Joshi J G
Department of Biochemistry, University of Tennessee, Knoxville 37996-0840.
Biofactors. 1990 Jul;2(3):163-9.
Experimental evidence is summarized to support the hypothesis that chronic exposure to low levels of aluminum may lead to neurological disorders. These disorders result from defective phosphorylation--dephosphorylation reactions, reduced glucose utilization and site-specific damage inflicted by free radicals produced by altered iron metabolism. The brain is a highly compartmentalized organ. Therefore, a co-localization of critical mass of metabolic errors rather than a single event may be essential to precipitate a neural disease. Aluminum appears to participate in formulating this critical mass. Patients with dialysis dementia get partial relief by desferroxamine which chelates aluminum. However, it also chelates iron and therefore limits its applicability. While the specific chelator for aluminum is yet to be made available, exercising a caution in aluminum intake appears prudent.
实验证据汇总如下，以支持长期接触低水平铝可能导致神经紊乱这一假说。这些紊乱是由磷酸化 - 去磷酸化反应缺陷、葡萄糖利用减少以及铁代谢改变产生的自由基造成的位点特异性损伤所致。大脑是一个高度分区化的器官。因此，关键代谢错误的临界质量共同定位而非单个事件，可能对于引发神经疾病至关重要。铝似乎参与形成了这一临界质量。透析性痴呆患者通过去铁胺（一种能螯合铝的物质）可获得部分缓解。然而，它也会螯合铁，因此限制了其适用性。虽然尚未有可用于铝的特异性螯合剂，但谨慎控制铝的摄入量似乎是明智的。
