triethyllead and Disease-Models--Animal

Alkyl leads (R x Pb) are environmentally prevalent compounds which have been shown to produce a variety of neurological and behavioral deficits in both laboratory animals and man. Due to the increasing commercial use of these compounds, the episodes of human poisoning, and the limited understanding of their sites and mechanisms of toxicity, the organoleads, as a class, remain potentially important environmental health hazards. Recent data indicate that the constellation of behavioral effects produced by these compounds resembles the behavioral sequelae of limbic system damage. For example, alterations in sensory responsiveness and/or behavioral reactivity and task-dependent changes in avoidance learning are observed following organolead exposure and experimental disruption of the limbic system. Furthermore, neurochemical changes induced by organoleads are regionally-specific and restricted to the limbic forebrain and frontal cortex. The present review will summarize the toxic properties of organoleads, discuss their neurobehavioral effects, and suggest that these effects might be attributable to a disruption of the limbic forebrain.

Topics: Animals; Behavior, Animal; Brain Diseases; Chemical Phenomena; Chemistry; Disease Models, Animal; Humans; Kinetics; Lead; Lead Poisoning; Limbic System; Organometallic Compounds; Rats; Tetraethyl Lead

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.

Topics: Animals; Brain; Brain Diseases; Cells, Cultured; Chick Embryo; Disease Models, Animal; Energy Metabolism; Lead; Myelin Sheath; Nerve Tissue Proteins; Organometallic Compounds; Rats