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大鼠心脏中线粒体功能的年龄相关损伤。

Age-associated damage in mitochondrial function in rat hearts.

作者信息

Takasawa M, Hayakawa M, Sugiyama S, Hattori K, Ito T, Ozawa T

机构信息

Department of Internal Medicine, Faculty of Medicine, University of Nagoya, Japan.

出版信息

Exp Gerontol. 1993 May-Jun;28(3):269-80. doi: 10.1016/0531-5565(93)90034-b.

DOI:10.1016/0531-5565(93)90034-b
PMID:8344397
Abstract

The aim of this study is to elucidate effects of aging on mitochondrial function and mitochondrial DNA (mtDNA) in rat heart and liver. The activities of complex I and complex IV of heart mitochondria of rats aged 100 weeks decreased significantly by 31% and 22%, respectively, compared with those of rats aged 7 weeks. No significant changes were observed in these two parameters in rats aged 7 weeks and aged 55 weeks. There were no significant differences in the specific activities of complex II and complex III among the age groups of 7, 55, and 100 weeks. The mtDNA content decreased by 58% in rats aged 100 weeks compared with that in rats aged 7 weeks. Content of 8-hydroxydeoxyguanosine (8-OH-dG), an oxidative product of deoxyguanosine (dG), increased by 130% in rats aged 100 weeks compared with that in rats aged 7 weeks. No significant changes were observed in these parameters between rats aged 7 weeks and 55 weeks. In contrast to heart mtDNA, these age-dependent changes were not observed in liver mitochondria at rats aged up to 100 weeks. From our results, age-associated decline in mitochondrial function might play an important role in cell aging, particularly in postmitotic cells such as heart muscle, and accumulation of oxidative damage to mtDNA might be involved in this mechanism.

摘要

本研究的目的是阐明衰老对大鼠心脏和肝脏线粒体功能及线粒体DNA(mtDNA)的影响。与7周龄大鼠相比,100周龄大鼠心脏线粒体复合物I和复合物IV的活性分别显著降低了31%和22%。7周龄和55周龄大鼠的这两个参数未观察到显著变化。7周、55周和100周龄组之间复合物II和复合物III的比活性无显著差异。与7周龄大鼠相比,100周龄大鼠的mtDNA含量降低了58%。脱氧鸟苷(dG)的氧化产物8-羟基脱氧鸟苷(8-OH-dG)的含量在100周龄大鼠中比7周龄大鼠增加了130%。7周龄和55周龄大鼠之间这些参数未观察到显著变化。与心脏mtDNA不同,在高达100周龄的大鼠肝脏线粒体中未观察到这些年龄依赖性变化。根据我们的结果,与年龄相关的线粒体功能下降可能在细胞衰老中起重要作用,特别是在心肌等有丝分裂后细胞中,mtDNA氧化损伤的积累可能参与了这一机制。

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