Oxidativestressisonefactorthatcantriggerprogrammedcelldeath.ActivatedneutrophilsrespondingtoinflammatorystimulationproducereactiveoxygenspecieslikesuperoxidefreerADIcalstokillinvadingbacteria,butthesereactiveoxygenspeciescanalsoattackendothelialcellsliningthevascularwallandtriggerapoptosis.Endothelialcellsalsoproducereactiveoxygenspeciesinsidethecellthatcancontributetooxidativestressandapoptosis,suchasduringreperfusioninjuryfollowingischemia.Superoxidedismutase(SOD)convertshighlyreactiveanddamagingsuperoxidefreeradicalstoperoxidesthatarelessreactivethansuperoxidebutstimulateapoptosis.Theglutathione(GSH)peptidereducingagentremovestoxicmetabolitesandrepairsdamagecreatedbyreactiveoxygenspecies.Glutathioneperoxidase(GPx),forexample,removesperoxidesusingglutathioneasareducingagent,andglutathionereductase(GSR)regeneratesreducedglutathione.Insidetheendothelialcellperoxidecanbeconvertedtohydroxylionsinthepresenceofiron.PeroxidesandhydroxylradicalsactivateNF-kBandactivateexpressionofinflammatorygenesincludingadhesionmolecules,TNFandIL-8.Theapoptoticresponseofendothelialcellstooxidativestressmaybeinvolvedinthedevelopmentandprogressionofatherosclerosis. Contributor:GlennCroston,PhD. REFERENCES: