衰老过程中心肌FoF1 atp合酶的功能及分子变化。

Cardioscience Pub Date : 1993-06-01
F Guerrieri, G Capozza, A Fratello, F Zanotti, S Papa
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引用次数: 0

摘要

我们研究了心肌线粒体FoF1 ATP合酶在衰老过程中的功能和分子变化。衰老大鼠(24个月)心脏制备的超声亚线粒体颗粒的ATP水解酶活性低于成年大鼠(12个月)心脏制备的线粒体颗粒。衰老大鼠心肌亚线粒体颗粒对寡霉素敏感的质子传导比成年大鼠大。在亚线粒体颗粒中免疫检测到的F1 β亚基在衰老大鼠中比在成年大鼠中少。成年大鼠心脏亚线粒体颗粒暴露于60Co产生的自由基中,导致ATP水解酶活性失活,F1含量降低。衰老过程中线粒体FoF1 ATP合酶的结构和功能改变可能会影响能量代谢,我们的研究结果表明,这可能源于线粒体内膜产生的自由基的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Functional and molecular changes in FoF1 ATP-synthase of cardiac muscle during aging.

We have studied the functional and molecular changes of mitochondrial FoF1 ATP synthase of cardiac muscle during aging. ATP hydrolase activity was lower in sonic submitochondrial particles prepared from hearts of senescent rats (24 months) than in those prepared from hearts of adult rats (12 months). Oligomycin-sensitive proton conduction of cardiac submitochondrial particles was greater in senescent rats than in adult rats. The beta subunit of F1, detected immunologically in submitochondrial particles, was less in senescent rats than in adult rats. Exposure of cardiac submitochondrial particles from adult rats to free radicals, generated by 60Co, resulted in inactivation of ATP hydrolase activity and a decreased content of F1. The structural and functional alterations of mitochondrial FoF1 ATP synthase during aging may be expected to affect energy metabolism, and our results suggest that they could originate from the action of free radicals generated in the inner mitochondrial membrane.

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