ALCOHOL INDUCED OXIDANT INJURY

该方案旨在解决自由基 在酒精诱导的肝损伤的明显模型中发生。 将完成自由基生成的定性评估 通过异前列烷的体内测量。 此外，调查人员 计划探索血栓素介导的血管收缩的理论， A2导致肝损伤加重。 三个具体目标 待检验的是：1）为了解决升高的8-epi PGF 2 α形成反映了明显的酒精诱导的肝病。 2)为了解决酒精诱导的肝损伤的假设， 与血栓素生物合成增加有关。3)解决 假设继发于铁过载的肝损伤与 8-epi PGF 2 α的生成量增加

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 PGF 2 alpha 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 PGF 2 alpha formation.