IMMUNOSTIMULATION PROTECTS MICROGLIAL CELLS FROM NITRIC OXIDE-MEDIATED APOPTOSIS

CELLULAR oxidative stress from excess free radicals can initiate apopt osis in some cell types. Thus, we hypothesize that cells expressing ni tric oxide synthase (NOS) will also express anti-oxidative stress mech anisms, in order to prevent self-intoxication by the free radical, nit ric oxide (NO). To test this hypothesis, we investigated the vulnerabi lity of microglial cells (BV-2 line) to NO produced by the NO donor so dium nitroprusside. Damage to the cells was measured by an in situ det ection method of DNA fragmentation, an indicator of apoptosis. Activat ion by lipopolysaccharide (LPS) dose-dependently protected BV-2 cells against NO toxicity (up to 67%) while unactivated BV-2 cells were vuln erable to NO. Our results indicate that activation of BV-2 cells induc es protection mechanisms against NO toxicity.