Worrall S, de Jersey J, Nicholls R, Wilce P
Department of Biochemistry, University of Queensland, Brisbane, Australia.
Dig Dis. 1993 Jul-Oct;11(4-5):265-77. doi: 10.1159/000171418.
Alcohol abuse is a major cause of liver disease. While ethanol itself has been shown to be hepatotoxic, its primary metabolite acetaldehyde has also been implicated in the pathogenesis of alcoholic liver disease. The majority of ethanol metabolism occurs in the liver and high concentrations of acetaldehyde accumulate during chronic ethanol abuse. Acetaldehyde has been shown to react with many proteins in vitro, forming stable covalent adducts. These modifications can act as neoantigens and may also alter biological function. Acetaldehyde-modified proteins have been detected in the livers of ethanol-fed rats and human alcoholics. Circulating antibodies reactive with modified proteins have also been detected. A direct linkage between acetaldehyde-modified proteins, antibodies and liver damage has yet to be established, but current research should clarify the picture in the next few years.
酒精滥用是肝脏疾病的主要原因。虽然乙醇本身已被证明具有肝毒性，但其主要代谢产物乙醛也与酒精性肝病的发病机制有关。大部分乙醇代谢发生在肝脏中，在慢性乙醇滥用期间会积累高浓度的乙醛。乙醛已被证明在体外能与许多蛋白质发生反应，形成稳定的共价加合物。这些修饰可作为新抗原，也可能改变生物学功能。在喂食乙醇的大鼠和人类酗酒者的肝脏中已检测到乙醛修饰的蛋白质。也已检测到与修饰蛋白反应的循环抗体。乙醛修饰的蛋白质、抗体与肝损伤之间的直接联系尚未确立，但目前的研究应能在未来几年阐明情况。
