Adaptation to the action of low temperature. Pathogenetic role of disadaptation to cold in the development of prenosological conditions in the conditions of the north Lyudmila Ivanovna Gerasimova
- 2036I will tell you about one of the most incredible, from the point of view of everyday ideas, practices - the practice of free adaptation to the cold.
According to generally accepted ideas, a person cannot be in the cold without warm clothes. The cold is absolutely fatal, and it is worth going out into the street without a jacket by the will of fate, as the unfortunate person is in for a painful freezing, and an inevitable bunch of diseases upon his return.
In other words, generally accepted ideas completely deny a person the ability to adapt to the cold. The comfort range is considered to be exclusively above room temperature.
Like you can't argue. You can't spend the whole winter in shorts and a T-shirt in Russia...
That's just the point, it's possible!!
No, not gritting your teeth, acquiring icicles to set a ridiculous record. And freely. Feeling, on average, even more comfortable than those around you. This is a real practical experience, crushingly breaking the generally accepted patterns.
It would seem, why own such practices? Yes, everything is very simple. New horizons always make life more interesting. Removing inspired fears, you become freer.
The range of comfort is vastly expanded. When the rest is either hot or cold, you feel good everywhere. Phobias disappear completely. Instead of the fear of getting sick, if you don’t dress warmly enough, you get complete freedom and self-confidence. It's really nice to run in the cold. If you go beyond your limits, then this does not entail any consequences.
How is this even possible? Everything is very simple. We are much better off than we think. And we have mechanisms that allow us to be free in the cold.
Firstly, with temperature fluctuations within certain limits, the metabolic rate, the properties of the skin, etc. change. In order not to dissipate heat, the outer contour of the body greatly reduces the temperature, while the core temperature remains very stable. (Yes, cold paws are normal!! No matter how we were convinced in childhood, this is not a sign of freezing!)
With an even greater cold load, specific mechanisms of thermogenesis are activated. We know about contractile thermogenesis, in other words, shivering. The mechanism is, in fact, an emergency. Trembling warms, but it turns on not from a good life, but when you really get cold.
But there is also non-shivering thermogenesis, which produces heat through the direct oxidation of nutrients in the mitochondria directly into heat. In the circle of people practicing cold practices, this mechanism was simply called the "stove". When the "stove" is switched on, heat is produced in the background in an amount sufficient for a long stay in the cold without clothes.
Subjectively, it feels rather unusual. In Russian, the word "cold" refers to two fundamentally different sensations: "it's cold outside" and "it's cold for you." They may be present independently. You can freeze in a fairly warm room. And you can feel the skin burning cold outside, but not freeze at all and not experience discomfort. Moreover, it's nice.
How can one learn to use these mechanisms? I will say emphatically that I consider “learning by article” risky. Technology must be handed over personally.
Non-contractile thermogenesis starts in fairly severe frost. And turning it on is quite inertial. The "stove" starts working not earlier than in a few minutes. Therefore, paradoxically, learning to walk freely in the cold is much easier in severe frost than on a cool autumn day.
It is worth going out into the cold, as you begin to feel the cold. An inexperienced person is seized with panic horror. It seems to him that if it is already cold now, then in ten minutes there will be a full paragraph. Many simply do not wait for the "reactor" to enter the operating mode.
When the “stove” nevertheless starts up, it becomes clear that, contrary to expectations, it is quite comfortable to be in the cold. This experience is useful in that it immediately breaks the patterns instilled in childhood about the impossibility of this, and helps to look at reality in a different way as a whole.
For the first time, you need to go out into the cold under the guidance of a person who already knows how to do it, or where you can return to warmth at any time!
And you have to go out naked. Shorts, better even without a T-shirt and nothing else. The body needs to be properly frightened so that it turns on the forgotten adaptation systems. If you get scared and put on a sweater, trowel, or something similar, then the heat loss will be enough to freeze very hard, but the "reactor" will not start!
For the same reason, gradual "hardening" is dangerous. Dropping the temperature of the air or bath "by one degree in ten days" leads to the fact that sooner or later there comes a moment when it is already cold enough to get sick, but not enough to trigger thermogenesis. Truly, only iron people can withstand such hardening. But almost everyone can immediately go out into the cold or dive into the hole.
After what has been said, one can already guess that adaptation not to frost, but to low positive temperatures is a more difficult task than jogging in frost, and it requires more highly trained. The "stove" at +10 does not turn on at all, and only non-specific mechanisms work.
It should be remembered that severe discomfort cannot be tolerated. When everything goes right, no hypothermia develops. If you start to feel very cold, then you need to stop the practice. Periodic exits beyond the limits of comfort are inevitable (otherwise, these limits cannot be pushed), but extreme should not be allowed to grow into pipets.
The heating system eventually gets tired of working under load. Endurance limits are very far. But they are. You can freely walk at -10 all day, and at -20 for a couple of hours. But it will not work to go skiing in one T-shirt. (Field conditions are generally a separate issue. In winter, you can’t save on clothes taken with you on a hike! You can put it in a backpack, but you can’t forget it at home. In snowless times, you can risk leaving extra things at home that are taken only because of fear of weather, but if you have experience)
For greater comfort, it is better to walk like this in more or less clean air, away from sources of smoke and smog - sensitivity to what we breathe in this state increases significantly. It is clear that practice is generally incompatible with smoking and booze.
Being in the cold can cause cold euphoria. The feeling is pleasant, but requires the utmost self-control, in order to avoid the loss of adequacy. This is one of the reasons why it is highly undesirable to start a practice without a teacher.
Another important nuance is a long reboot of the heating system after significant loads. Having caught the cold properly, you can feel pretty good, but when you enter a warm room, the “stove” turns off, and the body begins to warm up with a shiver. If at the same time you go out into the cold again, the “stove” will not turn on, and you can freeze very much.
Finally, you need to understand that the possession of practice does not guarantee not to freeze anywhere and never. The state changes, and many factors influence. But, the likelihood of getting into trouble from the weather is still reduced. Just as the probability of being physically blown away by an athlete is in any way lower than that of a squishy one.
Alas, it was not possible to create a complete article. I only outlined this practice in general terms (more precisely, a set of practices, because diving into an ice hole, jogging in a T-shirt in the cold and wandering through the forest in the style of Mowgli are different). Let me summarize what I started with. Owning your own resources allows you to get rid of fears, and feel much more comfortable. And it's interesting.
In the previous chapter, general (i.e., non-specific) patterns of adaptation were analyzed, but the human body responds in relation to specific factors and specific adaptive reactions. It is these reactions of adaptation (to temperature change, to a different mode of physical activity, to weightlessness, to hypoxia, to a lack of information, to psychogenic factors, as well as the features of human adaptation and adaptation management) that are considered in this chapter.
ADAPTATION TO TEMPERATURE CHANGES
The temperature of the human body, like that of any homoiothermic organism, is characterized by constancy and fluctuates within extremely narrow limits. These limits range from 36.4 ?C to 37.5 ?C.
Adaptation to the action of low temperature
The conditions under which the human body must adapt to the cold may be different. This can be work in cold shops (cold does not act around the clock, but alternating with normal temperature conditions) or adaptation to life in northern latitudes (a person in the conditions of the North is exposed not only to low temperatures, but also to a changed lighting regime and radiation level).
Work in cold shops. In the first days, in response to low temperatures, heat production increases uneconomically, excessively, and heat transfer is still insufficiently limited. After the establishment of the stable adaptation phase, the processes of heat production are intensified, heat transfers are reduced; eventually an optimal balance is established to maintain a stable body temperature.
Adaptation to the conditions of the North is characterized by an unbalanced combination of heat production and heat transfer. The decrease in heat transfer efficiency is achieved by reducing
and the cessation of sweating, narrowing of the arterial vessels of the skin and muscles. Activation of heat production is initially carried out by increasing blood flow in the internal organs and increasing muscle contractile thermogenesis. emergency stage. An obligatory component of the adaptive process is the inclusion of a stress response (activation of the central nervous system, an increase in the electrical activity of thermoregulation centers, an increase in the secretion of liberins in hypothalamic neurons, in pituitary adenocytes - adrenocorticotropic and thyroid-stimulating hormones, in the thyroid gland - thyroid hormones, in the adrenal medulla - catecholamines, and in their cortex - corticosteroids). These changes significantly modify the function of organs and physiological systems of the body, changes in which are aimed at increasing the oxygen transport function (Fig. 3-1).
Rice. 3-1.Ensuring the oxygen transport function during adaptation to cold
Persistent adaptation accompanied by an increase in lipid metabolism. The content of fatty acids in the blood increases and the level of sugar decreases slightly, fatty acids are washed out from adipose tissue due to increased “deep” blood flow. In mitochondria adapted to the conditions of the North, there is a tendency to uncouple phosphorylation and oxidation, and oxidation becomes dominant. Moreover, there are relatively many free radicals in the tissues of the inhabitants of the North.
Cold water.The physical agent through which low temperature affects the body is most often air, but it can also be water. For example, when in cold water cooling of the body occurs faster than in air (water has a 4 times greater heat capacity and 25 times greater thermal conductivity than air). So, in water, the temperature of which is + 12? C, heat is lost 15 times more than in air at the same temperature.
Only at a water temperature of + 33- 35? C, the temperature sensations of people in it are considered comfortable and the time spent in it is not limited.
At a water temperature of + 29.4 ? C, people can stay in it for more than a day, but at a water temperature of + 23.8 ? C, this time is 8 hours and 20 minutes.
In water with a temperature below + 20 ? C, the phenomena of acute cooling quickly develop, and the time of safe stay in it is calculated in minutes.
A person's stay in water, the temperature of which is + 10-12 ? C, for 1 hour or less causes life-threatening conditions.
Staying in water at a temperature of + 1 ? C inevitably leads to death, and at + 2-5? C, after 10-15 minutes it causes life-threatening complications.
The time of safe stay in ice water is no more than 30 minutes, and in some cases people die after 5-10 minutes.
The body of a person immersed in water experiences significant overloads due to the need to maintain a constant temperature of the “core of the body” due to the high thermal conductivity of water and the absence of auxiliary mechanisms that provide thermal insulation of a person in the air (the thermal insulation of clothing decreases sharply due to its wetting, thin a layer of heated air near the skin). In cold water, only two mechanisms are left for a person to maintain a constant temperature of the "core of the body", namely: increasing heat production and limiting the flow of heat from the internal organs to the skin.
Limitation of heat transfer from the internal organs to the skin (and from the skin to the environment) is provided by peripheral vasoconstriction, which is most pronounced at the level of the skin, and intramuscular vasodilation, the degree of which depends on the localization of cooling. These vasomotor reactions, by redistributing the volume of blood towards the central organs, are able to maintain the temperature of the “core of the body”. At the same time, there is a decrease in plasma volume due to an increase in capillary permeability, glomerular filtration, and a decrease in tubular reabsorption.
The increase in heat production (chemical thermogenesis) occurs through increased muscle activity, the manifestation of which is shivering. At a water temperature of + 25 ?C, shivering occurs when the skin temperature drops to + 28 ?C. There are three successive phases in the development of this mechanism:
The initial decrease in the temperature of the "core";
Its sharp increase, sometimes exceeding the temperature of the “core of the body” before cooling;
Reducing to a level dependent on water temperature. In very cold water (below + 10 ? C) trembling begins very abruptly, very intense, combined with rapid shallow breathing and a feeling of compression of the chest.
Activation of chemical thermogenesis does not prevent cooling, but is considered as an "emergency" way to protect against cold. A drop in the temperature of the “core” of the human body below + 35 ° C indicates that the compensatory mechanisms of thermoregulation cannot cope with the destructive effect of low temperatures, and deep hypothermia of the body sets in. The resulting hypothermia changes all the most important vital functions of the body, as it slows down the rate of chemical reactions in cells. An inevitable factor accompanying hypothermia is hypoxia. The result of hypoxia are functional and structural disorders, which in the absence of the necessary treatment lead to death.
