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衰老过程中心肌F1F0 ATP合酶的功能和分子变化

Functional and molecular changes in FoF1 ATP-synthase of cardiac muscle during aging.

作者信息

Guerrieri F, Capozza G, Fratello A, Zanotti F, Papa S

机构信息

Institute of Medical Biochemistry and Chemistry, University of Bari, Italy.

出版信息

Cardioscience. 1993 Jun;4(2):93-8.

PMID:8347797
Abstract

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.

摘要

我们研究了衰老过程中心肌线粒体F₀F₁ATP合酶的功能和分子变化。从老年大鼠(24个月)心脏制备的超声亚线粒体颗粒中的ATP水解酶活性低于从成年大鼠(12个月)心脏制备的颗粒。老年大鼠心脏亚线粒体颗粒对寡霉素敏感的质子传导性比成年大鼠更高。通过免疫检测在亚线粒体颗粒中发现的F₁的β亚基,老年大鼠比成年大鼠少。成年大鼠心脏亚线粒体颗粒暴露于由⁶⁰Co产生的自由基中,导致ATP水解酶活性失活和F₁含量降低。衰老过程中线粒体F₀F₁ATP合酶的结构和功能改变可能会影响能量代谢,我们的结果表明它们可能源于线粒体内膜产生自由基(的作用)。

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