Caco-2 cell metabolism of oxygen-derived radicals

Abstract

Reactive oxygen metabolites have been associated with gastrointestinal injury and may play a role as mediators of inflammation. The effect of oxygen metabolites on Caco-2 cell viability (trypan blue exclusion and⁵¹Cr release), hexose monophosphate shunt activity, and glutathione was assessed. Caco-2 cells were incubated with amino acid oxidase, xanthine oxidase, menadione, andt-butylhydroperoxide in the presence and absence of superoxide dismutase, catalase, mannitol, and butylated hydroxytoluene. With amino acid oxidase, trypan blue exclusion decreased (P51Cr release, oxidized glutathione, and shunt activity increased (PP51Cr release, oxidized glutathione, and shunt activity increased (P51Cr release, oxidized glutathione, and shunt activity (Pt-Butylhydroperoxide did not effect⁵¹Cr release or trypan blue exclusion, but oxidized glutathione and shunt activity increased (PP51Cr release, but caused an increase in oxidized glutathione and shunt activity (PP<0.001). Menadione also caused a depletion of total glutathione. Thus, Caco-2 cells are sensitive to oxidant injury and in all four systems increase in shunt activity and oxidized glutathione occurred at concentrations lower than those that caused cell injury, suggesting the shunt via the glutathione cycle is important in Caco-2 cell metabolism of oxidant species.