Effects of altered porphyrin synthesis on brain neurochemistry.
Lead is one of several environmentally significant substances which alter porphyrin synthesis in several organs. Biochemically, the consequences of both acute and chronic lead exposure, at relatively low dose, are increases in tissue and plasma levels of the porphyrin precursor aminolevulinic acid (ALA) and inhibition of the enzyme ALA dehydrase. These effects are considered for their possible role in the neurotoxicity associated with lead exposure. The effects of lead, on porphyrin metabolism and on neurochemistry and behavior, are compared to those associated with exposure to the "suicide" inhibitor of ALA dehydrase, succinylacetone. Similarities in both porphyrinopathy and in associated neurotoxicity suggest an etiologic role for altered porphyrin synthesis in lead neurotoxicity.
D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D004798:Enzymes / Q000097:blood; D005260:Female; D006427:Hemin / Q000494:pharmacology; D006537:Heptanoates / Q000494:pharmacology; D006591:Hexobarbital / Q000494:pharmacology; D007855:Lead Poisoning / Q000378:metabolism; D011164:Porphyrias / Q000139:chemically induced; D011166:Porphyrins / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000503:physiopathology; D012890:Sleep / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D004798:Enzymes; D006537:Heptanoates; D011166:Porphyrins; C020804:succinylacetone; D005680:gamma-Aminobutyric Acid; D006427:Hemin; D006591:Hexobarbital