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滥用酒精者易有扑热息痛引起的肝中毒,其机制可能是肝脏的细胞色素P-450激活药物的毒性代谢物过多,也可能是谷胱甘肽(GSH)与毒性代谢物形成解毒结合物的能力减弱。本文试图阐明此中机理。研究设计分两部份:①选5例男性无肝病的慢性酒精中毒者和5例健康对照者。禁食10h后各口服扑热息痛2g,并在服药前和服药后4h内每隔1h抽血检测GSH,并收集服药后6h的尿液,测定扑热息痛的两种主要解毒代谢物:胱氨酸-扑热息痛和N-乙酰胱氨酸-扑热息痛。②选慢性酒精性肝炎病者(8例)、用经皮肝活检法测定肝脏的GSH含量,并与取自外科活检的肝脏(3例),慢性持久性肝炎(5例)或非酒精性肝硬化病者(7例)的肝脏GSH作比较,观
Alcohol abuse is more likely to cause paracetamol-induced liver toxicity, the mechanism may be liver cytotoxic P-450 activator of toxic metabolites too much, it may be glutathione (GSH) and toxic metabolites form detoxification conjugates Weakened ability. This article attempts to clarify the mechanism. Study design is divided into two parts: ① 5 cases of chronic alcoholism in men without liver disease and 5 healthy controls were selected. After oral administration of Paracetamol 2g for 10h after fasting, GSH was taken every 1h before taking the medicine and 4h after taking the medicine. The urine of 6h after taking the medicine was collected and the two main detoxification metabolites of acetaminophen were determined: cystine-paracetamol And N-acetylcysteine-paracetamol. ② Chronic alcoholic hepatitis (n = 8) was selected. The hepatic GSH level was determined by percutaneous liver biopsy and was compared with the liver (3 cases), chronic persistent hepatitis (5 cases) or non-alcoholic Liver cirrhosis patients (7 cases) compared with the liver GSH view