Irving M G, Halliday J W, Powell L W
Department of Medicine, University of Queensland, Royal Brisbane Hospital, Australia.
Alcohol Clin Exp Res. 1988 Feb;12(1):7-13. doi: 10.1111/j.1530-0277.1988.tb00124.x.
Although alcoholic liver disease is often associated with some increase in hepatic iron stores, it is now established that when gross iron overload is present, this is due to genetic hemochromatosis. Furthermore, there appears to be a critical iron concentration necessary for the induction of hepatic fibrosis. Lipid peroxidation induced by ethanol and/or iron would appear to play a major role in hepatic damage in both humans and experimental animals. Although the exact mechanism(s) of induction of lipid peroxidation by ethanol and iron remains to be elucidated, both toxins can exert a synergistic effect upon hepatic lipid peroxidation. Iron overload has also been shown to stimulate directly hepatocyte and hepatic procollagen mRNA expression, which is further stimulated by ethanol. The observed synergism between iron and alcohol with respect to both hepatic lipid peroxidation and collagen biosynthesis offers a possible explanation of the apparent early onset of fibrosis and cirrhosis in patients with iron overload who have an excessive alcohol intake.
虽然酒精性肝病常伴有肝脏铁储存量的一定增加，但现已明确，当出现严重铁过载时，这是由遗传性血色素沉着症所致。此外，似乎存在诱导肝纤维化所需的临界铁浓度。乙醇和/或铁诱导的脂质过氧化似乎在人类和实验动物的肝损伤中起主要作用。尽管乙醇和铁诱导脂质过氧化的确切机制仍有待阐明，但这两种毒素均可对肝脏脂质过氧化产生协同作用。铁过载还被证明可直接刺激肝细胞和肝前胶原mRNA表达，乙醇可进一步增强这种刺激作用。铁与酒精在肝脏脂质过氧化和胶原生物合成方面所观察到的协同作用，为铁过载且饮酒过量的患者肝纤维化和肝硬化明显早发现象提供了一种可能的解释。
