ALCOHOL INDUCED OXIDANT INJURY

这一方案旨在解决这样一个假设，即自由基 发生在酒精诱导的肝损伤的显性模型中。 将完成自由基生成的定性评估 通过体内测量异前列腺素。此外，调查人员 计划探索血栓素介导的血管收缩理论 A2导致肝损伤加重。三个具体目标 需要检验的是：1)解决了升高8-epi PGF的假设 2α的形成反映了明显的酒精性肝病。 2)解决酒精引起的肝损伤是 与血栓素生物合成增加有关。3)解决 铁负荷过多导致继发性肝损伤的代谢 伴有升高的8-表位前列腺素F2α形成。

This protocol is designed to address the hypothesis that free radical generation occurs in overt models of alcohol inducead 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 vasconstriction 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 2alpha 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 hyothesis that liver injury secondary to iron overload is associated with elevated 8-epi PGF2alpha formation.