Mitochondrial DNA - all things bad?

被引：45

作者：

Lightowlers, RH

Jacobs, HT

Kajander, OA

机构：

[1] Newcastle Univ, Sch Med, Dept Neurol, Mol Neurol Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England

[2] Inst Med Technol, Tampere 33101, Finland

[3] Tampere Univ Hosp, Tampere 33101, Finland

[4] Univ Glasgow, Inst Biomed & Life Sci, Glasgow G12 8QQ, Lanark, Scotland

来源：

TRENDS IN GENETICS | 1999年 / 15卷 / 03期

关键词：

D O I：

10.1016/S0168-9525(98)01684-9

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Mutations in mitochondrial DNA (mtDNA) are undoubtedly associated with a diverse spectrum of human disorders. More controversially, it has been claimed that they accumulate during ageing, and that they are responsible for an age-related decline in bioenergetic function and tissue viability. Here, we review the evidence for this assertion, concluding that claims for the age-accumulation of mtDNA mutations are based largely on non-quantitative methods, and that no clear, functional deficit of mitochondrial respiration has been shown to result from such lesions in aged individuals. The mitochondrial theory of ageing, however attractive in principle, is supported by very little hard evidence.

引用

页码：91 / 93

页数：3

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