Relevance of the topic. Recent studies have 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 has been 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 action of reactive oxygen species, is essential.

Approbation of work. The results of the research 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 a scientific and 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).

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. Long-term (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 stress 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, the increased production of various signaling factors, including hormonal factors, 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 mechanisms of adaptation 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 that indicated 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-vitaminosis (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, the further transformations of glucose-6-phosphate, which is 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 restructuring 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 cold, but not E-avitaminous oxidative stress, is characterized by the prevalence of energy production over energy consumption (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.

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