W X Gao1, J Z Liu, L P Wu, M C Cai. 1. Department of Pathophysiology & Institute of High Altitude Medicine, Third Military Medical University, Chongqing 400038, China.
Abstract
AIM: To explore the effects of acute and chronic hypoxia on brain mitochondrial transcription activity in vitro of rats. METHODS: Animal grouping: Wistar rats were randomized into acute hypoxic group (AH), chronic hypoxic group (CH) and the control. Mitochondrial transcription activity in vitro was measured in each group respectively as well as mitochondrial F0F1-ATPase activity, and effects of environmental ATP concentration on mitochondrial transcription activity in vitro was observed. RESULTS: Brain mitochondrial transcription activity and F0F1-ATPase activity were marked depressed in AH while partly reversed in CH, and they were linearly related. Mitochondrial transcription activity in vitro was affected by ATP concentration diphasely. CONCLUSION: Acute hypoxia may impair brain mitochondria energy metabolism by way of depressing mitochondrial transcription and then partially recover during chronic hypoxia. And mitochondrial transcription in vitro might be precisely regulated by ATP concentration.
AIM: To explore the effects of acute and chronic hypoxia on brain mitochondrial transcription activity in vitro of rats. METHODS: Animal grouping: Wistar rats were randomized into acute hypoxic group (AH), chronic hypoxic group (CH) and the control. Mitochondrial transcription activity in vitro was measured in each group respectively as well as mitochondrial F0F1-ATPase activity, and effects of environmental ATP concentration on mitochondrial transcription activity in vitro was observed. RESULTS: Brain mitochondrial transcription activity and F0F1-ATPase activity were marked depressed in AH while partly reversed in CH, and they were linearly related. Mitochondrial transcription activity in vitro was affected by ATP concentration diphasely. CONCLUSION: Acute hypoxia may impair brain mitochondria energy metabolism by way of depressing mitochondrial transcription and then partially recover during chronic hypoxia. And mitochondrial transcription in vitro might be precisely regulated by ATP concentration.