Schanne F A, Zucker A H, Farber J L, Rubin E
Science. 1981 Apr 17;212(4492):338-40. doi: 10.1126/science.7209533.
In alcoholic liver injury, necrosis is involved in the progression from benign fatty liver to alcoholic hepatitis and cirrhosis. However, there is no practical model of alcohol-dependent liver cell necrosis. The calcium-dependent killing of cultured rat hepatocytes by two different membrane-active hepatotoxins, galactosamine and phalloidin, is potentiated by ethyl alcohol. This indicates that some general physical effect of alcohol on cellular membranes renders cells susceptible to otherwise nonlethal injuries. The in vitro model described in this report may thus be used to search for a general mechanism underlying alcohol-related tissue injury.
在酒精性肝损伤中，坏死参与了从良性脂肪肝发展为酒精性肝炎和肝硬化的过程。然而，目前尚无酒精依赖型肝细胞坏死的实用模型。两种不同的膜活性肝毒素，即半乳糖胺和鬼笔环肽，对培养的大鼠肝细胞的钙依赖性杀伤作用可被乙醇增强。这表明酒精对细胞膜的某些一般物理作用使细胞易于受到原本非致命性损伤的影响。因此，本报告中描述的体外模型可用于探寻酒精相关组织损伤的一般机制。
