Aluminum, a neurotoxin which affects diverse metabolic reactions.
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.
Department of Biochemistry, University of Tennessee, Knoxville 37996-0840.
J G
JG
Joshi
D000535:Aluminum / Q000009:adverse effects / Q000494:pharmacology* / Q000633:toxicity; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D015913:Chelation Therapy; D005293:Ferritins / Q000378:metabolism; D005609:Free Radicals; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007501:Iron / Q000378:metabolism; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000188:drug therapy / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats
D005609:Free Radicals; D005293:Ferritins; D000535:Aluminum; D007501:Iron; D005947:Glucose