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The effect of hypoxic hypoxia on the pyruvate kinase (PK) activity in the brain structures of white rats during ontogenesis in a comparative aspect has been studied. A clear dependence could be established in the increase of PK activity from an oxygen deficient state, the age of animals, the studied structure of the brain and the prolonged effect of hypoxia. Prenatal exposure to hypoxia has shown that the PK activity is not restored to the control value level in postnatal development. After postnatal exposure to hypoxia with increasing age in animals, the PK activity gets more resistant to the effect of stress-factors. The data analysis indicates that the increasing exhaustion of energy resources necessary for normal cell functioning makes an important contribution to the development of hypoxic state and the insufficiency of mitochondrial oxidative phosphorylation, the main energy forming system which underlies these disturbances. Energy-shortage, in its turn causes a variety of secondary negative metabolic alterations and gives rise to free radical oxidation in the cells. An explanation of the obtained results suggested can be considered as an evidence of the realization of the biological effect of hypoxia through the oxidative mechanism.
International Journal of Secondary Metabolite
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