AGE-ASSOCIATED DAMAGE IN MITOCHONDRIAL-FUNCTION IN RAT HEARTS

被引:113
作者
TAKASAWA, M
HAYAKAWA, M
SUGIYAMA, S
HATTORI, K
ITO, T
OZAWA, T
机构
[1] UNIV NAGOYA, FAC MED, DEPT INTERNAL MED, SHOWA KU, NAGOYA 466, JAPAN
[2] UNIV NAGOYA, FAC MED, DEPT BIOMED CHEM, SHOWA KU, NAGOYA 466, JAPAN
关键词
HEART; LIVER; MITOCHONDRIA; AGING; MITOCHONDRIAL DNA; 8-HYDROXYDEOXYGUANOSINE;
D O I
10.1016/0531-5565(93)90034-B
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
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.
引用
收藏
页码:269 / 280
页数:12
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