Hypoxia has a complex and diverse origin.
Circulatory hypoxia occurs due to bradycardia and peripheral circulatory disorders.
Hemodynamic hypoxia develops due to the displacement of the oxyhemoglobin dissociation curve to the left.
Hypoxic hypoxia occurs with inhibition of the respiratory center and convulsive contraction of the respiratory muscles.
Adaptation to the action of high temperature
High temperature can affect the human body in different situations (for example, at work, in case of fire, in combat and emergency conditions, in a bath). Adaptation mechanisms are aimed at increasing heat transfer and reducing heat production. As a result, body temperature (although rising) remains within the upper limit of the normal range. The manifestations of hyperthermia are largely determined by the ambient temperature.
When the external temperature rises to + 30-31 ? C, the skin arteries expand and blood flow increases in it, the temperature of the surface tissues increases. These changes are aimed at the release of excess heat by the body through convection, heat conduction and radiation, but as the ambient temperature rises, the effectiveness of these heat transfer mechanisms decreases.
At an external temperature of + 32-33? C and above, convection and radiation stop. Heat transfer by sweating and evaporation of moisture from the surface of the body and respiratory tract acquires leading importance. So, about 0.6 kcal of heat is lost from 1 ml of sweat.
In organs and functional systems during hyperthermia, characteristic shifts occur.
The sweat glands secrete kallikrein, which breaks down a,2-globulin. This leads to the formation of kallidin, bradykinin and other kinins in the blood. Kinins, in turn, provide twofold effects: expansion of the arterioles of the skin and subcutaneous tissue; potentiation of perspiration. These effects of kinins significantly increase the body's heat transfer.
In connection with the activation of the sympathoadrenal system, the heart rate and minute output of the heart increase.
There is a redistribution of blood flow with the development of its centralization.
There is a tendency to increase blood pressure.
In the future, the adaptation is due to a decrease in heat production and the formation of a stable redistribution of the blood filling of the vessels. Excessive sweating turns into adequate at high temperatures. The loss of water and salts through sweat can be compensated by drinking salted water.
ADAPTATION TO THE MODE OF MOTOR ACTIVITY
Often, under the influence of any requirements of the external environment, the level of physical activity changes in the direction of its increase or decrease.
Increased activity
If physical activity becomes high by necessity, then the human body must adapt to a new
condition (for example, to hard physical work, sports, etc.). Distinguish between "urgent" and "long-term" adaptation to increased physical activity.
"Urgent" adaptation - the initial, emergency stage of adaptation - is characterized by maximum mobilization of the functional system responsible for adaptation, pronounced stress reaction and motor excitation.
In response to the load, an intense irradiation of excitation occurs in the cortical, subcortical and underlying motor centers, leading to a generalized, but insufficiently coordinated motor reaction. For example, the heart rate increases, but there is also a generalized inclusion of "extra" muscles.
Excitation of the nervous system leads to the activation of stress-realizing systems: adrenergic, hypothalamic-pituitary-adrenocortical, which is accompanied by a significant release of catecholamines, corticoliberin, ACTH and somatotropic hormones. On the contrary, the concentration of insulin and C-peptide in the blood decreases under the influence of exercise.
Stress-realizing systems. Changes in the metabolism of hormones during a stress reaction (especially catecholamines and corticosteroids) lead to the mobilization of the body's energy resources; potentiate the activity of the functional system of adaptation and form the structural basis of long-term adaptation.
stress-limiting systems. Simultaneously with the activation of stress-realizing systems, there is an activation of stress-limiting systems - opioid peptides, serotonergic and others. For example, in parallel with an increase in the content of ACTH in the blood, an increase in the concentration in the blood β endorphins and enkephalins.
Neurohumoral restructuring during urgent adaptation to physical activity provides activation of synthesis nucleic acids and proteins, selective growth of certain structures in the cells of organs, an increase in the power and efficiency of the activity of the functional adaptation system during repeated physical exertion.
With repeated physical exertion, muscle mass increases and its energy supply increases. Along with the
there are changes in the oxygen transport system and the effectiveness of the functions of external respiration and myocardium:
The density of capillaries in skeletal muscles and myocardium increases;
The speed and amplitude of contraction of the respiratory muscles increase, the vital capacity of the lungs (VC), maximum ventilation, oxygen utilization coefficient increase;
Myocardial hypertrophy occurs, the number and density of coronary capillaries increases, the concentration of myoglobin in the myocardium increases;
The number of mitochondria in the myocardium and the energy supply of the contractile function of the heart increase; the rate of contraction and relaxation of the heart increases during exercise, the stroke and minute volumes increase.
As a result, the volume of the function comes in line with the volume of the organ structure, and the body as a whole becomes adapted to the load of this magnitude.
Reduced activity
Hypokinesia (limitation of motor activity) causes a characteristic symptom complex of disorders that significantly limit a person's working capacity. The most characteristic manifestations of hypokinesia:
Violation of the regulation of blood circulation during orthostatic effects;
Deterioration of indicators of efficiency of work and regulation of the oxygen regime of the body at rest and during physical exertion;
The phenomena of relative dehydration, violations of isoosmia, chemistry and tissue structure, impaired renal function;
Atrophy of muscle tissue, impaired tone and function of the neuromuscular apparatus;
Decrease in the volume of circulating blood, plasma and mass of red blood cells;
Violation of the motor and enzymatic functions of the digestive apparatus;
Violation of indicators of natural immunity.
emergencythe phase of adaptation to hypokinesia is characterized by the mobilization of reactions that compensate for the lack of motor functions. Such protective reactions include the excitation of sympathetic
adrenal system. The sympathetic-adrenal system causes temporary, partial compensation of circulatory disorders in the form of increased cardiac activity, increased vascular tone and, consequently, blood pressure, increased respiration (increased ventilation of the lungs). However, these reactions are short-lived and quickly fade with continued hypokinesia.
The further development of hypokinesia can be imagined as follows:
Immobility contributes, first of all, to the reduction of catabolic processes;
The release of energy decreases, the intensity of oxidative reactions decreases;
In the blood, the content of carbon dioxide, lactic acid and other metabolic products, which normally stimulate respiration and blood circulation, decreases.
Unlike adaptation to a changed gas composition, low ambient temperature, etc., adaptation to absolute hypokinesia cannot be considered complete. Instead of the resistance phase, there is a slow depletion of all functions.
ADAPTATION TO WEIGHTLESSNESS
Man is born, grows and develops under the influence of gravity. The force of attraction forms the functions of skeletal muscles, gravitational reflexes, and coordinated muscular work. When gravity changes in the body, various changes are observed, determined by the elimination of hydrostatic pressure and the redistribution of body fluids, the elimination of gravity-dependent deformation and mechanical stress of body structures, as well as a decrease in the functional load on the musculoskeletal system, the elimination of support, and a change in the biomechanics of movements. As a result, a hypogravitational motor syndrome is formed, which includes changes in sensory systems, motor control, muscle function, and hemodynamics.
Sensory systems:
Decreased level of reference afferentation;
Decrease in the level of proprioceptive activity;
Change in the function of the vestibular apparatus;
Change in the afferent supply of motor reactions;
Disorder of all forms of visual tracking;
Functional changes in the activity of the otolithic apparatus with a change in the position of the head and the action of linear accelerations.
Motor control:
Sensory and motor ataxia;
spinal hyperreflexia;
Changing the motion control strategy;
Increasing the tone of the flexor muscles.
Muscles:
Decreased speed-strength properties;
Atony;
Atrophy, change in the composition of muscle fibers.
Hemodynamic disorders:
Increased cardiac output;
Decreased secretion of vasopressin and renin;
Increased secretion of natriuretic factor;
Increased renal blood flow;
Decreased blood plasma volume.
The possibility of true adaptation to weightlessness, in which the regulation system is restructured, adequate to existence on Earth, is hypothetical and requires scientific confirmation.
ADAPTATION TO HYPOXIA
Hypoxia is a condition resulting from insufficient oxygen supply to tissues. Hypoxia is often combined with hypoxemia - a decrease in the level of tension and oxygen content in the blood. There are exogenous and endogenous hypoxia.
Exogenous types of hypoxia - normo- and hypobaric. The reason for their development: a decrease in the partial pressure of oxygen in the air entering the body.
Normobaric exogenous hypoxia is associated with the restriction of oxygen supply to the body with air at normal barometric pressure. Such conditions are formed when:
■ presence of people in a small and/or poorly ventilated space (room, shaft, well, elevator);
■ violations of air regeneration and/or supply of oxygen mixture for breathing in aircraft and submersible vehicles;
■ non-compliance with the technique of artificial lung ventilation. - Hypobaric exogenous hypoxia may occur:
■ when climbing mountains;
■ in people raised to great heights in open aircraft, on lift chairs, as well as when the pressure in the pressure chamber is reduced;
■ with a sharp drop in barometric pressure.
Endogenous hypoxia are the result of pathological processes of various etiologies.
There are acute and chronic hypoxia.
Acute hypoxia occurs with a sharp decrease in the access of oxygen to the body: when the subject is placed in a pressure chamber, from which air is pumped out, carbon monoxide poisoning, acute circulatory or respiratory disorders.
Chronic hypoxia occurs after a long stay in the mountains or in any other conditions of insufficient oxygen supply.
Hypoxia is a universal operating factor, to which effective adaptive mechanisms have been developed in the body over many centuries of evolution. The reaction of the body to hypoxic exposure can be considered on the model of hypoxia when climbing mountains.
The first compensatory reaction to hypoxia is an increase in heart rate, stroke and minute blood volumes. If the human body consumes 300 ml of oxygen per minute at rest, its content in the inhaled air (and, consequently, in the blood) has decreased by 1/3, it is enough to increase the minute volume of blood by 30% so that the same amount of oxygen is delivered to the tissues . The opening of additional capillaries in tissues realizes an increase in blood flow, since this increases the rate of oxygen diffusion.
There is a slight increase in the intensity of breathing, shortness of breath occurs only with pronounced degrees of oxygen starvation (pO 2 in the inhaled air is less than 81 mm Hg). This is explained by the fact that increased respiration in a hypoxic atmosphere is accompanied by hypocapnia, which inhibits an increase in pulmonary ventilation, and only
after a certain time (1-2 weeks) of staying in hypoxia, there is a significant increase in pulmonary ventilation due to an increase in the sensitivity of the respiratory center to carbon dioxide.
The number of erythrocytes and the concentration of hemoglobin in the blood increase due to the emptying of blood depots and thickening of the blood, and then due to the intensification of hematopoiesis. Decrease in atmospheric pressure by 100 mm Hg. causes an increase in hemoglobin in the blood by 10%.
The oxygen transport properties of hemoglobin change, the shift of the oxyhemoglobin dissociation curve to the right increases, which contributes to a more complete return of oxygen to the tissues.
In cells, the number of mitochondria increases, the content of respiratory chain enzymes increases, which makes it possible to intensify the processes of energy use in the cell.
Behavior modification occurs (limitation of motor activity, avoidance of exposure to high temperatures).
Thus, as a result of the action of all links of the neurohumoral system, structural and functional rearrangements occur in the body, as a result of which adaptive reactions to this extreme impact are formed.
PSYCHOGENIC FACTORS AND DEFICIENCY OF INFORMATION
Adaptation to the effects of psychogenic factors proceeds differently in individuals with different types of GNI (choleric, sanguine, phlegmatic, melancholic). In extreme types (cholerics, melancholics), such adaptation is not stable, sooner or later the factors affecting the psyche lead to a breakdown of the GNA and the development of neuroses.
The following are the main principles of anti-stress protection:
Isolation from the stressor;
Activation of stress-limiting systems;
Suppression of the focus of increased excitation in the central nervous system by creating a new dominant (switching attention);
Suppression of the negative reinforcement system associated with negative emotions;
Activation of the positive reinforcement system;
Restoration of the body's energy resources;
Physiological relaxation.
