ИСТИНА

The method of hypoxic postconditioning (PostC) is an exposure of injured organism to extreme factors of mild intensity in order to mobilize endogenous protective mechanisms. It consists of three sequential episodes of mild hypobaric hypoxia that follow the severe injurious hypoxia (SH). The SH was shown to cause cell death by both necrotic and apoptotic ways while the PostC corrected cellular damage (1). This effect was considered to be mediated by antioxidant defense systems. We investigated the cellular redox state, antioxidant capacity and the glutathione-dependent antioxidant system activity in rat hippocampus. In addition, as the protective effect of glutathione is dependent on the amount of reduced NADP, we estimated its quantity. According to the fact that the main source of NADPH is glucose-6-phosphate dehydrogenase (G6PD) (2), the key enzyme of pentose-phosphate pathway, we have analyzed its activity. In our model we observed decreased G6PD activity after SH accompanied with reduced NADPH amount. The level of total glutathione also dropped causing the same result for antioxidant capacity and cellular redox state. In contrast, the activity of G6PD recovered to control in response to PostC which caused the stabilization of NADPH level. The amount of total glutathione, antioxidant capacity and redox state also recovered. In addition, the immunohistochemical analysis has shown that G6PD is preferentially localized of in neuronal cells which was shown to contribute in neuronal survival in vitro (3). This data demonstrates the significant role of antioxidant systems and its processivity in neuronal survival after severe injurious hypoxia accompanied with hypoxic postconditioning.