Protein carbonyl accumulation in aging Dauer formation-defective (daf) mutants of Caenorhabditis elegans

被引:57
作者
Yasuda, K
Adachi, H
Fujiwara, Y
Ishii, N [1 ]
机构
[1] Tokai Univ, Sch Med, Dept Mol Life Sci, Kanagawa 2591193, Japan
[2] Lion Corp, Life Sci Res Ctr, Kanagawa, Japan
[3] Kobe Univ, Sch Med, Dept Radiat Biophys & Genet, Kobe, Hyogo 650, Japan
来源
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES | 1999年 / 54卷 / 02期
关键词
D O I
10.1093/gerona/54.2.B47
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
It is known that a dauer-constitutive gene, daf-2, controls both larval development and adult life span irt Caenorhabditis elegans. The increased life span caused by the daf-2 mutation can be enhanced by a daf-12 mutation and suppressed by a daf-16 mutation. In order to determine the correlation between longevity and oxidative stress in these mutants, protein carbonyl (a good indicator of oxidative damage during aging) was measured. Mean life spans of these mutants were in the order of daf-16 < daf-2;daf-16 congruent to wild type < daf-2 < daf-2;daf-12. Accumulations of protein carbonyl in these wild-type and daf mutants were in a mirror image of the order of their life spans. These results strongly support the notion that oxidative damage is one of the major causal factors for life-span determination in C. elegans.
引用
收藏
页码:B47 / B51
页数:5
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