학술논문
Inhibition of hypochlorous acid-induced cellular toxicity by nitrite
Document Type
Abstract
Source
Proceedings of the National Academy of Sciences of the United States. Sept 17, 2002, Vol. 99 Issue 19, p12061, 6 p.
Subject
Language
ISSN
0027-8424
Abstract
Chronic inflammation results in increased nitrogen monoxide (*NO) formation and the accumulation of nitrite (N[O.sup.-.sub.2]). Neutrophils stimulated by various inflammatory mediators release myeloperoxidase to produce the cytotoxic agent hypochlorous acid (HOCl). Exposure of chondrocytic SW1353 cells to HOCl resulted in a concentration- and time-dependent loss in viability, ATP, and glutathione levels. Treatment of cells with N[O.sup.-.sub.2] but not nitrate (N[O.sup.-.sub.3]) substantially decreased HOCl-dependent cellular toxicity even when N[O.sup.-.sub.2] was added at low ([micro]M) concentrations. In contrast, N[O.sup.-.sub.2] alone (even at 1 mM concentrations) did not affect cell viability or ATP and glutathione levels. These data suggest that N[O.sup.-.sub.2] accumulation at chronic inflammatory sites, where both HOCl and *NO are overproduced, may be cytoprotective against damage caused by HOCl. We propose that this is because HOCl is removed by reacting with N[O.sup.-.sub.2] to give nitryl chloride (N[O.sub.2]Cl), which is less damaging in our cell system. inflammation | cell toxicity | nitryl chloride | nitric oxide | arthritis