Information stress
One of the types of psychological stress is informational stress. The problem of information stress is a problem of the 21st century. If the flow of information exceeds the possibilities of the brain formed in the process of evolution for its processing, information stress develops. The consequences of information overload are so great that even new terms are introduced to denote not entirely clear states of the human body: chronic fatigue syndrome, computer addiction, etc.
Adapting to information scarcity
The brain needs not only minimal rest, but also some amount of excitement (emotionally meaningful stimuli). G. Selye describes this state as a state of eustress. The consequences of a lack of information include a lack of emotionally significant stimuli and growing fear.
The lack of emotionally significant stimuli, especially at an early age (sensory deprivation), often leads to the formation of the personality of the aggressor, and the significance of this factor in the formation of aggressiveness is an order of magnitude higher than physical punishment and other harmful educational factors.
In conditions of sensory isolation, a person begins to experience growing fear up to panic and hallucinations. E. Fromm calls the presence of a sense of unity as one of the most important conditions for the maturation of an individual. E. Erickson believes that a person needs to identify himself with other people (reference group), nation, etc., that is, say "I am like them, they are the same as me." It is preferable for a person to identify himself even with such subcultures as hippies or drug addicts than not to identify himself at all.
sensory deprivation (from lat. sensus feeling, feeling and deprivatio- deprivation) - prolonged, more or less complete deprivation of a person of visual, auditory, tactile or other sensations, mobility, communication, emotional experiences, carried out either for experimental purposes or as a result of
the current situation. With sensory deprivation, in response to the lack of afferent information, processes are activated that in a certain way affect figurative memory.
As the time spent in these conditions increases, people develop emotional lability with a shift towards low mood (lethargy, depression, apathy), which for a short time are replaced by euphoria, irritability.
There are memory impairments that are directly dependent on the cyclical nature of emotional states.
The rhythm of sleep and wakefulness is disturbed, hypnotic states develop, which drag on for a relatively long time, are projected outward and are accompanied by the illusion of involuntariness.
Thus, the restriction of movement and information are factors that violate the conditions for the development of the organism, leading to the degradation of the corresponding functions. Adaptation in relation to these factors is not of a compensatory nature, since typical features of active adaptation do not appear in it, and only reactions associated with a decrease in functions and ultimately leading to pathology predominate.
FEATURES OF ADAPTATION IN HUMANS
The features of human adaptation include a combination of the development of the physiological adaptive properties of the organism with artificial methods that transform the environment in its interests.
Adaptation management
Ways to manage adaptation can be divided into socio-economic and physiological.
Socio-economic methods include all activities aimed at improving living conditions, nutrition, and creating a safe social environment. This group of events is extremely important.
Physiological methods of adaptation control are aimed at the formation of nonspecific resistance of the organism. These include the organization of the regime (change of sleep and wakefulness, rest and work), physical training, hardening.
Physical training. The most effective means of increasing the body's resistance to disease and adverse environmental influences are regular exercise. Motor activity affects many systems of life. It extends to the balance of metabolism, activates the vegetative systems: blood circulation, respiration.
hardening. There are measures aimed at increasing the body's resistance, united by the concept of "hardening". A classic example of hardening is constant cold training, water procedures, exercises in the open air in any weather.
The dosed use of hypoxia, in particular in the form of a training stay of a person at an altitude of about 2-2.5 thousand meters, increases the nonspecific resistance of the body. The hypoxic factor contributes to an increased release of oxygen to tissues, its high utilization in oxidative processes, the activation of enzymatic tissue reactions, and the economical use of the reserves of the cardiovascular and respiratory systems.
The stress response from the link of adaptation can, under excessively strong environmental influences, transform into a link of pathogenesis and induce the development of diseases - from ulcers to severe cardiovascular and immune diseases.
QUESTIONS FOR SELF-CHECKING
1. What is the adaptation to the action of low temperature?
2. What are the differences between the adaptation to the action of cold water.
3. Name the mechanism of adaptation to high temperature.
4. What is the adaptation to high physical activity?
5. What is the adaptation to low physical activity?
6. Is adaptation to weightlessness possible?
7. What is the difference between adaptation to acute hypoxia and adaptation to chronic hypoxia?
8. Why is sensory deprivation dangerous?
9. What are the features of human adaptation?
10. What ways of managing adaptation do you know?
I'll tell you about one of the most incredible, from the point of view of ordinary ideas, practices - the practice of free adaptation to the cold.
According to generally accepted ideas, a person cannot be in the cold without warm clothes. The cold is absolutely fatal, and it is worth going out into the street without a jacket by the will of fate, as the unfortunate person is in for a painful freezing, and an inevitable bunch of diseases upon his return.
In other words, generally accepted ideas completely deny a person the ability to adapt to the cold. The comfort range is considered to be exclusively above room temperature.
Like you can't argue. You can’t spend the whole winter in Russia in shorts and a T-shirt ...
That's just the point, it's possible!!
No, not gritting your teeth, acquiring icicles to set a ridiculous record. And freely. Feeling, on average, even more comfortable than those around you. This is a real practical experience, crushingly breaking the generally accepted patterns.
It would seem, why own such practices? Yes, everything is very simple. New horizons always make life more interesting. Removing inspired fears, you become freer.
The range of comfort is vastly expanded. When the rest is either hot or cold, you feel good everywhere. Phobias disappear completely. Instead of the fear of getting sick, if you don’t dress warmly enough, you get complete freedom and self-confidence. It's really nice to run in the cold. If you go beyond your limits, then this does not entail any consequences.
How is this even possible? Everything is very simple. We are much better off than we think. And we have mechanisms that allow us to be free in the cold.
Firstly, with temperature fluctuations within certain limits, the metabolic rate, the properties of the skin, etc. change. In order not to dissipate heat, the outer contour of the body greatly reduces the temperature, while the core temperature remains very stable. (Yes, cold paws are normal!! No matter how we were convinced in childhood, this is not a sign of freezing!)
With an even greater cold load, specific mechanisms of thermogenesis are activated. We know about contractile thermogenesis, in other words, shivering. The mechanism is, in fact, an emergency. Trembling warms, but it turns on not from a good life, but when you really get cold.
But there is also non-shivering thermogenesis, which produces heat through the direct oxidation of nutrients in the mitochondria directly into heat. In the circle of people practicing cold practices, this mechanism was simply called the "stove". When the "stove" is switched on, heat is produced in the background in an amount sufficient for a long stay in the cold without clothes.
Subjectively, it feels rather unusual. In Russian, the word "cold" refers to two fundamentally different sensations: "it's cold outside" and "it's cold for you." They may be present independently. You can freeze in a fairly warm room. And you can feel the skin burning cold outside, but not freeze at all and not experience discomfort. Moreover, it's nice.
How can one learn to use these mechanisms? I will say emphatically that I consider “learning by article” risky. Technology must be handed over personally.
Non-shivering thermogenesis starts in a fairly severe frost. And turning it on is quite inertial. The "stove" starts working not earlier than in a few minutes. Therefore, paradoxically, learning to walk freely in the cold is much easier in severe frost than on a cool autumn day.
It is worth going out into the cold, as you begin to feel the cold. An inexperienced person is seized with panic horror. It seems to him that if it is already cold now, then in ten minutes there will be a full paragraph. Many simply do not wait for the "reactor" to enter the operating mode.
When the “stove” nevertheless starts up, it becomes clear that, contrary to expectations, it is quite comfortable to be in the cold. This experience is useful in that it immediately breaks the patterns instilled in childhood about the impossibility of this, and helps to look at reality in a different way as a whole.
For the first time, you need to go out into the cold under the guidance of a person who already knows how to do it, or where you can return to warmth at any time!
And you have to go out naked. Shorts, better even without a T-shirt and nothing else. The body needs to be properly frightened so that it turns on the forgotten adaptation systems. If you get scared and put on a sweater, trowel, or something similar, then the heat loss will be enough to freeze very hard, but the "reactor" will not start!
For the same reason, gradual "hardening" is dangerous. Dropping the temperature of the air or bath "by one degree in ten days" leads to the fact that sooner or later there comes a moment when it is already cold enough to get sick, but not enough to trigger thermogenesis. Truly, only iron people can withstand such hardening. But almost everyone can immediately go out into the cold or dive into the hole.
After what has been said, one can already guess that adaptation not to frost, but to low positive temperatures is a more difficult task than jogging in frost, and it requires higher preparation. The "stove" at +10 does not turn on at all, and only non-specific mechanisms work.
It should be remembered that severe discomfort cannot be tolerated. When everything goes right, no hypothermia develops. If you start to feel very cold, then you need to stop the practice. Periodic exits beyond the limits of comfort are inevitable (otherwise, these limits cannot be pushed), but extreme should not be allowed to grow into pipets.
The heating system eventually gets tired of working under load. Endurance limits are very far. But they are. You can freely walk at -10 all day, and at -20 for a couple of hours. But it will not work to go skiing in one T-shirt. (Field conditions are generally a separate issue. In winter, you can’t save on clothes taken with you on a hike! You can put it in a backpack, but you can’t forget it at home. In snowless times, you can risk leaving extra things at home that are taken only because of fear of weather, but if you have experience)
For greater comfort, it is better to walk like this in more or less clean air, away from sources of smoke and from smog - sensitivity to what we breathe in this state increases significantly. It is clear that practice is generally incompatible with smoking and booze.
Being in the cold can cause cold euphoria. The feeling is pleasant, but requires the utmost self-control, in order to avoid the loss of adequacy. This is one of the reasons why it is highly undesirable to start a practice without a teacher.
Another important nuance is a long reboot of the heating system after significant loads. Having caught the cold properly, you can feel pretty good, but when you enter a warm room, the “stove” turns off, and the body begins to warm up with a shiver. If at the same time you go out into the cold again, the “stove” will not turn on, and you can freeze very much.
Finally, you need to understand that the possession of practice does not guarantee not to freeze anywhere and never. The state changes, and many factors influence. But, the probability of getting into trouble from the weather is still reduced. Just as the probability of being physically blown away by an athlete is in any way lower than that of a squishy one.
Alas, it was not possible to create a complete article. I only outlined this practice in general terms (more precisely, a set of practices, because diving into an ice hole, jogging in a T-shirt in the cold and wandering through the forest in the style of Mowgli are different). Let me summarize what I started with. Owning your own resources allows you to get rid of fears, and feel much more comfortable. And it's interesting.
Dmitry Kulikov
- Specialty HAC RF03.00.16
- Number of pages 101
CHAPTER 1. MODERN CONCEPTS ON THE MECHANISM OF ADAPTATION OF THE ORGANISM TO COLD AND TOCOPHEROL DEFICIENCY.
1.1 New ideas about the biological functions of reactive oxygen species during adaptive transformations of metabolism.
1.2 Mechanisms of body adaptation to cold and the role of oxidative stress in this process.
1.3 Mechanisms of adaptation of the body to tocopherol deficiency and the role of oxidative stress in this process.
CHAPTER 2. MATERIAL AND RESEARCH METHODS.
2.1 Organization of the study.
2.1.1 Organization of experiments on the influence of cold.
2.1.2 Organization of experiments on the effect of tocopherol deficiency.
2.2 Research methods
2.2.1 Hematological parameters
2.2.2 Study of energy metabolism.
2.2.3 Study of oxidative metabolism.
2.3 Statistical processing of results.
CHAPTER 3. INVESTIGATION OF OXIDATIVE HOMEOSTASIS, BASIC MORPHOFUNCTIONAL PARAMETERS OF THE ORGANISM OF RATS AND ERYTHROCYTES UNDER LONG-TERM EXPOSURE TO COLD.
CHAPTER 4. INVESTIGATION OF OXIDATIVE HOMEOSTASIS, BASIC MORPHOFUNCTIONAL PARAMETERS OF THE ORGANISM OF RATS AND ERYTHROCYTES WITH LONG-TERM TOCOPHEROL DEFICIENCY.
