Butler B F, Topham R W
Department of Chemistry, University of Richmond, VA 23173.
Biochem Mol Biol Int. 1993 May;30(1):53-61.
Riboflavin deficiency in rats resulted in a reduction in the transfer of 59Fe from an intragastric dose to plasma compared to age-matched or weight-matched controls. The uptake of iron by brush-border membrane vesicles made from intestinal mucosa of riboflavin-deficient rats was much less than identically-prepared vesicles from control groups. Although the mucosal content of 59Fe was smaller in riboflavin-deficient rats thirty minutes after dosing, the relative distribution of 59Fe between the mucosal iron-binding proteins, ferritin and transferrin, was not changed compared to the control groups. These studies suggest that the impairment in iron absorption in riboflavin deficiency is primarily the result of a reduced uptake of iron into the mucosal cell and not a redistribution of iron between iron-binding proteins inside the mucosal cell.
与年龄匹配或体重匹配的对照组相比,大鼠核黄素缺乏导致胃内剂量的59Fe向血浆的转移减少。由核黄素缺乏大鼠的肠黏膜制成的刷状缘膜囊泡对铁的摄取远低于对照组同样制备的囊泡。给药30分钟后,虽然核黄素缺乏大鼠黏膜中的59Fe含量较少,但与对照组相比,黏膜铁结合蛋白、铁蛋白和转铁蛋白之间59Fe的相对分布没有变化。这些研究表明,核黄素缺乏时铁吸收受损主要是由于铁进入黏膜细胞的摄取减少,而非黏膜细胞内铁结合蛋白之间铁的重新分布。