Activities of monoamine oxidase B, Cu-Zn-dependent superoxide dismutase (SOD), and catalase, and concentration of enzyme-active ceruloplasmin were measured in brain preparations from 43 humans died at the age of 21-92 years. Activity of monoamine oxidase B in the neocortex, cerebellum, basal ganglia, and stem structures increased with age, while SOD activity decreased and catalase and ceruloplasmin concentrations slightly increased. A contribution of age-related increase of cerebral monoamine oxidase activity into ontogenetic impairment of the antioxidant defense in human brain is discussed.

The increased vulnerability of animals to ACVA due to hyperglycemia and increased sensitivity to acute hypoxic hypoxia was established. Reamberin and α-lipoic acid administered for 14 days in doses, which are equivalent to therapeutic range in humans, enhance the tolerance to ACVA and acute hypoxic hypoxia in mice with alloxan diabetes. These medications also decrease the intensity of hyperglycemia during concurrent insulin replacement therapy. The increased tolerance to ACVA in mice with alloxan diabetes caused by reamberin and alpha-lipoic acid is associated with an antihypoxic effect of these medications and does not depend on their effect on the intensity of hyperglycemia. Reamberin outperformed α-lipoic acid in the antihypoxic activity, protection against ACVA and the rate of onset of glucose reducing effect in experimental diabetes mellitus.