Recommended list of dissertations
Physiological aspects of cellular and molecular patterns of adaptation of animal organisms to extreme situations 2013, Doctor of Biological Sciences Cherkesova, Dilara Ulubievna
Mechanisms of participation of tocopherol in adaptive transformations in the cold 2000, Doctor of Biological Sciences Kolosova, Natalia Gorislavovna
Features of the functioning of the hypothalamic-pituitary-reproductive system at the stages of ontogenesis and under the conditions of the use of geroprotectors 2010, Doctor of Biological Sciences Kozak, Mikhail Vladimirovich
Ecological and physiological aspects of the formation of adaptive mechanisms of mammals to hypothermia under experimental conditions 2005, candidate of biological sciences Solodovnikova, Olga Grigoryevna
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Introduction to the thesis (part of the abstract) on the topic "Experimental study of antioxidant enzyme systems during adaptation to prolonged exposure to cold and tocopherol deficiency"
Relevance of the topic. Research recent years It has been shown that the so-called reactive oxygen species, such as superoxide and hydroxyl radicals, hydrogen peroxide, and others, play an important role in the mechanisms of organism adaptation to environmental factors (Finkel, 1998; Kausalya and Nath, 1998). It has been established that these free-radical oxygen metabolites, which until recently were considered only as damaging agents, are signaling molecules and regulate adaptive transformations of the nervous system, arterial hemodynamics, and morphogenesis. (Luscher, Noll, Vanhoute, 1996; ; Groves, 1999; Wilder, 1998; Drexler, Homig, 1999). The main source of reactive oxygen species is a number of enzymatic systems of the epithelium and endothelium (NADP-oxidase, cyclooxygenase, lipoxygenase, xanthine oxidase), which are activated upon stimulation of chemo- and mechanoreceptors located on the luminal membrane of the cells of these tissues.
At the same time, it is known that with increased production and accumulation in the body of reactive oxygen species, that is, with the so-called oxidative stress, their physiological function can be transformed into a pathological one with the development of peroxidation of biopolymers and damage to cells and tissues as a result. (Kausalua & Nath 1998; Smith & Guilbelrt & Yui et al. 1999). Obviously, the possibility of such transformation is determined primarily by the rate of ROS inactivation by antioxidant systems. In this regard, of particular interest is the study of changes in reactive oxygen species inactivators - enzymatic antioxidant systems of the body, with prolonged exposure of the body to such extreme factors as cold and deficiency of the vitamin antioxidant - tocopherol, which are currently considered as endo- and exogenous inducers of oxidative stress.
Purpose and objectives of the study. The aim of the work was to study changes in the main enzymatic antioxidant systems during adaptation of rats to prolonged exposure to cold and tocopherol deficiency.
Research objectives:
1. To compare changes in indicators of oxidative homeostasis with changes in the main morphological and functional parameters of the body of rats and erythrocytes during prolonged exposure to cold.
2. To compare changes in indicators of oxidative homeostasis with changes in the main morphological and functional parameters of the body of rats and erythrocytes in tocopherol deficiency.
3. Carry out a comparative analysis of changes in oxidative metabolism and the nature of the adaptive reaction of the body of rats during prolonged exposure to cold and tocopherol deficiency.
Scientific novelty. It has been established for the first time that prolonged intermittent exposure to cold (+5°C for 8 hours a day for 6 months) causes a number of adaptive morphofunctional changes in the body of rats: acceleration of body weight gain, an increase in the content of spectrin and actin in erythrocyte membranes , increased activity of key enzymes of glycolysis, the concentration of ATP and ADP, as well as the activity of ATPases.
For the first time, it has been shown that oxidative stress plays an important role in the mechanism of development of adaptation to cold, a feature of which is an increase in the activity of the components of the antioxidant system - enzymes of the NADPH-generating pentose phosphate pathway of glucose breakdown, superoxide dismutase, catalase, and glutathione pyroxidase.
It has been shown for the first time that the development of pathological morphological and functional changes in tocopherol deficiency is associated with severe oxidative stress occurring against the background of reduced activity of the main antioxidant enzymes and enzymes of the pentose phosphate pathway of glucose breakdown.
It was established for the first time that the result of metabolic transformations under the influence of environmental factors on the body depends on the adaptive increase in the activity of antioxidant enzymes and the associated severity of oxidative stress.
Scientific and practical significance of the work. The new facts obtained in the work expand the understanding of the mechanisms of adaptation of the body to environmental factors. The dependence of the result of adaptive transformations of metabolism on the degree of activation of the main enzymatic antioxidants was revealed, which indicates the need for directed development of the adaptive potential of this non-specific system of stress resistance of the body under changing environmental conditions.
The main provisions for defense:
1. Prolonged exposure to cold causes a complex of changes in the adaptive direction in the body of rats: an increase in resistance to the action of cold, which was expressed in the weakening of hypothermia; acceleration of body weight gain; increase in the content of spectrin and actin in erythrocyte membranes; an increase in the rate of glycolysis, an increase in the concentration of ATP and ADP; an increase in the activity of ATPases. The mechanism of these changes is associated with the development of oxidative stress in combination with an adaptive increase in the activity of the components of the antioxidant defense system - pentose-phosphate shunt enzymes, as well as the main intracellular antioxidant enzymes, primarily superoxide dismutase.
2. A long-term deficiency of tocopherol in the body of rats causes a persistent hypotrophic effect, damage to erythrocyte membranes, inhibition of glycolysis, a decrease in the concentration of ATP and ADP, and the activity of cellular ATPases. In the mechanism of development of these changes, insufficient activation of antioxidant systems - the NADPH-generating pentose-phosphate pathway and antioxidant enzymes, which creates conditions for the damaging effect of reactive oxygen species, is essential.
Approbation of work. The research results were reported at a joint meeting of the Department of Biochemistry and the Department of Normal Physiology of the Altai State Medical Institute (Barnaul, 1998, 2000), at a scientific conference dedicated to the 40th anniversary of the Department of Pharmacology of the Altai State medical university(Barnaul, 1997), at the scientific-practical conference "Modern problems of balneology and therapy", dedicated to the 55th anniversary of the sanatorium "Barnaul" (Barnaul, 2000), at the II International Conference of Young Scientists of Russia (Moscow, 2001).
Similar theses in the specialty "Ecology", 03.00.16 VAK code
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Biochemical changes in mammalian membranes during hibernation and hypothermia 2005, Doctor of Biological Sciences Klichkhanov, Nisred Kadirovich
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Dissertation conclusion on the topic "Ecology", Skuryatina, Yulia Vladimirovna
1. Long-term intermittent exposure to cold (+5°C for 8 hours a day for 6 months) causes a complex of adaptive changes in the body of rats: dissipation of the hypothermic reaction to cold, acceleration of body weight gain, an increase in the content of spectrin and actin in erythrocyte membranes, increased glycolysis, an increase in the total concentration of ATP and ADP and the activity of ATPases.
2. The state of adaptation of rats to prolonged intermittent exposure to cold corresponds to oxidative stress, which is characterized by increased activity of the components of enzymatic antioxidant systems - glucose-6-phosphate dehydrogenase, superoxide dismutase, catalase and glutathione peroxidase.
3. Prolonged (6 months) alimentary deficiency of tocopherol causes a persistent hypotrophic effect in the body of rats, anemia, damage to erythrocyte membranes, inhibition of glycolysis in erythrocytes, a decrease in the total concentration of ATP and ADP, as well as the activity of Na+,K+-ATPase.
4. Disadaptive changes in the body of rats with tocopherol deficiency are associated with the development of pronounced oxidative stress, which is characterized by a decrease in the activity of catalase and glutathione peroxidase, combined with a moderate increase in the activity of glucose-6-phosphate dehydrogenase and superoxide dismutase.
5. The result of adaptive transformations of metabolism in response to prolonged exposure to cold and alimentary tocopherol deficiency depends on the severity of oxidative stress, which is largely determined by an increase in the activity of antioxidant enzymes.
CONCLUSION
To date, a fairly clear idea has developed that the adaptation of the human and animal organism is determined by the interaction of the genotype with external factors (Meyerson and Malyshev, 1981; Panin, 1983; Goldstein and Brown, 1993; Ado and Bochkov, 1994). At the same time, it should be taken into account that the genetically determined inadequacy of the inclusion of adaptive mechanisms under the influence of extreme factors can lead to the transformation of a state of tension into an acute or chronic pathological process (Kaznacheev, 1980).
The process of adaptation of the organism to new conditions of the internal and external environment is based on the mechanisms of urgent and long-term adaptation (Meyerson, Malyshev, 1981). At the same time, the process of urgent adaptation, considered as a temporary measure that the body resorts to in critical situations, has been studied in sufficient detail (Davis, 1960, 1963; Isahakyan, 1972; Tkachenko, 1975; Rohlfs, Daniel, Premont et al., 1995; Beattie, Black, Wood et al., 1996; Marmonier, Duchamp, Cohen-Adad et al., 1997). During this period, increased production of various signaling factors, including hormonal ones, induces a significant local and systemic restructuring of metabolism in various organs and tissues, which ultimately determines true, long-term adaptation (Khochachka and Somero, 1988). Activation of biosynthetic processes at the level of replication and transcription determines the structural changes that develop in this case, which are manifested by hypertrophy and hyperplasia of cells and organs (Meyerson, 1986). Therefore, the study of the biochemical foundations of adaptation to long-term exposure to disturbing factors is not only of scientific but also of great practical interest, especially from the point of view of the prevalence of maladaptive diseases (Lopez-Torres et al., 1993; Pipkin, 1995; Wallace and Bell, 1995; Sun et al. al., 1996).
Undoubtedly, the development of long-term adaptation of the body is a very complex process, which is realized with the participation of the entire complex of a hierarchically organized system of metabolism regulation, and many aspects of the mechanism of this regulation remain unknown. According to the latest literature data, the adaptation of the body to long-acting disturbing factors begins with local and systemic activation of the phylogenetically most ancient process of free radical oxidation, leading to the formation of physiologically important signaling molecules in the form of reactive oxygen and nitrogen species - nitric oxide, superoxide and hydroxyl. radical, hydrogen peroxide, etc. These metabolites play a leading mediator role in the adaptive local and systemic regulation of metabolism by autocrine and paracrine mechanisms (Sundaresan, Yu, Ferrans et. al., 1995; Finkel, 1998; Givertz, Colucci, 1998).
In this regard, when studying the physiological and pathophysiological aspects of adaptive and maladaptive reactions, the issues of regulation by free-radical metabolites are occupied, and the issues of biochemical adaptation mechanisms during prolonged exposure to oxidative stress inducers are of particular relevance (Cowan, Langille, 1996; Kemeny, Peakman, 1998; Farrace, Cenni, Tuozzi et al., 1999).
Undoubtedly, the greatest information in this regard can be obtained from experimental studies on the corresponding "models" of common types of oxidative stress. As such, the best known models are exogenous oxidative stress caused by cold exposure and endogenous oxidative stress arising from a deficiency of vitamin E, one of the most important membrane antioxidants. These models were used in this work to elucidate the biochemical foundations of the organism's adaptation to long-term oxidative stress.
