Oxidative injury and other metabolic disorders in hepatic encephalopathy.

T Negru, V Ghiea, D Păsărică
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Abstract

Within the complex mechanism of hepatic encephalopathy resulting from alcohol poisoning, a significant pathogenic role seems to relate to lipid peroxides (free radicals generated by chronic alcohol poisoning itself). Oxidative aggression is emphasized by the diminishing antioxidative capacity of the body resulting from serious liver injury brought about by chronic ethyl poisoning. The poisoning influences the whole functional capacity of the liver, hepatic protein synthesis included, which also means ceruloplasmin and siderophilin synthesis; the two latter elements make up AOS Cp-Tr which neutralizes the harmful activity of Cu and Fe excess and stimulates release of free radicals of oxygen. The purpose of our research was to study the redox balance alteration in blood in a group of patients who were in a critical condition and had been admitted to the somatic patients ward of the "Prof. Dr. Alexandru Obregia" Neurology and Psychiatry Hospital and who were suffering from hepatic encephalopathy resulting from ethyl poisoning.

肝性脑病的氧化损伤及其他代谢紊乱。
在酒精中毒引起的肝性脑病的复杂机制中,脂质过氧化物(慢性酒精中毒本身产生的自由基)似乎起着重要的致病作用。慢性乙基中毒引起严重肝损伤,机体的抗氧化能力下降,强调了氧化攻击。中毒影响肝脏的整体功能,包括肝蛋白的合成,也包括铜蓝蛋白和嗜铁蛋白的合成;后两种元素构成AOS Cp-Tr,它中和过量的Cu和Fe的有害活性,并刺激氧自由基的释放。我们的研究目的是研究一组因乙基中毒而患肝性脑病的危重病人的血液氧化还原平衡变化,这些病人曾住进“Alexandru博士”神经病学和精神病学医院的躯体病人病房。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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