ALCOHOL INDUCED OXIDANT INJURY

该方案旨在解决自由基生成发生在酒精诱导肝损伤的显性模型中的假设。自由基生成的定性评估将通过体内异前列腺素的测量来完成。此外，研究人员计划探索血栓素A2介导的血管收缩导致肝损伤加重的理论。需要测试的三个具体目的是：1)验证8-epi PGF 2 α形成升高反映明显酒精诱导的肝脏疾病的假设。2)验证酒精诱导肝损伤与血栓素生物合成增加相关的假说。3)为了解决铁超载继发性肝损伤与8-epi PGF2alpha形成升高相关的假设。

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.