Swaiman K F, Machen V L
Neurochem Res. 1985 Dec;10(12):1635-44. doi: 10.1007/BF00988605.
Dynamic studies of iron metabolism in brain are generally unavailable despite the fact that a number of neurologic conditions are associated with excessive accumulation of iron in central nervous tissue. Cortical non-neuronal (glial) cultures were prepared from fetal mouse brain. After 13 days the cultures were exposed to radiolabeled iron. Brisk and linear total iron uptake and ferritin iron uptake occurred over 4 hours. When methylamine or ammonium chloride was added, (both known inhibitors of transferrin iron release because of their lysosomotropic properties), total iron uptake was diminished. Further studies indicated that methylamine inhibits glial cell ferritin iron incorporation. Glial cell iron transport is similar to previously reported neuronal cell iron transport (1) but glial cell iron uptake proceeds at a faster rate and is more susceptible to the inhibition of certain lysosomotropic agents. The data reinforces the likelihood that iron uptake by nervous tissues is transferrin-mediated.
尽管许多神经系统疾病与中枢神经组织中铁的过度积累有关,但大脑中铁代谢的动态研究通常难以开展。从胎鼠大脑制备皮质非神经元(神经胶质)培养物。13天后,将培养物暴露于放射性标记的铁。在4小时内发生了快速且线性的总铁摄取和铁蛋白铁摄取。当加入甲胺或氯化铵时(由于它们的溶酶体亲和特性,二者均为已知的转铁蛋白铁释放抑制剂),总铁摄取减少。进一步研究表明,甲胺抑制神经胶质细胞铁蛋白铁的掺入。神经胶质细胞铁转运与先前报道的神经元细胞铁转运相似(1),但神经胶质细胞铁摄取速率更快,并且更容易受到某些溶酶体亲和剂的抑制。这些数据进一步证明了神经组织摄取铁是由转铁蛋白介导的可能性。