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Titolo:
OXIDANT STRESS WITH HYDROGEN-PEROXIDE ATTENUATES CALCIUM PARADOX INJURY - ROLE OF PROTEIN-KINASE-C AND ATP-SENSITIVE POTASSIUM CHANNEL
Autore:
MIYAWAKI H; WANG YG; ASHRAF M;
Indirizzi:
UNIV CINCINNATI,MED CTR,DEPT PATHOL & LAB MED,231 BETHESDA AVE CINCINNATI OH 45267 UNIV CINCINNATI,MED CTR,DEPT PATHOL & LAB MED CINCINNATI OH 45267
Titolo Testata:
Cardiovascular Research
fascicolo: 3, volume: 37, anno: 1998,
pagine: 691 - 699
SICI:
0008-6363(1998)37:3<691:OSWHAC>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISOLATED RAT-HEART; MYOCARDIAL INJURY; PRECONDITIONING ELICITS; FREE-RADICALS; PROTECTION; ISCHEMIA; MYOCYTES; CONTRIBUTES; REPERFUSION; GENERATION;
Keywords:
CALCIUM; K-ATP CHANNEL; MYOCYTES; PROTEIN KINASE C; PRECONDITIONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
H. Miyawaki et al., "OXIDANT STRESS WITH HYDROGEN-PEROXIDE ATTENUATES CALCIUM PARADOX INJURY - ROLE OF PROTEIN-KINASE-C AND ATP-SENSITIVE POTASSIUM CHANNEL", Cardiovascular Research, 37(3), 1998, pp. 691-699

Abstract

Objective: We tested the hypotheses that low concentration of H2O2 attenuates the Ca2+ paradox (Ca2+ PD) injury, and that activation of protein kinase C (PKC) and/or ATP-sensitive potassium channel (K-ATP) areinvolved in the protective effects of H2O2. Methods: Langendorff-perfused rat hearts were subjected to the Ca2+ PD (10 min of Ca2+ depletion followed by 10 min of Ca2+ repletion). Functional and biochemical effects of H2O2 and other interventions on the cell injury induced by the Ca2+ PD were assessed. Results: In the Ca2+ PD hearts pretreated with 20 mu mol/l H2O2, left ventricular end-diastolic pressure and coronary flow were significantly preserved. Furthermore, peak lactate dehydrogenase release was significantly decreased and ATP contents were morepreserved, compared with non-treated Ca2+ PD hearts. H2O2-treated hearts also showed remarkable preservation of cell structure. Addition ofa specific PKC inhibitor, chelerythrine during H2O2 treatment completely abolished the beneficial effects of H2O2 on the Ca2+ PD, Similarly, an activator of PKC, Phorbol 12-myristate 13 acetate mimicked the protection by H2O2. Furthermore, pretreatment with a K-ATP opener, cromakalim also provided protection similar to H2O2 against the Ca2+ PD injury. However, a specific K-ATP inhibitor, glibenclamide was not able to completely block the effects of H2O2. Conclusions: These findings suggest that pretreatment with low concentration of H2O2 provides significant protection against the lethal injury of Ca2+ PD in rat hearts. PKC-mediated signaling pathways appear to play a crucial role in the protection against the Ca2+ PD injury. (C) 1998 Elsevier Science B.V.

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Documento generato il 04/04/20 alle ore 15:31:18