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Titolo:
NITRIC-OXIDE ATTENUATES CELLULAR HEXOSE-MONOPHOSPHATE SHUNT RESPONSE TO OXIDANTS IN ARTICULAR CHONDROCYTES AND ACTS TO PROMOTE OXIDANT INJURY
Autore:
CLANCY RM; ABRAMSON SB; KOHNE C; REDISKE J;
Indirizzi:
NYU,HOSP JOINT DIS,MED CTR,DEPT RHEUMATOL,301 E 17TH ST NEW YORK NY 10003 NYU,MED CTR,DEPT MED,DIV RHEUMATOL NEW YORK NY 10003 CIBA GEIGY CORP,RES DEPT SUMMIT NJ 07901
Titolo Testata:
Journal of cellular physiology
fascicolo: 2, volume: 172, anno: 1997,
pagine: 183 - 191
SICI:
0021-9541(1997)172:2<183:NACHSR>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYDROGEN-PEROXIDE; GLUTATHIONE-PEROXIDASE; PROTEOGLYCAN SYNTHESIS; SUPEROXIDE-DISMUTASE; INHIBITION; CELLS; CYTOTOXICITY; PEROXYNITRITE; APOPTOSIS; DEPLETION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
R.M. Clancy et al., "NITRIC-OXIDE ATTENUATES CELLULAR HEXOSE-MONOPHOSPHATE SHUNT RESPONSE TO OXIDANTS IN ARTICULAR CHONDROCYTES AND ACTS TO PROMOTE OXIDANT INJURY", Journal of cellular physiology, 172(2), 1997, pp. 183-191

Abstract

Nitric oxide (NO) has been implicated in both cartilage degradation and cell survival. Importantly, NO has been shown, in a cell-type-dependent manner, to directly cause cell death or indirectly promote cell death by compromising the ability of cells to detoxify intra- or extracellular oxidants. In this study we examined the role of NO in the survival of bovine chondrocytes exposed to catabolic cytokines (interleukin-l (IL-l); tumor necrosis factor [TNF]) with or without the addition of an exogenous oxidant stress (e.g., H2O2, HOOCl, etc.). The exposureof chondrocytes to a mixture of IL-l and TNF (IL-1/TNF) results in the release of NO but did not alter cell viability. However, there was evidence of NO-dependent oxidative responses in the IL-1/TNF group, as we observed an increased level of intracellular oxidants as well as the appearance of a 55 kD nitrated protein which reflects the formation of peroxynitrite. We next analyzed viability with H2O2. The LD50 for IL-1/TNF-treated cells was 0.1 mM (vs. 1 mM for control). The enhanced sensitivity was completely reversed when cells were incubated with theNO synthase inhibitor 1-n5-1-iminoethylornithine (NIO). To test whether cell death was caused by compromising the ability of cells to detoxify extracellular oxidants, we examined the hexose monophosphate shunt(HMPS) response in cells given H2O2. Treatment of control cells with H2O2 resulted in a fourfold increase in HMPS activity. In contrast, IL-1/TNF cells exhibited no increase in HMPS activity. The attenuation of stimulated HMPS activity was reversed by the coaddition of NIO. Thus, these data indicate that 1) endogenous NO mediates cytokine-dependent susceptibility to oxidant injury and 2) this effect is in part due to impaired activation of the HMPS. In inflamed joints replete with cytokines and oxidants, NO may contribute to chondrocyte death and progressive joint destruction. (C) 1997 Wiley-Liss, Inc.

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Documento generato il 21/09/20 alle ore 06:27:16