Olynyk J, Hall P, Reed W, Williams P, Kerr R, Mackinnon M
University Department of Medicine, Fremantle Hospital, Australia.
J Hepatol. 1995 Jun;22(6):671-6. doi: 10.1016/0168-8278(95)80222-3.
BACKGROUND/AIMS: The hypothesis that chronic alcohol ingestion potentiates iron-associated liver injury was investigated in the 'carbonyl iron-overload rat model'.
Newborn male and female Wistar-Furth rats (seven per group) were used to investigate iron-alcohol interaction over a 26-week period. Groups 1 and 2 were iron loaded from birth, while the others received normal diet. At 10 weeks all rats commenced Lieber-DeCarli liquid diet; additional treatments were: group 1 6 g carbonyl iron/1000 ml diet plus alcohol; group 2 carbonyl iron in the liquid diet; group 3 alcohol in the liquid diet; group 4, the controls, received liquid diet only.
This study confirmed our previous observation that iron-loading from birth resulted in grade III-IV siderosis, in both male and female rats, and caused fibrosis associated with periportal macrophages. Alcohol-feeding, in addition to iron-feeding for 26 weeks significantly lowered the hepatic iron concentration in both male and female rats compared to those fed iron only (p < 0.05). Alcohol feeding did increase hepatic fibrosis in the iron-loaded animals. However, serum alanine aminotransferase activity was significantly higher in the iron-alcohol group than in the other groups (p < 0.05).
Thus, contrary to expectation, chronic alcohol feeding failed to potentiate hepatic fibrosis in iron-overloaded rats, although there was rather more hepatocyte necrosis, and the serum alanine aminotransferase activity was significantly higher in the iron-alcohol group than in the other groups.
背景/目的：在“羰基铁过载大鼠模型”中研究慢性酒精摄入增强铁相关肝损伤这一假说。
采用新生雄性和雌性Wistar - Furth大鼠（每组7只），在26周的时间内研究铁与酒精的相互作用。第1组和第2组从出生起就进行铁负荷，而其他组给予正常饮食。在10周时，所有大鼠开始给予Lieber - DeCarli液体饮食；额外的处理为：第1组，6 g羰基铁/1000 ml饮食加酒精；第2组，液体饮食中含羰基铁；第3组，液体饮食中含酒精；第4组为对照组，仅给予液体饮食。
本研究证实了我们之前的观察结果，即从出生起进行铁负荷会导致雄性和雌性大鼠出现III - IV级铁沉着症，并引起与门周巨噬细胞相关的纤维化。与仅喂食铁的大鼠相比，在26周内同时喂食酒精和铁显著降低了雄性和雌性大鼠的肝铁浓度（p < 0.05）。酒精喂养确实增加了铁负荷动物的肝纤维化。然而，铁 - 酒精组的血清丙氨酸氨基转移酶活性显著高于其他组（p < 0.05）。
因此，与预期相反，慢性酒精喂养未能增强铁过载大鼠的肝纤维化，尽管肝细胞坏死更多，且铁 - 酒精组的血清丙氨酸氨基转移酶活性显著高于其他组。