In accordance with numerous literature data (Spirichev, Matusis, Bronstein, 1979; Aloia, Raison, 1989; Glofcheski, Borrelli, Stafford, Kruuv, 1993; Beattie, Black, Wood, Trayhurn, 1996), we found that the daily 8-hour cold exposure for 24 weeks led to a pronounced increase in the concentration of malondialdehyde in erythrocytes. This indicates the development of chronic oxidative stress under the influence of cold. Similar changes took place in the body of rats kept for the same period on a diet devoid of vitamin E. This fact is also consistent with the observations of other researchers (Masugi,
Nakamura, 1976; Tamai., Miki, Mino, 1986; Archipenko, Konovalova, Dzhaparidze et al., 1988; Matsuo, Gomi, Dooley, 1992; Cai, Chen, Zhu et al., 1994). However, the causes of oxidative stress in long-term intermittent exposure to cold and oxidative stress in long-term tocopherol deficiency are different. If in the first case the cause of the stress state is the impact of an external factor - cold, which causes an increase in the production of oxyradicals due to the induction of the synthesis of an uncoupling protein in mitochondria (Nohl, 1994; Bhaumik, Srivastava, Selvamurthy et al., 1995; Rohlfs, Daniel, Premont et al. ., 1995; Beattie, Black, Wood et al., 1996; Femandez-Checa, Kaplowitz, Garcia-Ruiz et al., 1997; Marmonier, Duchamp, Cohen-Adad et al., 1997; Rauen, de Groot, 1998 ), then with a deficiency of the membrane antioxidant tocopherol, the cause of oxidative stress was a decrease in the rate of neutralization of oxyradical mediators (Lawler, Cline, He, Coast, 1997; Richter, 1997; Polyak, Xia, Zweier et. al., 1997; Sen, Atalay, Agren et al., 1997; Higashi, Sasaki, Sasaki et al., 1999). Given the fact that prolonged exposure to cold and vitamin E deficiency cause the accumulation of reactive oxygen species, one could expect the transformation of the physiological regulatory role of the latter into a pathological one, with cell damage due to peroxidation of biopolymers. In connection with the generally accepted idea until recently about the damaging effect of reactive oxygen species, cold and tocopherol deficiency are considered as factors provoking the development of many chronic diseases (Cadenas, Rojas, Perez-Campo et al., 1995; de Gritz, 1995; Jain, Wise , 1995; Luoma, Nayha, Sikkila, Hassi., 1995; Barja, Cadenas, Rojas et al., 1996; Dutta-Roy, 1996; Jacob, Burri, 1996; Snircova, Kucharska, Herichova et al., 1996; Va- Squezvivar, Santos, Junqueira, 1996; Cooke, Dzau, 1997; Lauren, Chaudhuri, 1997; Davidge, Ojimba, Mc Laughlin, 1998; Kemeny, Peakman, 1998; Peng, Kimura, Fregly, Phillips, 1998; Nath, Grande, Croatt et al., 1998; Newaz and Nawal, 1998; Taylor, 1998). Obviously, in the light of the concept of the mediator role of reactive oxygen species, the realization of the possibility of transforming physiological oxidative stress into pathological one largely depends on the adaptive increase in the activity of antioxidant enzymes. In accordance with the concept of an antioxidant enzyme complex as a functionally dynamic system, there is a recently discovered phenomenon of substrate induction of gene expression of all three major antioxidant enzymes - superoxide dismutase, catalase, and glutathione peroxidase (Peskin, 1997; Tate, Miceli, Newsome, 1995; Pinkus, Weiner, Daniel, 1996; Watson, Palmer. , Jauniaux et al., 1997; Sugino, Hirosawa-Takamori, Zhong 1998). It is important to note that the effect of such induction has a fairly long lag period, measured in tens of hours and even days (Beattie, Black, Wood, Trayhurn, 1996; Battersby, Moyes, 1998; Lin, Coughlin, Pilch, 1998). Therefore, this phenomenon can lead to an acceleration of the inactivation of reactive oxygen species only under prolonged exposure to stress factors.
The studies carried out in the work showed that long-term intermittent exposure to cold caused a harmonious activation of all the studied antioxidant enzymes. This is consistent with the opinion of Bhaumik G. et al (1995) on the protective role of these enzymes in limiting complications during prolonged cold stress.
At the same time, only superoxide dismutase activation was recorded in the erythrocytes of vitamin E-deficient rats at the end of the 24-week observation period. It should be noted that such an effect was not observed in previous similar studies (Xu, Diplock, 1983; Chow, 1992; Matsuo, Gomi, Dooley, 1992; Walsh, Kennedy, Goodall, Kennedy, 1993; Cai, Chen, Zhu et al. , 1994; Tiidus, Houston, 1994; Ashour, Salem, El Gadban et al., 1999). However, it should be noted that the increase in the activity of superoxide dismutase was not accompanied by an adequate increase in the activity of catalase and glutathione peroxidase and did not prevent the development of the damaging effect of reactive oxygen species. The latter was evidenced by a significant accumulation in erythrocytes of the product of lipid peroxidation - malonidialdehyde. It should be noted that the peroxidation of biopolymers is currently considered as the main cause of pathological changes in avitaminosis E (Chow, Ibrahim, Wei and Chan, 1999).
The effectiveness of antioxidant protection in experiments on the study of cold exposure was evidenced by the absence of pronounced changes in hematological parameters and the preservation of erythrocyte resistance to the action of various hemolytics. Similar results were previously reported by other researchers (Marachev, 1979; Rapoport, 1979; Sun, Cade, Katovich, Fregly, 1999). On the contrary, in animals with E-avitaminosis, a complex of changes was observed indicating the damaging effect of reactive oxygen species: anemia with intravascular hemolysis, the appearance of erythrocytes with reduced resistance to hemolytics. The latter is considered a very characteristic manifestation of oxidative stress in E-avitaminosis (Brin, Horn, Barker, 1974; Gross, Landaw, Oski, 1977; Machlin, Filipski, Nelson et al., 1977; Siddons, Mills, 1981; Wang, Huang, Chow, 1996). The foregoing convinces of the body's significant capabilities to neutralize the consequences of oxidative stress of external origin, in particular, caused by cold, and the inferiority of adaptation to endogenous oxidative stress in the case of E-avitaminosis.
The group of antioxidant factors in erythrocytes also includes the NADPH generation system, which is a cofactor for heme oxygenase, glutathione reductase, and thioredoxin reductase, which reduce iron, glutathione, and other thio compounds. In our experiments, a very significant increase in the activity of glucose-6-phosphate dehydrogenase in rat erythrocytes was observed both under the influence of cold and with tocopherol deficiency, which was previously observed by other researchers (Kaznacheev, 1977; Ulasevich, Grozina, 1978;
Gonpern, 1979; Kulikov, Lyakhovich, 1980; Landyshev, 1980; Fudge, Stevens, Ballantyne, 1997). This indicates activation in experimental animals of the pentose phosphate shunt, in which NADPH is synthesized.
The mechanism of development of the observed effect becomes clearer in many respects when analyzing changes in carbohydrate metabolism parameters. An increase in glucose uptake by erythrocytes of animals was observed both against the background of oxidative stress caused by cold and during oxidative stress induced by tocopherol deficiency. This was accompanied by a significant activation of membrane hexokinase, the first enzyme of intracellular carbohydrate utilization, which is in good agreement with the data of other researchers (Lyakh, 1974, 1975; Panin, 1978; Ulasevich, Grozina, 1978; Nakamura, Moriya, Murakoshi. et al., 1997; Rodnick , Sidell, 1997). However, further transformations of glucose-6-phosphate, which was intensively formed in these cases, differed significantly. Upon adaptation to cold, the metabolism of this intermediate increased both in glycolysis (as evidenced by an increase in the activity of hexophosphate isomerase and aldolase) and in the pentose phosphate pathway. The latter was confirmed by an increase in the activity of glucose-6-phosphate dehydrogenase. At the same time, in E-avitaminous animals, the rearrangement of carbohydrate metabolism was associated with an increase in the activity of only glucose-6-phosphate dehydrogenase, while the activity of key glycolysis enzymes did not change or even decreased. Therefore, in any case, oxidative stress causes an increase in the rate of glucose metabolism in the pentose phosphate shunt, which ensures the synthesis of NADPH. This seems to be very appropriate in the context of increasing cell demand for redox equivalents, in particular NADPH. It can be assumed that in E-avitaminous animals this phenomenon develops to the detriment of glycolytic energy-producing processes.
The noted difference in the effects of exogenous and endogenous oxidative stress on glycolytic energy production also affected the energy status of cells, as well as energy consumption systems. Under cold exposure, there was a significant increase in the concentration of ATP + ADP with a decrease in the concentration of inorganic phosphate, an increase in the activity of total ATP-ase, Mg-ATP-ase and Na+,K+-ATP-ase. Conversely, in the erythrocytes of rats with E-avitaminosis, a decrease in the content of macroergs and ATPase activity was observed. At the same time, the calculated ATP + ADP / Pn index confirmed the available information that for cold, but not for E-avitaminous oxidative stress, the prevalence of energy production over energy consumption is characteristic (Marachev, Sorokovoy, Korchev et al., 1983; Rodnick, Sidell, 1997; Hardewig, Van Dijk, Portner, 1998).
Thus, with prolonged intermittent exposure to cold, the restructuring of the processes of energy production and energy consumption in the animal body had a clear anabolic character. This is confirmed by the observed acceleration of the increase in body weight of animals. The disappearance of the hypothermic reaction to cold in rats by the 8th week of the experiment indicates a stable adaptation of their organism to cold and, consequently, the adequacy of adaptive metabolic transformations. At the same time, judging by the main morphofunctional, hematological, and biochemical parameters, changes in energy metabolism in E-avitaminous rats did not lead to an adaptively appropriate result. It seems that the main reason for such an organism's response to tocopherol deficiency is the outflow of glucose from energy-producing processes into the processes of formation of the endogenous antioxidant NADPH. It is likely that the severity of adaptive oxidative stress is a kind of regulator of glucose metabolism in the body: this factor is able to turn on and enhance the production of antioxidants during glucose metabolism, which is more significant for the survival of the body under conditions of a powerful damaging effect of reactive oxygen species than the production of macroergs.
It should be noted that, according to modern data, oxygen radicals are inducers of the synthesis of individual replication and transcription factors that stimulate adaptive proliferation and differentiation of cells in various organs and tissues (Agani and Semenza, 1998). At the same time, one of the most important targets for free radical mediators are transcription factors of the NFkB type, which induce the expression of genes for antioxidant enzymes and other adaptive proteins (Sundaresan, Yu, Ferrans et. al, 1995; Finkel, 1998; Givertz, Colucci, 1998). Thus, one can think that it is this mechanism that is activated during cold-induced oxidative stress and provides an increase in the activity of not only specific antioxidant defense enzymes (superoxide dismutase, catalase, and glutathione peroxidase), but also an increase in the activity of enzymes of the pentose phosphate pathway. With a more pronounced oxidative stress caused by a deficiency of the membrane antioxidant tocopherol, the adaptive substrate inducibility of these components of the antioxidant defense is realized only partially and, most likely, is not effective enough. It should be noted that the low efficiency of this system ultimately led to the transformation of physiological oxidative stress into pathological.
The data obtained in the work allow us to conclude that the result of adaptive transformations of metabolism in response to disturbing environmental factors, in the development of which reactive oxygen species are involved, is largely determined by the adequacy of the associated increase in the activity of the main antioxidant enzymes, as well as enzymes of the NADPH-generating pentose phosphate pathway. breakdown of glucose. In this regard, when the conditions for the existence of a macroorganism change, especially during the so-called environmental disasters, the severity of oxidative stress and the activity of enzymatic antioxidants should become not only an object of observation, but also one of the criteria for the effectiveness of the body's adaptation.
List of references for dissertation research candidate of biological sciences Skuryatina, Yulia Vladimirovna, 2001
1. Abrarov A.A. Effect of fat and fat-soluble vitamins A, D, E on the biological properties of erythrocytes: Diss. doc. honey. Sciences. M., 1971.- S. 379.
2. Ado A. D., Ado N. A., Bochkov G. V. Pathological physiology.- Tomsk: Publishing House of TSU, 1994.- P. 19.
3. Asatiani V. S. Enzymatic methods of analysis. M.: Nauka, 1969. - 740 p.
4. Benisovich V. I., Idelson L. I. Formation of peroxides and composition of fatty acids in erythrocyte lipids of patients with Marchiafava Micheli’s disease // Probl. hematol. and transfusion, blood. - 1973. - No. 11. - S. 3-11.
