HYPOXIA STRESS ON THE ACTIVITY OF ANTIOXIDANT ENZYMES, NEURONAL APOPTOSIS AND EXPRESSION OF RELATED GENES OF TELENCEPHALON IN GYMNOCYPRIS PRZEWALSKII

To explore the physiological response of Qinghai Lake naked carp (Gymnocypris przewalskii) telencephalon cells to hypoxia, the carp with body weight (97.68±0.12) g and body length (24.11±0.12) cm were challenged with hypoxia stress dissolved oxygen content of (0.7±0.1) mg/L and normoxia dissolved oxygen content of (8.4±0.1) mg/L for 24h to measure mitochondrial ultrastructure, membrane potential, antioxidant enzyme activities, telencephalon cells apoptosis, apoptotic-related genes (Caspase 3, Bax and Bcl-2) and hypoxia-induced response-related gene (Hif-2α and EGLN1). The results showed that: (1) nerve cells mitochondria swelled and their cristae dissolved during hypoxia stress, the mitochondrial membrane potential increased significantly at 8h and then significantly decreased at 24h, indicating the destroyed mitochondria of telencephalon cells with the increased hypoxia time. (2) hypoxia enhanced cell apoptosis and the expression levels of Caspase 3, Hif-2α, Bax and Bcl-2 genes in telencephalon cells, and significantly decreased the ratio of Bcl-2/Bax and the expression of EGLN1. (3) the increased content of hydrogen peroxide (H₂O₂) in telencephalon cells only happened at 8h. Hypoxia significantly induced the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA) and the total antioxidant capacity (T-AOC) only at 24h. Furthermore, there was no significant difference in glutathione peroxidase (GPX) between the groups. These results suggest that hypoxia stress mediates the permeability of mitochondrial membrane and the expression of Caspase 3, Bax and Bcl-2 genes via ROS production in telencephalon cells to induce telencephalon cells apoptosis, which might be balanced by increasing the activities of T-AOC and SOD and the expression levels of Hif-2α and decreasing the expression levels of EGLN1.