Fletcher L M, Halliday J W, Powell L W
The Clinical Sciences Unit, The Queensland Institute of Medical Research, Brisbane, Australia.
J Gastroenterol Hepatol. 1999 Mar;14(3):202-14. doi: 10.1046/j.1440-1746.1999.01836.x.
It is known that the regular consumption of alcohol is responsible for the disruption of normal iron metabolism in humans, resulting in the excess deposition of iron in the liver in approximately one-third of alcoholic subjects. The mechanisms involved are largely unknown; however, it is likely that the two major proteins of iron metabolism, ferritin and transferrin are intimately involved in the process. Tissue damage in alcoholic liver disease and the inherited iron-overload disease, haemochromatosis, are caused by excess alcohol and iron, respectively. The mechanisms of this damage are believed to be similar in both disease conditions and involve free radical-mediated toxicity. A high proportion of haemochromatosis sufferers consume excessive amounts of alcohol and synergistic hepatotoxic events may occur leading to the earlier development of liver cirrhosis. This review describes briefly the role of ferritin and transferrin in normal iron metabolism and in iron overload disease and explores the possible involvement of these proteins in the pathophysiology of excess iron deposition in alcoholic subjects.
众所周知，经常饮酒会破坏人体正常的铁代谢，导致约三分之一的酒精性肝病患者肝脏中铁过量沉积。其中涉及的机制很大程度上尚不清楚；然而，铁代谢的两种主要蛋白质，即铁蛋白和转铁蛋白，很可能密切参与了这一过程。酒精性肝病和遗传性铁过载疾病血色素沉着症中的组织损伤分别是由过量酒精和铁引起的。人们认为，这两种疾病状态下这种损伤的机制相似，都涉及自由基介导的毒性。很大一部分血色素沉着症患者饮酒过量，可能会发生协同肝毒性事件，导致肝硬化的提前发展。本文简要描述了铁蛋白和转铁蛋白在正常铁代谢和铁过载疾病中的作用，并探讨了这些蛋白质可能参与酒精性肝病患者铁过量沉积病理生理学的情况。