5. Bobyrev VN, Voskresensky ON Changes in the activity of antioxidant enzymes in lipid peroxidation syndrome in rabbits // Vopr. honey. chemistry. 1982. - Vol. 28(2). - S. 75-78.
6. Viru A. A. Hormonal mechanisms of adaptation and training. M.: Nauka, 1981.-S. 155.
7. Goldstein D. L., Brown M. S. Genetic aspects of diseases // Internal diseases / Under. ed. E. Braunwald, K. D. Isselbacher, R. G. Petersdorf and others - M .: Medicine, 1993.- T. 2.- P. 135.
8. Datsenko Z. M., Donchenko G. V., Shakhman O. V., Gubchenko K. M., Khmel T. O. The role of phospholipids in the functioning of various cell membranes in conditions of antioxidant system disturbance // Ukr. biochem. j.- 1996.- v. 68(1).- S. 49-54.
9. Yu. Degtyarev V. M., Grigoriev G. P. Automatic recording of acid erythrograms on the EFA-1 densitometer //Lab. case.- 1965.- No. 9.- S. 530-533.
10. P. Derviz G. V., Byalko N. K. Refinement of the method for determining hemoglobin dissolved in blood plasma // Lab. case.- 1966.- No. 8.- S. 461-464.
11. Deryapa N. R., Ryabinin I. F. Human adaptation in the polar regions of the Earth.- L .: Medicine, 1977.- P. 296.
12. Jumaniyazova K. R. Effect of vitamins A, D, E on peripheral blood erythrocytes: Diss. cand. honey. Sciences. - Tashkent, 1970. - S. 134.
13. Donchenko G. V., Metalnikova N. P., Palivoda O. M. et al. Regulation of ubiquinone and protein biosynthesis in rat liver with E-hypovitaminosis by a-tocopherol and actinomycin D, Ukr. biochem. J.- 1981.- T. 53(5).- S. 69-72.
14. Dubinina E. E., Salnikova L. A., Efimova L. F. Activity and isoenzyme spectrum of erythrocyte and plasma superoxide dismutase // Lab. case.- 1983.-№10.-S. 30-33.
15. Isahakyan JI. A. Metabolic structure of temperature adaptations D.: Nauka, 1972.-S. 136.
16. Kaznacheev V.P. Biosystem and adaptation // Report at the II session of the Scientific Council of the USSR Academy of Sciences on the problem of applied human physiology. - Novosibirsk, 1973.-S. 74.
17. Kaznacheev V.P. Problems of human adaptation (results and prospects) // 2nd All-Union. conf. on adaptation of the person to various. geographical, climatic, and industrial conditions: abstract. dokl.- Novosibirsk, 1977.- v. 1.-S. 3-11.
18. Kaznacheev V.P. Modern aspects of adaptation. - Novosibirsk: Nauka, 1980.-S. 191.
19. Kalashnikov Yu. K., Geisler B. V. On the method of determining blood hemoglobin using acetone cyanohydrin // Lab. case.- 1975.- No. 6.- SG373-374.
20. Kandror I. S. Essays on human physiology and hygiene in the Far North. - M .: Medicine, 1968. - P. 288.
21. Kashevnik L. D. Metabolism in beriberi S.- Tomsk., 1955.- S. 76.
22. Korovkin B.F. Enzymes in the diagnosis of myocardial infarction.- L: Nauka, 1965.- P. 33.
23. Kulikov V. Yu., Lyakhovich V. V. Reactions of free radical oxidation of lipids and some indicators of oxygen metabolism // Mechanisms of human adaptation in high latitudes / Ed. V. P. Kaznacheeva.- L .: Medicine, 1980.- S. 60-86.
24. Landyshev S.S. Adaptation of erythrocyte metabolism to the action of low temperatures and respiratory failure // Adaptation of humans and animals in various climatic zones / Ed. M. 3. Zhits.- Chita, 1980.- S. 51-53.
25. Lankin V. Z., Gurevich S. M., Koshelevtseva N. P. The role of lipid peroxides in the pathogenesis of atherosclerosis. Detoxification of lipoperoxides by the glutathione peroxidase system in the aorta // Vopr. honey. Chemistry. - 1976. - No. 3, - S. 392-395.
26. Lyakh L.A. On the stages of formation of adaptation to cold // Theoretical and practical problems of the effect of low temperatures on the body: Tez. IV All-Union. Conf.- 1975.- S. 117-118.
27. Marachev A. G., Sorokovoi V. I., Korchev A. V. et al. Bioenergetics of erythrocytes in the inhabitants of the North // Human Physiology.- 1983.- No. 3.- P. 407-415.
28. Marachev A.G. Structure and function of human erythron in the conditions of the North // Biological problems of the North. VII symposium. Human adaptation to the conditions of the North / Ed. V.F. Burkhanova, N.R. Deryapy.- Kirovsk, 1979.- S. 7173.
29. Matusis I. I. Functional relationships of vitamins E and K in the metabolism of the animal organism // Vitamins.- Kyiv: Naukova Dumka, 1975.- Vol. 8.-S. 71-79.
30. Meyerson F. 3., Malyshev Yu. I. The phenomenon of adaptation and stabilization of structures and protection of the heart.- M: Medicine, 1981.- P. 158.
31. Meyerson F. 3. Basic patterns of individual adaptation // Physiology of adaptation processes. M.: Nauka, 1986.- S. 10-76.
32. Panin JI. E. Some biochemical problems of adaptation // Medico-biological aspects of adaptation processes / Ed. J.I. P. Nepomnyashchikh.-Novosibirsk.: Science.-1975a.-S. 34-45.
33. Panin L. E. The role of hormones of the pituitary-adrenal system and pancreas in the violation of cholesterol metabolism in some extreme conditions: Diss. doc. honey. nauk.- M., 19756.- S. 368.
34. Panin L. E. Energy aspects of adaptation. - L.: Medicine, 1978. - 192 p. 43. Panin L. E. Features of energy metabolism // Mechanisms of human adaptation to high latitude conditions / Ed. V. P. Kaznacheeva.- L .: Medicine, 1980.- S. 98-108.
35. Peskin A. V. Interaction of active oxygen with DNA (Review) // Biochemistry.- 1997.- T. 62.- No. 12.- P. 1571-1578.
36. Poberezkina N. B., Khmelevsky Yu. V. Disturbances in the structure and function of erythrocyte membranes E in beriberi rats and its correction with antioxidants // Ukr. biochem. j.- 1990.- v. 62(6).- S. 105-108.
37. Pokrovsky A. A., Orlova T. A., Pozdnyakov A. JL Influence of tocopherol deficiency on the activity of certain enzymes and their isoenzymes in the testes of rats // Vitamins and reactivity of the body: Proceedings of the MOIP.- M., 1978.-T. 54.- S. 102-111.
38. Rapoport Zh. Zh. Adaptation of the child in the North.- L .: Medicine, 1979.- P. 191.
39. Rossomahin Yu. I. Features of thermoregulation and body resistance to contrasting effects of heat and cold under different modes of temperature adaptation: Abstract of the thesis. diss. cand. biol. Sciences.- Donetsk, 1974.- S. 28.
40. Seits, I.F., On the quantitative determination of adenosine tri- and adenosine diphosphates, Byull. exp. biol. and medical - 1957. - No. 2. - S. 119-122.
41. Sen I. P. Development of E-vitamin deficiency in white rats fed with qualitatively different fats: Diss. cand. honey. nauk.- M., 1966.- S. 244.
42. Slonim, A.D., Physiological mechanisms of natural adaptations of animals and humans, Dokl. for the yearly session Academic Council dedicated. memory of acad. K. M. Bykova. - JL, 1964.
43. Slonim A. D. Physiological adaptations and peripheral structure of reflex responses of the organism // Physiological adaptations to heat and cold / Ed. A. D. Slonim.- JL: Science, 1969.- S. 5-19.
44. Spirichev V. B., Matusis I. I., Bronstein JL M. Vitamin E. // In the book: Experimental vitaminology / Ed. Yu. M. Ostrovsky.- Minsk: Science and Technology, 1979.- S. 18-57.
45. Stabrovsky E. M. Energy metabolism of carbohydrates and its endocrine regulation under the influence of low environmental temperature on the body: Avto-ref. diss. doc. biol. nauk.- JL, 1975.- S. 44.
46. Tepliy D. JL, Ibragimov F. Kh. Changes in the permeability of erythrocyte membranes in rodents under the influence of fish oil, vitamin E and fatty acids // J. Evolution. Biochemistry and Physiology.- 1975.- v. 11(1).- S. 58-64.
47. Terskov I. A., Gitelzon I. I. Erythrograms as a method of clinical blood testing.- Krasnoyarsk, 1959.- P. 247.
48. Terskov I. A., Gitelzon I. I. The value of dispersion methods for the analysis of erythrocytes in normal and pathological conditions // Questions of biophysics, biochemistry and pathology of erythrocytes.- M.: Nauka, 1967.- P. 41-48.
49. Tkachenko E. Ya. On the ratio of contractile and non-contractile thermogenesis in the body during adaptation to cold // Physiological adaptation to cold, mountain and subarctic conditions / Ed. K. P. Ivanova, A. D. Slonim.-Novosibirsk: Nauka, 1975.- P. 6-9.
50. Uzbekov G. A., Uzbekov M. G. Highly sensitive micromethod for photometric determination of phosphorus // Lab. case.- 1964.- No. 6.- S. 349-352.
51. Khochachka P., Somero J. Biochemical adaptation: Per. from English. M.: Mir, 1988.-576 p.
52. Shcheglova, AI, Adaptive Changes in Gas Exchange in Rodents with Different Ecological Specializations, Physiological Adaptations to Heat and Cold, Ed. A. D. Slonim.- L.: Nauka, 1969.- S. 57-69.
53. Yakusheva I. Ya., Orlova LI Method for determination of adenosine triphosphatases in hemolysates of blood erythrocytes // Lab. case.- 1970.- No. 8.- S. 497-501.
54. Agani F., Semenza G. L. Mersalyl is a novel inducer of vascular endothelial growth factor gene expression and hypoxia-inducible factor 1 activity // Mol. Pharmacol.- 1998.- Vol. 54(5).-P. 749-754.
55. Ahuja B. S., Nath R. A kinetik study of superoxide dismutase in normal human erytrocytes and its possible role in anemia and radiation damage // Simpos. on control in mechanisms cell, processes. - Bombey, 1973. - P. 531-544.
56. Aloia R. C., Raison J. K. Membrane function in mammalian hibernation // Bio-chim. Biophys. Acta.- 1989.- Vol. 988.- P. 123-146.
57. Asfour R. Y., Firzli S. Hematologic stadies in undernourished children with low serum vitamin E levels // Amer. J.Clin. Nutr.- 1965.- Vol. 17(3).-P. 158-163.
58. Ashour M. N., Salem S. I., El Gadban H. M., Elwan N. M., Basu T. K. Antioxidant status in children with protein-energy malnutrition (PEM) living in Cairo, Egypt // Eur. J.Clin. Nutr.- 1999.- Vol. 53(8).-P. 669-673.
59. Bang H. O., Dierberg J., Nielsen A. B. Plasma lipid and lipoprotein pattern in Greenlandic west coast Eskimos // Lancet.- 1971.- Vol. 7710(1).-P. 1143-1145.
60. Barja G., Cadenas S., Rojas C., et al. Effect of dietary vitamin E levels on fatty acid profiles and nonenzymatic lipid peroxidation in the guinea pig liver // Lipids.-1996.- Vol. 31(9).-P. 963-970.
61. Barker M. O., Brin M. Mechanisms of lipid peroxidation in erythrocytes of vitamin E deficients rats and in phospholipid model sistems // Arch. Biochem. and Biophys.- 1975.- Vol. 166(1).-P. 32-40.
