Triethyllead and cerebral development: an overview.
The immature brain is unduly vulnerable to the toxic effects of triethyllead (Et3Pb). Both brain growth and main developmental events in the tissue are appreciably restrained by this neurotoxin. Generally, the susceptibility of brain cells to Et3Pb appears to diminish with age. The major cellular alterations in the affected tissue include the destruction of cell processes, and swelling and vacuolization in the pericaryon. The effect of Et3Pb-induced poisoning is one of hypomyelination as seen from the prominent reduction in the content of cerebral myelin. Myelin-producing cells (oligodendrocytes) seem to be particularly vulnerable to Et3Pb relative to other components of the tissue. Furthermore, the toxin specifically hampers the process of myelin membrane assembly. The inhibitory effects of Et3Pb can be attributed to the interaction of this amphiphilic compound with cellular membranes and with the process of their biogenesis.
D000818:Animals; D001921:Brain / Q000254:growth & development* / Q000378:metabolism; D001927:Brain Diseases / Q000139:chemically induced*; D002478:Cells, Cultured; D002642:Chick Embryo; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects; D007854:Lead / Q000633:toxicity*; D009186:Myelin Sheath / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009942:Organometallic Compounds / Q000633:toxicity*; D051381:Rats
D009419:Nerve Tissue Proteins; D009942:Organometallic Compounds; D007854:Lead; C010360:triethyllead