title: Antioxidant effects of alpha tocopherol, ascorbic acid and L-methionine on lead induced oxidative stress to the liver, kidney and brain in rats.
abstract: Lead exposure related oxidative stress has been incriminated, at least in part, to its toxic effects in different organs. The present investigation was carried out to study the ameliorative effects of antioxidant (ascorbic acid, alpha tocopherol or L-methionine) alone and antioxidant (alpha tocopherol) plus a conventional chelator (CaNa2 EDTA) on some of the parameters indicative of oxidative stress in the liver, kidney and brain in lead-exposed rats. Rats were given 0 (n=6, healthy controls) or 1 mg of Pb(2+)/kg b.w (n=30) as lead acetate solution in sterile normal saline ip for a period of 4 weeks. The ip injections were then withdrawn and lead exposed rats were randomly divided into five equal groups. Six lead-exposed rats were given no treatment during the 5th week (Pb group) to serve as positive controls. The rest four groups received either ascorbic acid, alpha tocopherol or L-methionine in the 5th week at the daily dose of 100 mg/kg b.w orally or alpha tocopherol as above plus CaNa2 EDTA at the rate of 110 mg/kg b.w twice a day ip for a period of 4 days. All the animals were sacrificed 1 day after the end of the experiment, and the liver, kidney and brain were quickly excised for the estimation of lead burden and alteration in the oxidative indices. Lead exposure for a period of 4 weeks followed by a period of 1 week to recover, resulted in significantly (P<0.05) higher accumulation of lead, associated with significant (P<0.05) increases in lipid peroxide level in the liver and brain, and non-protein bound thiol contents in the brain. Changes in the superoxide dismutase and catalase activities in lead-exposed rats did not reach statistical (P<0.05) significance. Treatment with antioxidants alone resulted in reversal of oxidative stress without significant decline in tissue lead burden. Tissue specific changes, following lead exposure and responses to the treatment with different antioxidants were recorded in the parameters of oxidative damage viz. lipid peroxide level, antioxidant enzymes and thiol contents.
authors.affiliation: Environmental Medicine Laboratory, Division of Medicine, Indian Veterinary Research Institute, Izatnagar, India. patrarc@ivri.up.nic.in
authors.forename: R C
authors.initials: RC
authors.lastname: Patra
authors.forename: D
authors.initials: D
authors.lastname: Swarup
authors.forename: S K
authors.initials: SK
authors.lastname: Dwivedi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002614:Chelating Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004492:Edetic Acid / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007854:Lead / Q000378:metabolism / Q000633:toxicity; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008715:Methionine / Q000494:pharmacology*; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D002614:Chelating Agents; D008054:Lipid Peroxides; D014810:Vitamin E; D007854:Lead; D004492:Edetic Acid; D008715:Methionine; D001205:Ascorbic Acid