Subtitle:

Age-related Fragmentation of Mitochondrial DNA Associated with Oxygen Damage

Publisher:

Komitet Biotechnologii PAN ; Instytut Chemii Bioorganicznej PAN

Description:

Zeszyt specjalny. Polish - Japan Issue

Abstract:

In normal human hearts, a progressive age-related fragmentation of mitochondrial (mt) DNAinto various-sized deleted (A) mtDNA up to 358 types was documented by a novel total-detectionsystem for deletions. The AmtDNA lacking replication origin(s), minicircles, accumulated up to280 types out of the 358, suggesting a yet unknown replication mechanism in human. Wild-typemtDNA decreased linearly down to 11% of the total with age negatively correlated with AmtDNAand oxidized nucleoside, 8-hydroxy-deoxyguanosine. A remarkable mirror image observed inAmtDNA size distribution as well implies that random hydroxyl-radical attacks resulted in doublestrand break and rejoining of mtDNA as a preferable mechanism to form various AmtDNA ofclosed circular duplex. In the patients with mitochondrial cardiomyopathy, similar fragmentationand oxidative damage in mtDNA was documented at their age 7 to 19 equivalent to the normalsubjects of age over 80. Exposure of a cultured cell line under oxygen stress, 95% oxygen, coldmimic these changes in mtDNA* within 3 days leading an apoptotic cell death, whereas mtDNAlacking cells are relatively immune. These facts support the ‘redox mechanism of ageing’.

Relation:

Biotechnologia, vol.35, 4 (1996)-.

Volume:

35

Issue:

4

Start page:

208

End page:

222

Detailed Resource Type:

Artykuł

Format:

application/pdf

Resource Identifier:

0860-7796 ; oai:rcin.org.pl:146571 ; IChB B-31

Source:

Biblioteka Instytutu Chemii Bioorganicznej PAN

Language:

pol

Language of abstract:

eng

Temporal coverage:

1988-2010

Rights:

Licencja Creative Commons Uznanie autorstwa-Na tych samych warunkach 4.0

Terms of use:

-

Digitizing institution:

Instytut Chemii Bioorganicznej Polskiej Akademii Nauk

Original in:

Instytut Chemii Bioorganicznej Polskiej Akademii Nauk

Projects co-financed by:

Program Operacyjny Polska Cyfrowa, lata 2014-2020, Działanie 2.3 : Cyfrowa dostępność i użyteczność sektora publicznego; środki z Europejskiego Funduszu Rozwoju Regionalnego oraz współfinansowania krajowego z budżetu państwa

Access:

Otwarty