ALCOHOL INDUCED OXIDANT INJURY

这一方案旨在解决这样一个假设，即自由基 在酒精性肝损伤的显性模型中发生。 自由基生成的定性评估将通过以下方式完成 异前列腺素的活体测量。此外，调查人员计划 血栓素A_2介导血管收缩的理论探讨 结果肝损伤加重。三个具体目标是 测试结果如下：1)解决8-epi-PGF2pha升高的假设 其形成反映了明显的酒精性肝病。2)至 解决酒精引起的肝损伤与酒精相关的假设 随着血栓素生物合成的增加。3)解决假设 铁超载引起的继发性肝损伤与升高有关 8-表观PGF2Alpha形成。

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.