The effect of nitric oxide (NO) on the oxidative burst was analyzed in purified murine microglial cells in vitro. The generation of reactive oxygen derivatives was monitored with the use of luminol-dependent chemiluminescence. After inducing the endogenous NO production with interleukin 1beta (IL-1beta) and interferon-gamma (IFN-gamma) the superoxide anion release was significantly reduced, which was reversed by the inhibition of the NO synthase. Additionally, chemical NO-releasing compounds reduced the generation of reactive oxygen derivatives rapidly and independently of the pathway used to trigger the oxidative burst. This effect of NO was not mediated via guanylyl cyclase and cGMP, or due to the scavenging of released superoxide anions. This attenuation of superoxide anion generation by NO may limit deleterious effects of the release of reactive oxygen derivatives in tissue inflammation or injury.
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