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Titolo:
Targeted disruption of the mouse Sod I gene makes the hearts vulnerable toischemic reperfusion injury
Autore:
Yoshida, T; Maulik, N; Engelman, RM; Ho, YS; Das, DK;
Indirizzi:
Univ Connecticut, Sch Med, Cardiovasc Res Ctr, Dept Surg, Farmington, CT 06030 USA Univ Connecticut Farmington CT USA 06030 t Surg, Farmington, CT 06030 USA Wayne State Univ, Inst Chem Toxicol, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 Chem Toxicol, Detroit, MI 48201 USA
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 3, volume: 86, anno: 2000,
pagine: 264 - 269
SICI:
0009-7330(20000218)86:3<264:TDOTMS>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
SUPEROXIDE-DISMUTASE; TRANSGENIC MICE; ISCHEMIA/REPERFUSION INJURY; GLUTATHIONE-PEROXIDASE; OXIDATIVE STRESS; FREE-RADICALS; HUMAN-DISEASE; RAT-HEART; OVEREXPRESSION; CARDIOPROTECTION;
Keywords:
transgenic; knockout; ischemia/reperfusion; free radicals; oxidative stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Das, DK Univ Connecticut, Sch Med, Cardiovasc Res Ctr, Dept Surg, Farmington, CT 06030 USA Univ Connecticut Farmington CT USA 06030 Farmington, CT 06030 USA
Citazione:
T. Yoshida et al., "Targeted disruption of the mouse Sod I gene makes the hearts vulnerable toischemic reperfusion injury", CIRCUL RES, 86(3), 2000, pp. 264-269

Abstract

The role of Cu/Zn-superoxide dismutase (SOD) in myocardial ischemic reperfusion injury was studied by using a mouse model with targeted disruption ofthe mouse Sod I gene. Inactivation of the functional mouse Sod I gene in hearts by gene targeting (Sod I+/-) resulted in a 50% reduction of Cu/Zn-SODmRNA and significant reduction of Cu/Zn-SOD enzyme activity compared with that of wild-type Son I+/+ mice. Cu/Zn-SOD mRNA could not be detected in Son I-/- heart. The isolated buffer-perfused hearts from the knockout mice devoid of any functional copy of the Sod I (Sod I-/-) and matched nontransgenic control mice were subjected to 30 minutes of global ischemia followed by2 hours of reperfusion. For both groups of mice, the postischemic functional recovery for the hearts was lower than the baseline, but the recovery for the Sod I-/- was less compared with the wild-type mice. Thus, the postischemic recovery of the developed force and the maximum first derivative of the developed force were consistently lower for the Sod I(-/-)mouse hearts compared with wild-type control hearts. The coronary flow was lower comparedwith the baseline levels for both groups of hearts, but there was no significant difference between the groups. The myocardial infarction determined from the ratio of infarct size/area of risk was higher for the Sod I-/- mice compared with the control mice. The amount of creatine kinase release from the wild-type mouse hearts was less compared with the Sod I-/- mouse hearts. In concert, a reduced amount of oxidative stress was found in the hearts of wild-type mice compared with Sod I-/- mouse hearts. These results documented that Sod I-/- mouse hearts were more susceptible to ischemic reperfusion injury compared with corresponding wild-type mouse hearts, suggesting that the Sod I gene constitutes an important defense element for the hearts.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 13:41:27