Transferrin glycans: a possible link between alcoholism and hepatic siderosis.
Transferrin glycans: a possible link between alcoholism and hepatic siderosis.
复制标题
转铁蛋白聚糖：酗酒和肝铁质沉着症之间可能存在的联系。
DOI：
10.1111/j.1530-0277.1984.tb05513.x
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
M. Debanne
中科院分区：
文献类型：
--
作者：
E. Regoeczi;P. Chindemi;M. Debanne
在1小时的实验中，研究了大鼠肝脏对去铁蛋白、兔去铁蛋白和缺乏唾液酸基残基的人转铁蛋白对~(59)Fe的摄取。与未经修饰的母体蛋白引入的59Fe相比，附着在这两种制剂上的59Fe从血浆中消失的速度更快。大部分从循环中消失的~(59)Fe活度可以通过肝脏恢复。对双标记(125I，59Fe)制剂的研究表明，增强的59Fe清除与修饰的转铁蛋白的分解代谢增加无关。如其他人所示，长期大量饮酒会导致人血清中出现唾液酸缺乏的转铁蛋白(缺少两个残基)。我们认为，缺乏唾液酸的转铁蛋白选择性地在肝细胞内沉积铁的能力增强，可能对酒精中毒所观察到的肝铁质沉着症的发生具有重要意义。
The hepatic uptake of 59Fe from diferric rat and rabbit asialotransferrins and from human transferrin lacking two sialyl residues was investigated in rats in experiments lasting for 1 hr. The 59Fe attached to either of these preparations disappeared from the plasma more rapidly than the 59Fe introduced with the unmodified respective parent proteins. Most of the 59Fe activity that had disappeared from the circulation could be recovered with the liver. Studies with double-labeled (125I, 59Fe) preparations showed that the enhanced 59Fe clearance was not associated with increased catabolism of the modified transferrins. Prolonged, heavy alcohol consumption, as shown by others, results in the appearance of sialic acid-deficient transferrin (two residues missing) in human serum. We suggest that the increased capacity of transferrin deficient in sialic acid to selectively deposit iron in the hepatocyte may be of significance for the development of the hepatic siderosis observed in alcoholism.