急慢性缺氧对大鼠心肌和肝细胞线粒体~3H－亮氨酸掺入量及DNA含量的影响

Effect of hypoxia on incorporation of ￣3H-Leucine into mitochondria protein and mitochondrial DNA content

本文采用￣３Ｈ－亮氨酸活体注入法观测了急性连续缺氧（模拟高原５０００ｍ）３、１２，３６和７２小时以及慢性间断缺氧１４，２８和４２（每天８小时）对大鼠肝脏及心肌线粒体的￣３Ｈ－亮氨酸掺入的影响。结果显示心肌线粒体的￣３Ｈ－亮氨酸掺入量多于肝脏。急性缺氧可显著抑制亮氨酸掺入，随后逐渐上升。缺氧７２小时末心肌和肝线粒体的亮氨酸掺入量分别达１７３％和１４８％。慢性缺氧可致心肌及肝脏线粒体的亮氨酸掺入量降低。以荧光法测定慢性缺氧心肌线粒体的ＤＮＡ含量，结果显示缺氧１４天无显著变化，２８天及４２天ＤＮＡ量显著升高。本实验结果提示，急性缺氧可显著抑制￣３Ｈ－亮氨酸掺入线粒体，但随后线粒体蛋白合成增强，慢性缺氧动物心肌线粒体蛋白合成受抑而ＤＮＡ复制增加。

Wistar rats were divided into 3 groups:1(the normoxic control,2)acutehypoxia group in which rats were exposed to continuous hypoxia(at simulated altitude of5000m)for 3,12,36,and 72 hours respectively,3)chronic hypoxia group in whichrats were subjected to intermittent hypoxia(at simulated altitude of 5000m 8 hr/day,for 14,28,and 42 days respectively).To observe the effect of hypoxia on mitochon-drial protein synthesis,amino acid(￣3H-Leucine)incorporation into liver and heart mito-chondrial protein were measured. Decreases in ￣3H-Leucine incorporation were observedboth in rats exposed to chronic hypoxia and in acute hypoxia at the end of 3 and 12hours.The incorporation at the end of 3 hours was the lowest,while at the end of 72hour the incorporation increased to 173%and 140%in heart and liver respyctively. Theheart mitochondrial DNA contents in chronic hypoxia groups were determined by 3,5-diaminobenzoic acid.At 14 th day of hypoxia,no difference was observed between thehypoxic and the control animals,but at 28 th or 42 nd days,mit-DNA increased signifi-cantly. These results indicated that mitochondrial protein synthesis was depressed in acutehypoxia, especially at the early stage(end of the third hour),then enhanced.The repli-cation of mitochondrial DNA increased while mitochondrial protein synthesis decreased inchronic hypoxia.