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Titolo:
Hydrogen peroxide- and peroxynitrite-induced mitochondrial DNA damage and dysfunction in vascular endothelial and smooth muscle cells
Autore:
Ballinger, SW; Patterson, C; Yan, CN; Doan, R; Burow, DL; Young, CG; Yakes, FM; Van Houten, B; Ballinger, CA; Freeman, BA; Runge, MS;
Indirizzi:
Univ Texas, Med Branch, Div Cardiol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 h, Div Cardiol, Galveston, TX 77555 USA Univ Texas, Med Branch, Sealy Ctr Mol Cardiol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 tr Mol Cardiol, Galveston, TX 77555 USA Vanderbilt Univ, Dept Biochem, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 t Biochem, Nashville, TN 37232 USA Univ Alabama, Dept Anesthesiol, Birmingham, AL USA Univ Alabama Birmingham AL USA ama, Dept Anesthesiol, Birmingham, AL USA
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 9, volume: 86, anno: 2000,
pagine: 960 - 966
SICI:
0009-7330(20000512)86:9<960:HPAPMD>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; MANGANESE SUPEROXIDE-DISMUTASE; RAT-LIVER MITOCHONDRIA; NITRIC-OXIDE; OXIDATIVE STRESS; HEART-MITOCHONDRIA; GENERATION; RADICALS; LDL; ATHEROSCLEROSIS;
Keywords:
reactive oxygen species; reactive nitrogen species; atherosclerosis; oxidative damage;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Runge, MS Univ Texas, Med Branch, Div Cardiol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 diol, Galveston, TX 77555 USA
Citazione:
S.W. Ballinger et al., "Hydrogen peroxide- and peroxynitrite-induced mitochondrial DNA damage and dysfunction in vascular endothelial and smooth muscle cells", CIRCUL RES, 86(9), 2000, pp. 960-966

Abstract

The mechanisms by which reactive species (RS) participate in the development of atherosclerosis remain incompletely understood, The present study wasdesigned to test the hypothesis that RS produced in the vascular environment cause mitochondrial damage and dysfunction in vitro and, thus, may contribute to the initiating events of atherogenesis. DNA damage was assessed invascular cells exposed to superoxide, hydrogen peroxide, nitric oxide, andperoxynitrite. In both vascular endothelial and smooth muscle cells, the mitochondrial DNA (mtDNA) was preferentially damaged relative to the transcriptionally inactive nuclear beta-globin gene. Similarly, a dose-dependent decrease in mtDNA-encoded mRNA transcripts was associated with RS treatment. Mitochondrial protein synthesis was also inhibited in a dose-dependent manner by ONOO-, resulting in decreased cellular ATP levels and mitochondrial redox function. Overall, endothelial cells were more sensitive to RS-mediated damage than were smooth muscle cells. Together, these data link RS-mediated mtDNA damage, altered gene expression, and mitochondrial dysfunction incell culture and reveal how RS may mediate vascular cell dysfunction in the setting of atherogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 06:08:35