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XXVII conference

Antioxidants –adaptogen to stress

Zhigacheva I.V.

N.M.Emanuel Institute of Biochemical Physics Russian Academy of Sciences

Introduction. Stress factors lead to a shift in the antioxidant – prooxidant balance towards an increase in the content of ROS in the cell. The main source of ROS in these conditions are mitochondria in animals [Zorov D. B. et al., 2007], mitochondria and chloroplasts in plants [Tailor N. L et al, 2003]. Excessive generation of ROS leads to oxidation of thiol groups of proteins, lipid peroxidation (LPO) of membranes and swelling of mitochondria, which leads to the development of a number of pathological conditions [Todorov I. N., 2007]. In this regard, there is a need to search for drugs-adaptogens that increase the body's resistance to stress factors. Antioxidants claim this role. The aim of the work was to study the effects of antioxidants from the class of spatially hindered phenols and 3-oxypyridines on the functional state of rat liver mitochondria and mitochondria of etiolated pea seedlings under stress. The model of acute hypobaric hypoxia (AHH) (for rats) and water deficiency (WD) (for pea seedlings) were used as a stress influence.

Methods. The functional state of mitochondria was assessed by mitochondrial respiration rate (polarographic method), lipid peroxidation level (by Schiff base fluorescence spectra) and by studying the fatty acid composition of mitochondrial membranes by chromatography.

Results. AHH led to the activation of LPO in rat liver mitochondrial membranes and pea seedling mitochondria. At the same time, the fluorescence intensity of the final LPO products increased by 3-4 times. Changes in the physical and chemical properties of mitochondrial membranes caused by lipid peroxidation of membranes had an impact on the activity of mitochondrial respiratory chain enzymes: there were a decrease in the maximum oxidation rates of NAD-dependent substrates by 25-29% and a decrease in the efficiency of oxidative phospholylation by 30%. Administration to rats of 10-6 M sodium anphen 10-13 M potassium phenosan or 10-6 M N-acetylcysteinate 2-ethyl-6-methyl-3-hydroxypyridine 45 minutes before exposure prevented the activation of LPO. A similar effect were exerted by the preparations on the LPO intensity and bioenergetic characteristics of the mitochondria of pea seedlings. The preparations increased the life expectancy of mice by 3.5–4.5 times under the conditions of AHH and prevented the inhibition of the growth of seedlings in the conditions of WD.

Conclusion. By preventing the activation of LPO, the drugs seem to help preserve the functional state of the mitochondria, which probably ensures the resistance of organisms to the action of stress factors.

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