62. Battersby B. J., Moyes C. D. Influence of acclimation temperature on mitochondrial dna, rna and enzymes in skeletal muscle // APStracts.- 1998.- Vol. 5.- P. 195.
63. Beattie J. H., Black D. J., Wood A. M., Trayhurn P. Cold-induced expression of the metallothionein-1 gene in brown adipose tissue of rats, Am. J. Physiol.-1996.-Vol. 270(5).- Pt 2.- P. 971-977.
64. Bhaumik G., Srivastava K. K., Selvamurthy W., Purkayastha S. S. The role of free radicals in cold injuries // Int. J. Biometeorol.- 1995.- Vol. 38(4).-P. 171-175.
65. Brin M., Horn L. R., Barker M. O. Relationship between fatty acid composition oferithrocytes and susceptibility to vitamin E deficiency // Amer. J.Clin. Nutr.-%1974.-Vol. 27(9).-P. 945-950.
66. Caasi P. I., Hauswirt J. W., Nair P. P. Biosynthesis of heme in vitamin E deficiency // Ann. N. Y. Acad. Sci.- 1972.- Vol. 203.- P. 93-100.
67. Cadenas S., Rojas C., Perez-Campo R., Lopez-Torres M., Barja G. Vitamin E protects guinea pig liver from lipid peroxidation without depressing levels of antioxidants//Int. J Biochem. cell. Biol.- 1995.-Vol. 27(11).-P. 1175-1181.
68 Cai Q. Y., Chen X. S., Zhu L. Z., et al. Biochemical and morphological changes in the lenses of selenium and/or vitamin E deficient rats // Biomed. Environ. Sci.-1994.-Vol. 7(2).-P. 109-115.
69. Cannon R. O. Role of nitric oxide in cardiovascular disease: focus on the endothelium // Clin. Chem.- 1998.- Vol. 44.- P. 1809-1819.
70. Chaudiere J., Clement M., Gerard D., Bourre J. M. Brain alterations induced by vitamin E deficiency and intoxication with methyl ethyl ketone peroxide // Neuro-toxicology.- 1988.- Vol. 9(2).-P. 173-179.
71. Chow C. K. Distribution of tocopherols in human plasma and red blood cells // Amer. J.Clin. Nutr.- 1975.- Vol. 28(7).-P. 756-760.
72. Chow C. K. Oxidative damage in the red cells of vitamin E-deficient rats // Free. Radic. Res. Commun.- 1992 vol. 16(4).-P. 247-258.
73. Chow C. K., Ibrahim W., Wei Z., Chan A. C. Vitamin E regulates mitochondrial hydrogen peroxide generation // Free Radic. Biol. Med.- 1999.- Vol. 27 (5-6).- P. 580-587.
74. Combs G. F. Influences of dietary vitamin E and selenium on the oxidant defense system of the chick//Poult. Sci.- 1981.- Vol. 60(9).- P. 2098-2105.
75. Cooke J. P., Dzau V. J. Nitric oxide synthase: Role in the Genesis of Vascular Disease // Ann. Rev. Med.- 1997.- Vol. 48.- P. 489-509.
76. Cowan D. B., Langille B. L. Cellular and molecular biology of vascular remodeling // Current Opinion in Lipidology.- 1996.- Vol. 7.- P. 94-100.
77. Das K. S., Lewis-Molock Y., White C. W. Elevation of manganese superoxide dismutase gene expression by thioredoxin, Am. J. Respir. Cell Mol. Biol.- 1997.-Vol. 17(6).-P. 12713-12726.
78. Davidge S. T., Ojimba J., McLaughlin M. K. Vascular Function in the Vitamin E Deprived Rat. An Interaction Between Nitric Oxide and Superoxide Anions // Hypertension.- 1998.- Vol. 31.- P. 830-835.
79. Davis T. R. A. Shivering and nonshivering heat production in animals and man, Cold Injury: Ed. S. H. Horvath.- N. Y., I960.- P. 223-269.
80. Davis T. R. A. Nonshivering thermogenesis, Feder. Proc.- 1963.- Vol. 22(3).-P. 777-782.
81. Depocas F. Calorigenesis from various organ systems in the whole animal // Feder. Proc.-I960.-Vol. 19(2).-P. 19-24.
82. Desaultes M., Zaror-Behrens G., Hims-Hagen J. Increased purine nucleotide binding, altered polipeptide composition and thermogenesis in brown adipose tissue mitochondria of cold-acclimated rats // Can. J. Biochem.- 1978.- Vol. 78(6).-P. 378-383.
83. Drexler H., Hornig B. Endothelial dysfunction in human disease // J. Mol. cell. Cardiol.- 1999.- Vol. 31(1).-P. 51-60.
84. Dutta-Roy A. K. Therapy and clinical trials // Current Opinion in Lipidology.-1996.-Vol. 7.-P. 34-37.
85. Elmadfa I., Both-Bedenbender N., Sierakowski B., Steinhagen-Thiessen E. Significance of vitamin E in aging // Z. Gerontol.- 1986.- Vol. 19(3).-P. 206-214.
86. Farrace S., Cenni P., Tuozzi G., et al. Endocrine and psychophysiological aspects of human adaptation to the extreme //Physiol. Behav.- 1999.- Vol.66(4).- P.613-620.
87. Fernandez-Checa, J. C., Kaplowitz N., Garcia-Ruiz C., et al. Importance and characteristics of glutahione transport in mitochondria: defense against TNF-induced oxidative stress and defect induced by alcohol // APStracts.- 1997.-Vol.4.- P. 0073G.
88. Finkel T. Oxygen radicals and signaling // Current Opinion in Cell Biology.-1998.- Vol. 10.-p. 248-253.
89. Photobiol.- 1993.- Vol. 58(2).-P. 304-312.
90. Fudge D. S., Stevens E. D., Ballantyne J. S. Enzyme adaptation along a hetero-thermic tissue the visceral retia mirabilia of the bluefin tuna // APStracts.- 1997.-Vol. 4, - P. 0059R.
91. Givertz M. M., Colucci W. S. New targets for heart-failure therapy: endothelin, inflammatory cytokines, and oxidative stress // Lancet.- 1998.- Vol.352- Suppl 1.-P. 34-38.
92. Glofcheski D. J., Borrelli M. J., Stafford D. M., Kruuv J. Induction of tolerance to hypothermia and hyperthermia by a common mechanism in mammalian cells // J. Cell. Physiol.- 1993.- Vol. 156.- P. 104-111.
93. Chemical Biology.- 1999.- Vol. 3.- P. 226-235.1 ll. Guarnieri C., Flamigni F., Caldarera R. C:, Ferrari R. Myocardial mitochondrial functions in alpha-tocopherol-deficient and -refed rabbits // Adv. Myocardiol.-1982.-Vol.3.-P. 621-627.
94. Hardewig I., Van Dijk P. L. M., Portner H. O. High energy turnover at low temperatures: recovery from exhaustive exercise in antarctic and temperate eelpouts (zoarcidae) // APStracts.- 1998.- Vol. 5.- P. 0083R.
95. Hassan H., Hashins A., van Italie T. B., Sebrell W. H. Syndrom in premature infants anemia associated with low plasma vitamin E level and high poliunsaturated fatty acid diet // Amer. J.Clin. Nutr.-1966.-Vol. 19(3).-P. 147-153.
96. Hauswirth G. W., Nair P. P. Some aspects of vitamin E in expression of biological information, Ann. N. Y. Acad. Sci.- 1972.- Vol. 203.- P. 111-122.
97. Henle E. S., Linn S. Formation, prevention, and repair of DNA damage by iron/hydrogen peroxide // J. Biol, chem.- 1997.- Vol. 272(31).- P. 19095-19098.
98. Higashi Y., Sasaki S., Sasaki N., et al. Daily aerobic exercise improves reactive hyperemia in patients with essential hypertension // Hypertension.- 1999.- Vol. 33(1).-Pt 2.-P. 591-597.
99. Howarth P. H Pathogenic mechanisms: a rational basis for treatment // V. M. J.-1998.-Vol. 316.-p. 758-761.
100. Hubbell R. B., Mendel L. B., Wakeman A. J. A new salt mixture for use in experimental diets // J. Nutr.- 1937.- Vol. 14.- P. 273-285.
101. Jacob R. A., Burri B. J. Oxidative damage and defense // Am. J.Clin. Nutr.-1996.-Vol. 63.- P. 985S-990S.
102. Jain S. K., Wise R. Relationship between elevated lipid peroxides, vitamin E deficiency and hypertension in preeclampsia, Mol. cell. Biochem.- 1995.- Vol. 151(1).-P. 33-38.
103. Karel P., Palkovits M., Yadid G., et al. Heterogeneous neurochemical responses to different stressors: a test of selye's doctrine of nonspecificity // APStracts.-1998.-Vol. 5.-P. 0221R.
104. Kausalya S., Nath J. Interactive role of nitric oxide and superoxide anion in neu-trophil-mediated endothelial cell in injury // J. Leukoc. Biol.- 1998.- Vol. 64(2).-P. 185-191.
105. Kemeny M., Peakman M. Immunology // B. M. J. - 1998.- Vol. 316.- P. 600-603.
106. Kozyreva T. V., Tkachenko E. Y., Kozaruk V. P., Latysheva T. V., Gilinsky M. A. The effects of slow and rapid cooling on catecholamine concentration in arterial plasma and the skin // APStracts.- 1999.- Vol. 6.- P. 0081R.
107. Lauren N., Chaudhuri G. Estrogens and atherosclerosis, Ann. Rev. Pharmacol. Toxicol.- 1997.- Vol. 37.- P. 477-515.
108. Lawler J. M., Cline C. C., Hu Z., Coast J. R. Effect of oxidative stress and acidosis on diaphragm contractile function // Am. J. Physiol.- 1997.- Vol. 273(2).-Pt 2.-P. 630-636.
109. Lin B., Coughlin S., Pilch P. F. Bi-directional regulation of uncoupling protein-3 and glut4 mrna in skeletal muscle by cold // APStracts.- 1998.- Vol. 5.- P. 0115E.
110. Lindquist J. M., Rehnmark S. Ambient temperature regulation of apoptosis in brown adipose tissue // J. Biol. Chem.- 1998.- Vol. 273(46).-P. 30147-30156.
111. Lowry O. H., Rosenbrough N. G., Farr A. L., Randell R. I. Protein measurement with the Folin phenol reagent // J. Biol. Chem.-195L-Vol. 193.- P. 265-275.
112. Luoma P. V., Nayha S., Sikkila K., Hassi J. High serum alpha-tocopherol, albumin, selenium and cholesterol, and low mortality from coronary heart disease in northern Finland//J. Intern. Med.- 1995.-Vol. 237(1).-P. 49-54.
113. Luscher T. F., Noll G., Vanhoutte P. M. Endothelial dysfunction in hypertension // J. Hypertens.- 1996.- Vol. 14(5).-P. 383-393.
114. Machlin L. J., Filipski R., Nelson J., Horn L. R., Brin M. Effect of progressive vitamin E deficiency in the rat // J. Nutr.- 1977.- Vol. 107(7).-P. 1200-1208.
115. Marmonier F., Duchamp C., Cohen-Adad F., Eldershaw T. P. D., Barra H. Hormonal control of thermogenesis in perfused muscle of muscovy ducklings // AP-Stracts.-1997.- Vol. 4.- P. 0286R.
116. Marvin H. N. Erythrocyte survival of rat deficient in vitamin E or vitamin B6 // J. Nutr.- 1963.-Vol. 80(2).-P. 185-190.
117. Masugi F., Nakamura T. Effect of vitamin E deficiency on the level of superoxide dismutase, glutathione peroxidase, catalase and lipid peroxide in rat liver, Int. J. Vitam. Nutr. Res.- 1976.- Vol. 46(2).-P. 187-191.
