| Summary: | 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.
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