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Titolo:
UV light synergistically enhances the cardiotoxic effects of interleukin 1beta through peroxynitrite formation
Autore:
Combes, A; McTiernan, C; Brooks, SS; Feldman, AM;
Indirizzi:
Univ Pittsburgh, Med Ctr, Inst Cardiovasc, Cardiovasc Res Labs, Pittsburgh, PA 15213 USA Univ Pittsburgh Pittsburgh PA USA 15213 es Labs, Pittsburgh, PA 15213 USA
Titolo Testata:
JOURNAL OF CARDIAC FAILURE
fascicolo: 2, volume: 7, anno: 2001,
pagine: 165 - 175
SICI:
1071-9164(200106)7:2<165:ULSETC>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR; CARDIAC ALLOGRAFT-REJECTION; GROWTH-FACTOR-BETA; GENE-EXPRESSION; FACTOR-ALPHA; MYOCYTES; INDUCTION; SUPEROXIDE; CYTOKINES;
Keywords:
free radicals; calcium transients; cardiomyocytes; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Feldman, AM Univ Pittsburgh, Med Ctr, Inst Cardiovasc, Cardiovasc Res Labs, S572 Scaife Hall,200 Lothrop St, Pittsburgh, PA 15213 USA Univ PittsburghS572 Scaife Hall,200 Lothrop St Pittsburgh PA USA 15213
Citazione:
A. Combes et al., "UV light synergistically enhances the cardiotoxic effects of interleukin 1beta through peroxynitrite formation", J CARD FAIL, 7(2), 2001, pp. 165-175

Abstract

Background: Proinflammatory cytokines play an important role in chronic cardiac diseases. Methods and Results: Neonatal rat cardiomyocytes were exposed to interleukin (IL)-I beta (2 ng/mL) for 4 days. We assessed contractility through videomicroscopy and calcium transients with the Ca2+-sensitive dye fura-2. In IL-1 beta -treated cells, the UV excitation (380 nm) necessary to induce dyefluorescence effected a rapid cessation of Ca2+ transients and contraction, accompanied by calcium overload originating from an intracellular compartment. This occurred in the absence of fura-2 but required UV illumination. Incubation with 10 mmol/L N-acetylcysteine prevented this response, suggesting a free radical-mediated event. However, exposure to IL-1 beta either increased or did not change the activity of the free radical scavengers superoxide dismutase, catalase, and glutathione peroxidase. In contrast, lipid peroxidation increased by 600% (P less than or equal to .0001) in the IL-1 beta plus W-treated cells, an effect eliminated by L-NMMA. L-NMMA also completely abolished the UV-mediated cytotoxicity. We used immunohistochemistry to localize nitrotyrosine accumulation in the myocytes cotreated with IL-1 beta and UV, an effect that was also blocked by L-NMMA. Conclusions: We hypothesize that the toxic radical peroxynitrite, arising from nitric oxide and superoxide anion, may be responsible for tetany and acute cardiomyocyte death. These results demonstrate the potential role of peroxynitrite in cardiotoxicity, which may be important in cardiac diseases associated with proinflammatory cytokines.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 09:53:10