118. Matsuo M., Gomi F., Dooley M. M. Age-related alterations in antioxidant capacity and lipid peroxidation in brain, liver, and lung homogenates of normal and vitamin E-deficient rats // Mech. Ageing Dev.- 1992.- Vol. 64(3).-P. 273-292.
119. Mazor D., Brill G., Shorer Z., Moses S., Meyerstein N. Oxidative damage in red blood cells of vitamin E deficient patients // Clin. Chim. Acta.- 1997.- Vol. 265(l).-P. 131-137.
120. Mircevova L. The role of Mg++-ATPase (actomyosine-like protein) in maintaining the biconcave shape of erythrocytes // Blut.- 1977.- vol 35(4).- P. 323-327.
121. Mircevova L., Victora L., Kodicek M., Rehackova H., Simonova A. The role of spectrin dependent ATPase in erytrocyte shape maintenance // Biomed. biochim. Acta.- 1983.- Vol. 42(11/12).- P. 67-71.
122. Nair P. P. Vitamin E and metabolic regulation // Ann. N. Y. Acad. Sci.-1972a.-Vol. 203.- P. 53-61.
123. Nair P. P. Vitamine E regulation of the biosintesis of porphirins and heme // J. Agr. and Food Chem.- 1972b.- Vol. 20(3).-P. 476-480.
124. Nakamura T., Moriya M., Murakoshi N., Shimizu Y., Nishimura M. Effects of phenylalanine and tyrosine on cold acclimation in mice // Nippon Yakurigaku Zasshi.-1997.-Vol. 110(1).-P. 177-182.
125. Nath K. A., Grande J., Croatt A., et al. Redox regulation of renal DNA synthesis, transforming growth factor-betal and collagen gene expression // Kidney Int.-1998.- Vol. 53(2).-P. 367-381.
126. Nathan C. Perspectives Series: Nitric Oxide and Nitric Oxide Synthases Inducible Nitric Oxide Synthase: What Difference Does It Make? // J. Clin. Invest.1997.- Vol. 100(10).-P. 2417-2423.
127. Newaz M. A., Nawal N. N. Effect of alpha-tocopherol on lipid peroxidation and total antioxidant status in spontaneously hypertensive rats // Am J Hypertens.1998.-Vol. 11(12).-P. 1480-1485.
128. Nishiyama H., Itoh K., Kaneko Y., et al. Glycine-rich RNA-binding Protein Mediating Cold-inducible Suppression of Mammalian Cell Growth // J. Cell. Biol.- 1997.- Vol. 137(4).-P. 899-908.
129. Nohl H. Generation of superoxide radicals as byproduct of cellular respiration, Ann. Biol. Clin. (Paris).- 1994.- Vol. 52(3).-P. 199-204.
130. Pendergast D. R., Krasney J. A., De Roberts D. Effects of immersio in cool water on lung-exhaled nitric oxide at rest and during exercise // Respir. Physiol.-1999.-Vol. 115(1).-P. 73-81.
131. Peng J. F., Kimura B., Fregly M., Phillips M. I. Reduction of cold-induced hypertension by antisense oligodeoxynucleotides to angiotensinogen mRNA and ATi receptor mRNA in brain and blood // Hypertension.- 1998.- Vol. 31.- P. 13171323.
132. Pinkus R., Weiner L. M., Daniel V. Role of oxidants and antioxidants in the induction of AP-1, NF-kappa B and glutathione S~transferase gene expression // J. Biol. Client.- 1996.- Vol. 271(23).- P. 13422-13429.
133. Pipkin F. B. Fortnightly Review: The hypertensive disorders of pregnancy // BMJ.- 1995.-Vol. 311.-P. 609-613.
134. Reis S. E., Blumenthal R. S., Gloth S. T., Gerstenblith R. G., Brinken J. A. Estrogen acutely abolishes cold-induced coronary vasoconstriction in postmenopausal women // Circulation.- 1994.- Vol. 90.- P. 457.
135. Salminen A., Kainulainen H., Arstila A. U., Vihko V. Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles // Acta Physiol. Scand.- 1984.- Vol. 122(4).-P. 565-570.
136. Sampson G. M. A., Muller D. P. Studies on the neurobiology of vitamin E (al-pha-tocopherol) and some other antioxidant systems in the rat // Neuropathol. Appl. Neurobiol.- 1987.- Vol. 13(4).-P. 289-296.
137. Sen C. K., Atalay M., Agren J., Laaksonen DE, Roy S., Hanninen O. Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise // APStracts.- 1997.- Vol. . 4.- P. 0101 A.
138. Shapiro S. S., Mott D. D., Machlin L. J. Altered binding of glyceraldehyde 3 -phosphate dehydrogenase to its binding site in vitamine E - deficient red blood cells // Nutr. Rept. Int.- 1982.- Vol. 25(3).-P. 507-517.
139. Sharmanov A. T., Aidarkhanov V. V., Kurmangalinov S. M. Effect of vitamin E deficiency on oxidative metabolism and antioxidant enzyme activity of macrophages // Ann. Nutr. Metab.- 1990.- Vol. 34(3).-P. 143-146.
140. Siddons R. C., Mills C. F. Glutatione peroxidase activity and erythrocyte stability in calves differing in selenium and vitamin E status, Brit. J. Nutr.-1981.-Vol. 46(2).-P. 345-355.
141. Simonoff M., Sergeant C., Gamier N., et al. Antioxidant status (selenium, vitamins A and E) and aging // EXS.- 1992.- Vol. 62.- P. 368-397.
142. Sklan D., Rabinowitch H. D., Donaghue S. Superoxide dismutase: effect of vitamins A and E, Nutr. Rept. Int.- 1981.- Vol. 24(3).-P. 551-555.
143. Smith S. C., Guilbert L. J., Yui J., Baker P. N., Davidge S. T. The role of reactive nitrogen/oxygen intermediates in cytokine-induced trophoblast apoptosis // Placenta.- 1999.- Vol. 20(4).-P. 309-315.
144. Snircova M., Kucharska J., Herichova I., Bada V., Gvozdjakova A. The effect of an alpha-tocopherol analog, MDL 73404, on myocardial bioenergetics // Bratisl Lek Listy.- 1996.- Vol. 97. P. 355-359.
145. Soliman M. K. Uber die Blutveranderungen bei Ratten nach verfuttem einer Tocopherol und Ubichinon Mangeldiat. 1. Zytologische und biochemische Veranderungen im Blut von vitamin E Mangelratten // Zbl. Veterinarmed.- 1973.-Vol. 20(8).-P. 624-630.
146. Stampfer M. J., Hennekens C. H., Manson J. E., et al. Vitamin E consumption and the risk of coronary disease in women // N. Engl. J. Med.- 1993.- Vol. 328.- P. 1444-1449.
147. Sun J. Z., Tang X. L., Park S. W., et al. Evidence for an Essential Role of Reactive Oxygen Species in the Genesis of Late Preconditioning Against Myocardial Stunning in Conscious Pigs // J. Clin. Invest. 1996, Vol. 97(2).-P. 562-576.
148. Sun Z., Cade J. R., Fregly M. J. Cold-induced hypertension. A model of miner-alocorticoid-induced hypertension// Ann.N.Y.Acad.Sci.- 1997.- Vol.813.- P.682-688.
149. Sun Z., Cade R, Katovich M. J., Fregly M. J. Body fluid distribution in rats with cold-induced hypertension // Physiol. Behav.- 1999.- Vol. 65(4-5).-P. 879-884.
150. Sundaresan M., Yu Z.-X., Ferrans VJ, Irani K., Finkel T. Requirement for generation of H202 for platelet-derived growth factor signal transduction // Science (Wash. DC).- 1995.- Vol . 270.- P. 296-299.
151. Suzuki J., Gao M., Ohinata H., Kuroshima A., Koyama T. Chronic cold exposure stimulates microvascular remodeling preferentially in oxidative muscles in rats // Jpn. J. Physiol.- 1997.- Vol. 47(6).-P. 513-520.
152. Tamai H., Miki M., Mino M. Hemolysis and membrane lipid changes induced by xanthine oxidase in vitamin E deficient red cells // J. Free Radic. Biol. Med.-1986.-Vol. 2(1).-P. 49-56.
153. Tanaka M., Sotomatsu A., Hirai S. Aging of the brain and vitamin E // J. Nutr. sci. Vitaminol. (Tokyo).- 1992.- Spec. No.-P. 240-243.
154. Tappel, A. L. Free radical lipid peroxidation damage and its inhibition by vitamin E and selenium, Fed. Proc.- 1965.- Vol. 24(1).-P. 73-78.
155. Tappel, A. L. Lipid peroxidation damage to cell components, Fed. Proc.- 1973.-Vol. 32(8).-P. 1870-1874.
156. Taylor A.J. N. Asthma and allergy // B. M. J.- 1998.- Vol. 316.- P. 997-999.
157. Tate D. J., Miceli M. V., Newsome D. A. Phagocytosis and H2C>2 induce catalase and metaliothionein irene expression in human retinal pigment epithelial cells // Invest. Onithalmol. Vis. Sci.- 1995.- Vol. 36.- P. 1271-1279.
158. Tensuo N. Effect of daily infusion of noradrenaline on metabolism and skin temperature in rabbits // J. Appl. Physiol.- 1972.- Vol. 32(2).-P. 199-202.
159. Tiidus P. M., Houston M. E. Antioxidant and oxidative enzyme adaptations to vitamin E deprivation and training // Med. sci. sports. Exerc.- 1994.- Vol. 26(3).-P. 354-359.
160. Tsen C. C., Collier H. B. The protective action of tocopherol against hemolisis of rat eritrocites by dialuric acid // Canada. J Biochem. Physiol.-I960.-Vol. 38(9).-P. 957-964.
161. Tudhope G. R., Hopkins J. Lipid peroxidation in human erythrocytes in tocopherol deficiency // Acta Haematol.- 1975.- Vol. 53(2).-P. 98-104.
162. Valentine J. S., Wertz D. L., Lyons T. J., Liou L.-L., Goto J. J., Gralla E. B. The dark side of dioxygen biochemistry // Current Opinion in Chemical Biology.-1998.-Vol. 2.-P. 253-262.
163. Vransky V. K. Red blood cell membrane resistanse // Biophys. Membrane Transport.- Wroclaw.- 1976.- Part 2.- P. 185-213.
164. Vuillanine R. Role biologiqe et mode d" action des vitamins E // Rec. med vet.-1974.-Vol. 150(7).-P. 587-592.
165. Wang J., Huang C. J., Chow C. K. Red cell vitamin E and oxidative damage: a dual role of reducing agents, Free Radic. Res.- 1996 Vol. 24(4).-P. 291-298.
166. Wagner B. A., Buettner G. R., Burns C. P. Vitamin E slows the rate of free radical-mediated lipid peroxidation in cells // Arch. Biochem. Biophys.- 1996.- Vol. 334.-p. 261-267.
167. Wallace J. L., Bell C. J. Gastroduodenal mucosal defense // Current Opinion in Gastroenterology 1994 .-Vol. 10.-p. 589-594.
168. Walsh D. M., Kennedy D. G., Goodall E. A., Kennedy S. Antioxidant enzyme activity in the muscles of calves depleted of vitamin E or selenium or both // Br. J. Nutr.- 1993.- Vol. 70(2).-P. 621-630.
169. Watson A. L., Palmer M. E., Jauniaux E., Burton G. J. Variations in expression of copper/zinc superoxide dismutase in villous trophoblast of the human placenta with gestational age // Placenta.- 1997.- Vol. 18(4).-P. 295-299.
170. Young J. B., Shimano Y. Effects of rearing temperature on body weight and abdominal fat in male and female rats // APStracts.-1991.- Vol. 4.- P. 041 OR.
171. Zeiher A. M., Drexler H., Wollschlager H., Just H. Endothelial dysfunction of the coronary microvasculature is associated with coronary blood flow regulation in patients with early atherosclerosis // Circulation.- 1991.- Vol. 84.- P. 19841992.
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