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Titolo:
EFFECT OF ALPHA-LIPOIC ACID AND DIHYDROLIPOIC ACID ON ISCHEMIA-REPERFUSION INJURY OF THE HEART AND HEART-MITOCHONDRIA
Autore:
SCHONHEIT K; GILLE L; NOHL H;
Indirizzi:
VET UNIV VIENNA,INST PHARMACOL & TOXICOL,LINKE BAHNGASSE 11 A-1030 VIENNA AUSTRIA VET UNIV VIENNA,INST PHARMACOL & TOXICOL A-1030 VIENNA AUSTRIA
Titolo Testata:
Biochimica et biophysica acta. Molecular basis of disease
fascicolo: 2-3, volume: 1271, anno: 1995,
pagine: 335 - 342
SICI:
0925-4439(1995)1271:2-3<335:EOAAAD>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREE-RADICAL GENERATION; POSTISCHEMIC REPERFUSION; MOLECULAR-OXYGEN; RESPIRATION; SCAVENGER;
Keywords:
HEART; MITOCHONDRIA; DIHYDROLIPOIC ACID; ALPHA-LIPOIC ACID; SUPEROXIDE RADICAL; UBISEMIQUINONE;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
K. Schonheit et al., "EFFECT OF ALPHA-LIPOIC ACID AND DIHYDROLIPOIC ACID ON ISCHEMIA-REPERFUSION INJURY OF THE HEART AND HEART-MITOCHONDRIA", Biochimica et biophysica acta. Molecular basis of disease, 1271(2-3), 1995, pp. 335-342

Abstract

The aim of the present study was to evaluate a possible interference of or-lipoic acid (LA) or its reduced form (dithiol dihydrolipoic acid= DHLA) in the cardiac ischemia/reperfusion injury both at the level of the intact organ and at the subcellular level of mitochondria. In order to follow the effect of LA on the ischemia/reperfusion injury of the heart the isolated perfused organ was subjected to total global ischemia and reperfusion in the presence and absence of different concentrations of LA, Treatment with 0.5 mu M LA improved the recovery of hemodynamic parameters; electrophysiological parameters were not influenced. However, application of 10 mu M LA to rat hearts further impairedthe recovery of hemodynamic functions and prolonged the duration of severe rhythm disturbances in comparison to reperfusion of control hearts. Treatment of isolated mitochondria with any concentration of DHLA could not prevent the impairment of respiratory-linked energy conservation caused by the exposure of mitochondria to 'reperfusion' conditions. However, DHLA was effective in decreasing the formation and the existence of mitochondrial superoxide radicals (O-2(-)). Apart from its direct O-2(-)-scavenging activities DHLA was also found to control mitochondrial O-2(-) formation indirectly by regulating redox-cycling ubiquinone. It is suggested that impairment of this mitochondrial O-2(-) generator mitigates postischemic oxidative stress which in turn reducesdamage to hemodynamic heart function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/08/20 alle ore 23:03:44