Chou A C, Broun G O, Fitch C D
Blood. 1978 Jul;52(1):187-95.
Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3-4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.
喂食维生素E缺乏饮食的兔子在3 - 4周内出现严重的肌肉营养不良，但未出现贫血。然而，与对照兔子（0.9%）相比，缺乏维生素E的兔子网织红细胞计数增加（3.2%），骨髓中红系增生明显。将缺乏维生素E的兔子与对照兔子相比，血浆铁浓度较低（134.4对206.6微克/分升）；总铁结合力较高（335.9对228.3微克/分升）；全血原卟啉浓度较高（131.6对81.7微克/分升）；脾脏中铁的总含量较低（71对153微克），骨骼肌中较高（4956对3054微克），骨髓、肝脏和心脏中的铁含量无变化。使用59Fe进行的铁吸收和排泄研究表明，缺乏维生素E的兔子没有异常。然而，铁动力学存在异常。59Fe消失的半衰期较短（100.6对169.4分钟），血浆铁周转率较高（1.25对0.95毫克/分升血液/天），缺乏维生素E的兔子在第9天时循环红细胞中59Fe的再次出现率较高（77.2%对57.2%）。放血诱导的贫血加剧了缺乏维生素E的兔子的铁代谢异常，这些动物无法纠正贫血。这些发现表明，兔子维生素E缺乏会导致与铁代谢异常和铁在骨骼肌中蓄积相关的异常红细胞生成。
