Altomare E, Vendemiale G, Albano O
Istituto di Clinica Medica I, Universita' di Bari, Italy.
Life Sci. 1988;43(12):991-8. doi: 10.1016/0024-3205(88)90544-9.
Reduced and oxidized hepatic glutathione was evaluated during alcoholic and non alcoholic liver injury. We studied 35 chronic alcoholics, 20 patients with non alcoholic liver diseases, 15 control subjects. Hepatic glutathione was measured in liver biopsies and correlated with histology and laboratory tests. Alcoholic and non alcoholic patients exhibited a significant decrease of hepatic glutathione compared to control subjects (controls: 4.14 +/- 0.1 mumol/g liver; alcoholics: 2.55 +/- 0.1, p less than 0.001; non alcoholics 2.77 +/- 0.1, p less than 0.001). Oxidized glutathione was significantly higher in the two groups of patients compared to controls (controls: 4.4 +/- 0.2% of total; alcoholics 8.2 +/- 0.3, p less than 0.001; non alcoholics: 8.5 +/- 0.8, p less than 0.001). The decreased hepatic glutathione levels in patients with alcoholic and non alcoholic liver diseases may represent a contributing factor of liver injury and may enhance the risk of toxicity in these patients.
在酒精性和非酒精性肝损伤过程中，对肝脏中还原型和氧化型谷胱甘肽进行了评估。我们研究了35名慢性酒精中毒者、20名非酒精性肝病患者以及15名对照者。在肝活检中测定肝脏谷胱甘肽，并将其与组织学和实验室检查结果进行关联。与对照者相比，酒精性和非酒精性患者的肝脏谷胱甘肽显著降低（对照者：4.14±0.1μmol/g肝脏；酒精中毒者：2.55±0.1，p<0.001；非酒精性患者：2.77±0.1，p<0.001）。与对照者相比，两组患者的氧化型谷胱甘肽显著更高（对照者：占总量的4.4±0.2%；酒精中毒者：8.2±0.3，p<0.001；非酒精性患者：8.5±0.8，p<0.001）。酒精性和非酒精性肝病患者肝脏谷胱甘肽水平降低可能是肝损伤的一个促成因素，并可能增加这些患者的毒性风险。
