期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2002
卷号：99
期号：19
页码：12061-12066
DOI：10.1073/pnas.152462399
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Chronic inflammation results in increased nitrogen monoxide (*NO) formation and the accumulation of nitrite (NO[IMG]f1.gif" ALT="Formula" BORDER="0">). 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 NO[IMG]f1.gif" ALT="Formula" BORDER="0"> but not nitrate (NO[IMG]f2.gif" ALT="Formula" BORDER="0">) substantially decreased HOCl-dependent cellular toxicity even when NO[IMG]f1.gif" ALT="Formula" BORDER="0"> was added at low ({micro}M) concentrations. In contrast, NO[IMG]f1.gif" ALT="Formula" BORDER="0"> alone (even at 1 mM concentrations) did not affect cell viability or ATP and glutathione levels. These data suggest that NO[IMG]f1.gif" ALT="Formula" BORDER="0"> 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 NO[IMG]f1.gif" ALT="Formula" BORDER="0"> to give nitryl chloride (NO2Cl), which is less damaging in our cell system.
