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Titolo:
Oxidative stress is not an obligate mediator of disease provoked by mitochondrial DNA mutations
Autore:
Mott, JL; Zhang, DK; Stevens, M; Chang, SW; Denniger, G; Zassenhaus, HP;
Indirizzi:
St Louis Univ, Hlth Sci Ctr, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA St Louis Univ St Louis MO USA 63104 iol & Immunol, St Louis, MO 63104 USA
Titolo Testata:
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
fascicolo: 1-2, volume: 474, anno: 2001,
pagine: 35 - 45
SICI:
1386-1964(20010301)474:1-2<35:OSINAO>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; DEGENERATIVE DISEASES; HEART-FAILURE; RINR-38 CELLS; HUMAN TISSUES; DAMAGE; MOUSE; GLUTATHIONE; PROTEINS; BCL-2;
Keywords:
mitochondrial DNA mutations; mtDNA; oxidative stress; pathogenesis; cardiomyopathy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Zassenhaus, HP St Louis Univ, Hlth Sci Ctr, Dept Mol Microbiol & Immunol, 1402 S Grand Blvd, St Louis, MO 63104 USA St Louis Univ 1402 S Grand Blvd St Louis MO USA 63104 4 USA
Citazione:
J.L. Mott et al., "Oxidative stress is not an obligate mediator of disease provoked by mitochondrial DNA mutations", MUT RES-F M, 474(1-2), 2001, pp. 35-45

Abstract

With age. mitochondrial DNA mutations and oxidative stress increase, leading to the hypothesis that the production of reactive oxygen species causes the pathogenic effects of mitochondrial DNA mutations. We tested this hypothesis using transgenic mice that develop cardiomyopathy due to the accumulation of mitochondrial DNA mutations specifically in the heart. Surprisingly, the mechanism of pathogenesis does not involve increased oxidative stress. The amounts of DNA and protein oxidative adducts are not elevated in the transgenic heart. Neither are signs of increased oxidative stress detected by measurements of enzyme function or oxidative defense systems. Rather, wefind that the mitochondrial DNA mutations induce a cytoprotective responseincluding increases in the levels of Bcl-2 and Bfl-1, pro-survival proteins that inhibit apoptosis. and atrial natriuretic factor. Bcl-2 is elevated in nearly all cardiomyocytes before the onset of dilated cardiomyopathy. These results raise the possibility that a signaling pathway between the mitochondrion and the nucleus mediates the pathogenic effect of mitochondrial DNA mutations. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 01:43:09