Modifications of the expression of thioredoxins and superoxide dismutases in the rat hippocampus that were induced by prenatal hypoxia are preserved in mature animals

Prenatal hypoxia induces structural and functional disturbances in the brain that develop during the following postnatal ontogeny. Some cognitive and behavioral disorders that are induced by prenatal hypoxia are preserved even in adults. Oxidative stress is a key factor of damage during hypoxia. Hence, the relationship between the pro- and antioxidant systems plays an important role in the development of both pathological and adaptive processes that were induced by hypoxia. Here, using immunocytochemistry we studied the expression of four endogenous protein antioxidants (Cu,Zn-superoxide dismutase, Mn-superoxide dismutase, thioredoxin-1, and thioredoxin-2) in hippocampal neurons of adult rats that were subjected to triple hypoxia at the 14th, 15th, and 16th days of their prenatal development. We found that in a number of cases prenatal hypoxia substantially modified the expression of endogenous antioxidants in hippocampal neurons of rats that achieved an adult age (80–90 days of postnatal ontogeny). The directions of these changes, however, are different for different antioxidants and areas of the hippocampus. It seems that this multidirectionality of changes in the expression of different antioxidants in different areas reflects an inextricable connection between the pathological consequences of prenatal hypoxia and adaptation processes that are induced by this hypoxia.