Localization of Abasic Sites and Single-Strand Breaks in Mitochondrial DNA from Brain of Aged Rat, Treated or not with Caloric Restriction Diet

被引：10

作者：

Lezza, A. M. S. ^{[1
]}

Fallacara, F. P. ^{[1
]}

Pesce, V. ^{[1
]}

Leeuwenburgh, C. ^{[2
]}

Cantatore, P. ^{[1
,3
]}

Gadaleta, M. N. ^{[1
,3
]}

机构：

[1] Univ Bari, Dept Biochem & Mol Biol Ernesto Quagliariello, I-70125 Bari, Italy

[2] Univ Florida, Coll Med, Dept Aging & Geriatr, Gainesville, FL 32611 USA

[3] CNR, Inst Biomembranes & Bioenerget, I-70126 Bari, Italy

来源：

NEUROCHEMICAL RESEARCH | 2008年 / 33卷 / 12期

关键词：

Aging; Caloric restriction; Rat brain; Mitochondrial DNA damage; Abasic sites; Ss-breaks;

D O I：

10.1007/s11064-008-9866-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

According to the "mitochondrial theory of aging'' the lifelong accumulation of various kinds of damage to mitochondrial DNA ( mtDNA) has been related to the age-dependent mitochondrial bioenergetic dysfunction. Caloric restriction (CR) diet is able to prevent or delay the onset of several age-related damages to mtDNA. The effects of aging and CR on the presence of abasic sites and single-strand breaks of the sugar-phosphate backbone in mtDNA have been analyzed by applying Ligation Mediated-PCR to a H strand region of brain mtDNA from young and old ad libitum-fed and old CR-treated rats. The region, encompassing the Direct Repeat 1 of the 4,834 bp-long deletion, is highly damaged in the old ad libitum- fed animals with respect to the young ones, whereas in the CR rats it shows a much lower extent of damage. The data confirm, at single nucleotide resolution, the protective effect of CR on the age-related mtDNA damage.

引用

页码：2609 / 2614

页数：6

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