nitryl-chloride and Inflammation

nitryl-chloride has been researched along with Inflammation* in 1 studies

Other Studies

1 other study(ies) available for nitryl-chloride and Inflammation

Article	Year
Inhibition of hypochlorous acid-induced cellular toxicity by nitrite. Proceedings of the National Academy of Sciences of the United States of America, 2002, Sep-17, Volume: 99, Issue:19 Chronic inflammation results in increased nitrogen monoxide (.NO) formation and the accumulation of nitrite (NO(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 NO(2-) but not nitrate (NO(3-)) substantially decreased HOCl-dependent cellular toxicity even when NO(2-) was added at low (microM) concentrations. In contrast, NO(2-) alone (even at 1 mM concentrations) did not affect cell viability or ATP and glutathione levels. These data suggest that NO(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 NO(2-) to give nitryl chloride (NO2Cl), which is less damaging in our cell system. Topics: Adenosine Triphosphate; Cell Line; Cell Survival; Chondrocytes; Glutathione; Humans; Hypochlorous Acid; Inflammation; L-Lactate Dehydrogenase; Nitrates; Nitric Oxide; Nitrites	2002

Article

Year

Inhibition of hypochlorous acid-induced cellular toxicity by nitrite.

Proceedings of the National Academy of Sciences of the United States of America, 2002, Sep-17, Volume: 99, Issue:19

Chronic inflammation results in increased nitrogen monoxide (.NO) formation and the accumulation of nitrite (NO(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 NO(2-) but not nitrate (NO(3-)) substantially decreased HOCl-dependent cellular toxicity even when NO(2-) was added at low (microM) concentrations. In contrast, NO(2-) alone (even at 1 mM concentrations) did not affect cell viability or ATP and glutathione levels. These data suggest that NO(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 NO(2-) to give nitryl chloride (NO2Cl), which is less damaging in our cell system.

Topics: Adenosine Triphosphate; Cell Line; Cell Survival; Chondrocytes; Glutathione; Humans; Hypochlorous Acid; Inflammation; L-Lactate Dehydrogenase; Nitrates; Nitric Oxide; Nitrites

2002