title: Relationship between oxidative stress, pathology, and behavioral signs of lead poisoning in mallards.
abstract: Some of the adverse effects of lead (Pb) may be associated with oxidative damage of lipids, proteins, or DNA. In a previous study a linkage was observed between the susceptibilities of waterfowl species to Pb poisoning with oxidative stress. To investigate this relationship among the individuals of a single species, for 3 wk 4 groups of 12 mallards were fed diets containing high or low levels of vitamin E (20 or 220 UI/kg) and high or low levels of Pb (0 or 2 g/kg). During the first week of Pb exposure, mallards developed hemolytic anemia, and during the second week, signs of neurological impairment. Histological findings in the Pb-exposed mallards were hemosiderosis, demyelinization of sciatic and brachial nerves, and tumefaction of renal tubular epithelium with the presence of intranuclear inclusion bodies. Lipid peroxidation increased with Pb exposure in blood, liver, bile, and brain, but decreased in nerves. Glutathione (GSH) increased with Pb exposure in liver and bile, and its oxidized/reduced ratio only increased in bile. Pb exposure inhibited GSH peroxidase activity (GPX) in plasma, liver, and brain, and decreased protein thiols (PSH) in blood and liver. Vitamin E resulted in significantly lower lipid peroxidation in nerves of control birds relative to unsupplemented controls, but did not alleviate any sign of lead posioning. Pb-induced pathological changes associated with hepatic and nervous functions were significantly correlated with lower GPX activity and PSH concentrations in these tissues rather than lipid peroxidation. Data suggest that inhibition of antioxidant enzymes and interaction with sulfhydryl groups of proteins may play a more important role in Pb poisoning of waterfowl than lipid peroxidation.
authors.affiliation: Laboratory of Toxicology, Faculty of Veterinary Medicine, Univerisitat Autònoma de Barcelona, Bellaterra, Spain. Rafael.Mateo@uab.es
authors.forename: Rafael
authors.initials: R
authors.lastname: Mateo
authors.forename: W Nelson
authors.initials: WN
authors.lastname: Beyer
authors.forename: James W
authors.initials: JW
authors.lastname: Spann
authors.forename: David J
authors.initials: DJ
authors.lastname: Hoffman
authors.forename: Antonio
authors.initials: A
authors.lastname: Ramis
mesh_terms: D000743:Anemia, Hemolytic / Q000139:chemically induced / Q000178:diet therapy / Q000517:prevention & control; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D001715:Bird Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D002493:Central Nervous System Diseases / Q000139:chemically induced / Q000178:diet therapy / Q000517:prevention & control; D004372:Ducks; D007854:Lead / Q000633:toxicity*; D007855:Lead Poisoning / Q000178:diet therapy / Q000517:prevention & control / Q000662:veterinary*; D015227:Lipid Peroxidation / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D013997:Time Factors; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D014810:Vitamin E; D007854:Lead