ALCOHOL INDUCED OXIDANT INJURY

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This protocol is designed to address the hypothesis that free radical generation occurs in overt models of alcohol induced liver injury. Qualitative assessment of free radical generation will be accomplished by in vivo measurement of isoprostanes. In addition, the investigators plan to explore the theory that vasoconstriction mediated by thromboxane A2 results in exacerbation of hepatic injury. The three specific aims to be tested are: 1) To address the hypothesis that elevated 8-epi PGF2alpha formation is reflective of overt alcohol induced liver disease. 2) To address the hypothesis that alcohol induced liver injury is associated with increased thromboxane biosynthesis. 3) To address the hypothesis that liver injury secondary to iron overload is associated with elevated 8-epi PGF2alpha formation.