Rouach H, Houze P, Orfanelli M T, Gentil M, Bourdon R, Nordmann R
Department of Biomedical Research on Alcoholism, Faculté de Médecine, Paris, France.
Biochem Pharmacol. 1990 Mar 15;39(6):1095-100. doi: 10.1016/0006-2952(90)90289-w.
An acute ethanol load (50 mmol/kg, i.p.) produced altogether a decrease in the non-heme iron content of the serum and an increase in the iron content in liver and cerebellum. Subcellular fractionation studies indicated that the non-heme iron accumulated by the liver, 4 hr after the ethanol load, was recovered in light mitochondria, microsomes and cytosol, and that iron accumulated by the cerebellum was localized in heavy mitochondria, light mitochondria, microsomes and cytosol. The low molecular weight chelatable (LMWC) iron content as well as the percentage of total non-heme iron represented by LMWC-iron were increased in the cytosol of liver and cerebellum after the ethanol load. These results suggest that an acute ethanol load induces (i) a shift in the distribution between circulating and tissular non-heme iron; (ii) an increase in the cytosolic LMWC-iron which, by favouring the biosynthesis of reactive free radicals, may contribute to lipid peroxidation in liver and cerebellum.
急性乙醇负荷（50 mmol/kg，腹腔注射）总体上导致血清中非血红素铁含量降低，肝脏和小脑中的铁含量增加。亚细胞分级分离研究表明，乙醇负荷4小时后肝脏积累的非血红素铁在线粒体轻组分、微粒体和胞质溶胶中被发现，而小脑积累的铁定位于线粒体重组分、线粒体轻组分、微粒体和胞质溶胶中。乙醇负荷后，肝脏和小脑胞质溶胶中的低分子量可螯合（LMWC）铁含量以及LMWC-铁占总非血红素铁的百分比均增加。这些结果表明，急性乙醇负荷诱导：（i）循环和组织中非血红素铁分布的改变；（ii）胞质溶胶中LMWC-铁增加，这可能通过促进活性自由基的生物合成，导致肝脏和小脑的脂质过氧化。
