Stimulation of macroautophagy can rescue older cells from 8-OHdG mtDNA accumulation: A safe and easy way to meet goals in the SENS agenda

被引：27

作者：

Donati, Alessio ^{[1
]}

Taddei, Michele ^{[1
]}

Cavallini, Gabriella ^{[1
]}

Bergamini, Ettore ^{[1
]}

机构：

[1] Univ Pisa, Ctr Res Biol & Pathol Aging, I-56126 Pisa, Italy

来源：

REJUVENATION RESEARCH | 2006年 / 9卷 / 03期

关键词：

D O I：

10.1089/rej.2006.9.408

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：

Reduction of oxidative stress within mitochondria is a major focus and important part in the SENS agenda. The age-related accumulation of mitochondria rich in oxidatively altered DNA may be a biomarker of malfunctioning and increased oxidative stress. Macroautophagy is the cell repair mechanism responsible for the disposal of excess or altered mitochondria tinder the inhibitory control of nutrition and insulin, and may mediate the antiaging effects of caloric restriction. The authors investigated the effects of stimulation of macroautophagy by the injection of an antilipolytic agent on the age-related accumulation of oxidatively altered mitochondrial DNA (mtDNA) in rat liver cells. Results showed that treatment rescued older cells from the accumulation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the mtDNA in less than 6 hours. It is concluded that the age-related changes in mtDNA and function are likely to be the consequence of a failure of macroautophagy in the recognition and disposal of a Small number of severely injured mitochondria, and that easy and safe ways are available to counteract this change.

引用

页码：408 / 412

页数：5

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