摘要
目的 :探讨模拟高原低氧对大鼠脑线粒体蛋白合成功能的影响。方法 :雄性wistar大鼠随机分为急性低氧组、慢性低氧组和平原对照组。急、慢性低氧组动物分别连续暴露于模拟 4 0 0 0m高原 3d和 4 0d ,分离脑线粒体 ,用 [3 H]-亮氨酸掺入法测定线粒体体外翻译活性 ,[3 5S]-蛋氨酸掺入并对翻译后产物经SDS -PAGE和放射自显影进行分子量鉴定。结果 :急性低氧脑线粒体蛋白翻译活性明显低于对照组 6 0 % (P <0 0 1) ,慢性低氧时线粒体翻译活性与对照组无显著差异 (P >0 0 5 ) ,但显著高于急性低氧组 (P <0 0 5 )。急性与慢性低氧暴露均未发现线粒体蛋白体外翻译产物与平原对照组有质的差异。结论 :低氧可影响线粒体DNA编码蛋白合成 ,并且与低氧暴露时间有关。
AIM: To investigate the effect of simulated high altitude hypoxia on rat brain mitochondrial translation activity. METHODS: Animals were continuously exposed to simulated 4 000 m high altitude in hypobaric chamber for three days and forty days. Mitochondria of rat brain were isolated by homogenizing brain tissue and following centrifuging program. Protein translation activity in isolated mitochondria in vitro was measured with -Lencine incorporation method. Products labeled with -methionine in isolated mitochondrial protein synthesis system in vitro were separated on SDS-PAGE and identified by autoradiography. RESULTS: Mitochondrial translation activity in vitro in acute hypoxia exposure were significantly lower than control( P< 0 01). Mitochondrial translation activity in chronic hypoxia exposure were significantly higher than that in acute hypoxia exposure( P< 0.05), but showed no statistical difference between chronic and control. No differences in electrophoretic-autoradiography pattern of -methionine incorporation into translational products was observed among three groups. CONCLUSION: These results indicated that acute hypoxia exposure depressed synthesis of mitochondrial protein encoded by mitochondrial DNA in vitro and the changes in mitochondrial protein synthesis were related with hypoxia exposure time. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第9期1038-1041,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (39730 190 )
关键词
线粒体
翻译
低氧
大鼠
WTBZ]Mitochondria
Translating
Anoxia
Rats