Lead toxicity part II: the role of free radical damage and the use of antioxidants in the pathology and treatment of lead toxicity.
Lead is an environmentally persistent toxin that causes neurological, hematological, gastrointestinal, reproductive, circulatory, and immunological pathologies. The propensity for lead to catalyze oxidative reactions and generate reactive oxygen species has been demonstrated in multiple studies. These reactive oxygen species (ROS) inhibit the production of sulfhydryl antioxidants, inhibit enzyme reactions impairing heme production, cause inflammation in vascular endothelial cells, damage nucleic acids and inhibit DNA repair, and initiate lipid peroxidation in cellular membranes. These wide-ranging effects of ROS generation have been postulated to be major contributors to lead-exposure related disease. Antioxidants - vitamins B6, C and E, zinc, taurine, N-acetylcysteine, and alpha-lipoic acid, either alone or in conjunction with standard pharmaceutical chelating agents - have been studied in lead-exposed animals. The evidence for their use in lead exposure, alone and in conjunction with chelating agents, is reviewed in this article.
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D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology; D007854:Lead / Q000378:metabolism; D007855:Lead Poisoning / Q000150:complications / Q000378:metabolism / Q000628:therapy; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000378:metabolism
D000975:Antioxidants; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D007854:Lead; D009569:Nitric Oxide; D005978:Glutathione