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eISSN: 1643-3750

Cellular mechanisms of lead neurotoxicity.

Anibal Garza, Rosario Vega, Enrique Soto

Med Sci Monit 2006; 12(3): RA57-65

ID: 447121

Available online: 2006-03-01

Published: 2006-03-01

Lead (Pb[sup]2+[/sup]), a heavy metal, has been used by humans for many technologicalpurposes, which is the main reason for its present widespread distribution. Although various actionshave been taken to decrease the use and distribution of lead in the environment, it remains a significanthealth hazard. The toxic mechanism of lead is caused by its ability to substitute for other polyvalentcations (particularly divalent cations, such as calcium [Ca[sup]2+[/sup]] and zinc [Zn[sup]2+[/sup]]) in the molecularmachinery of living organisms. These interactions allow lead to affect different biologically significantprocesses, including metal transport, energy metabolism, apoptosis, ionic conduction, cell adhesion,inter- and intracellular signaling, diverse enzymatic processes, protein maturation, and genetic regulation.Membrane ionic channels and signaling molecules seem to be one of the most relevant molecular targetscontributing to lead's neurotoxicity; the developing central nervous system is particularly susceptible.At critical times in development, lead may have a disorganizing influence with long-lasting effects thatmay continue into teenage years and beyond. Pediatric lead poisoning is more common than adult lead poisoning,and its effects may occur at reduced blood levels with subclinical symptoms, thus a high index of suspicionis necessary for physicians when dealing with pediatric patients. Long-term effects of lead poisoningmay produce cognitive and motor impairment, with behavioral alterations. This review is centered on thedescription of the molecular mechanisms of lead toxicity and its repercussions on cellular functions.

Keywords: Calcium Channels - toxicity, Calcium - metabolism, Lead - toxicity, Lead Poisoning - metabolism, Neurotoxicity Syndromes - metabolism, Zinc - metabolism