DIET, SMOKING & ALCOHOL INDUCED OXIDANT INJURY

饮食、吸烟

• 批准号: 6263593
• 负责人: EMMA MEAGHER
• 金额: $ 2.51万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-12-01 至 1999-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6263593
• 关键词: alcoholic liver cirrhosis; alcoholism /alcohol abuse; clinical research; diet; eicosanoid metabolism; free radicals; human subject; liver disorder; prostaglandin F; smoking; thromboxanes; tobacco abuse

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.

该方案旨在解决自由基产生发生在酒精诱导肝损伤的明显模型中的假设。将通过体内测量异前列腺素完成自由基生成的定性评估。 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。 待测试的三个具体目的是：1）解决升高的8-epi PGF 2 α形成反映明显的酒精诱导的肝病的假设。 2)探讨酒精诱导的肝损伤与血栓素生物合成增加相关的假设。 3)探讨继发于铁过载的肝损伤与8-epi PGF 2 α形成升高相关的假说。