Geology topics

R. Mateo

Publications and source records attributed to R. Mateo.

4 recordsLinked to original sources

USGS2016

Zinc and lead poisoning in wild birds in the Tri-State Mining District (Oklahoma, Kansas, Missouri)

contaminated with Pb, Cd, and Zn from mining, milling and smelting. Metals have been dispersed heterogeneously throughout the District in the form of milled mine waste ('chat'), as flotation tailings and from smelters as aerial deposition or slag. This study was conducted to determine if the habitat has been contaminated to the extent that the assessment populations of wild birds are exposed to toxic concentrations of metals. American robins (Turdus migratorius), northern cardinals (Cardinalis cardinalis), and waterfowl had increased Pb tissue concentrations (p < 0.05) compared with Pb tissue concentrations from reference birds, and the exposure of songbirds to Pb was comparable with that of birds observed at other sites severely contaminated with Pb. Mean activities of the Pb-sensitive enzyme delta-aminolevulinic acid dehydratase (ALAD) were decreased by >50% in red blood cells in these birds (p < 0.05). Several birds had tissue concentrations of Pb that have been associated with impaired biological functions and external signs of poisoning. Cadmium was increased in kidneys of songbirds (p < 0.05), but no proximal tubule cell necrosis associated with Cd poisoning was observed. Zinc concentrations in liver and kidney of waterfowl were significantly higher (p < 0.05) than reference values. The increased environmental concentrations of Zn associated with mining in the District accounted for the pancreatitis previously observed in five waterfowl from the District. The District is the first site at which free-flying wild birds have been found to be suffering severe effects of Zn poisoning.

Kansas, Missouri, Oklahoma↗

USGS2011

Relationship between oxidative stress, pathology, and behavioral signs of lead poisoning in mallards

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 72 mallards were fed diets containing high or low levels of vitamin E (20 or 220 Ul/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.

Journal of Toxicology and Environmental Health, Pa↗

USGS2003

Relation of fatty acid composition in lead-exposed mallards to fat mobilization, lipid peroxidation and alkaline phosphatase activity

The increase of n-6 polyunsaturated fatty acids (PUFA) in animal tissues has been proposed as a mechanism of lead (Pb) poisoning through lipid peroxidation or altered eicosanoids metabolism. We have studied fatty acid (FA) composition in liver and brain of mallards ( Anas platyrhynchos ) feeding for 3 weeks on diets containing combinations of low or high levels of vitamin E (20 or 200 UI/kg) and Pb (0 or 2 g/kg). Saturated FA, n-6 PUFA and total concentrations of FA were higher in livers of Pb-exposed mallards, but not in their brains. The percentage of n-6 PUFA in liver and brain was slightly higher in Pb-exposed mallards. The increase of n-6 PUFA in liver was associated with decreased triglycerides and increased cholesterol in plasma, thus could be in part attributed to feed refusal and fat mobilization. The hepatic ratios between adrenic acid (22:4 n-6) and arachidonic acid (20:4 n-6) or between adrenic acid and linoleic acid (18:2 n-6) were higher in Pb exposed birds, supporting the existing hypothesis of increased fatty acid elongation by Pb. Among the possible consequences of increased n-6 PUFA concentration in tissues, we found increased lipid peroxidation in liver without important histopathological changes, and decreased plasma alkaline phosphatase activity that may reflect altered bone metabolism in birds.

Comparative Biochemistry and Physiology, Part C: T↗

USGS2001

Differences in oxidative stress between young Canada geese and mallards exposed to lead-contaminated sediment

Lead (Pb) exposure results in an increase in tissue lipid peroxides and variation in glutathione (GSH) concentrations, which can be related to peroxidative damage of cell membranes in Pb-poisoned animals. Species and individual variation in sensitivity to Pb poisoning among animals may be due to differential resistance to oxidative stress. The effects of oxidative stress caused by Pb exposure (1.7, 414, and 828 µg/g of diet) were compared for the first 6 wk in growing young of two species of waterfowl, Canada geese ( Branta canadensis ) and mallards ( Anas platyrhynchos ), with the first species being possibly more sensitive to Pb poisoning based on previous field and laboratory observations. Blood and liver Pb concentrations increased more in mallards than in geese. This may be explained on the basis of body weight, being 3.2 times higher in geese, and by hepatic metabolism, where GSH S -transferase (GST) activity is 2.9-fold higher in geese and presumably has a role in the binding of Pb to GSH and subsequent biliary excretion. In contrast, mallards showed higher hepatic levels of GSH and activities of GSH peroxidase (GPX) and GSH reductase (GR). Although both species showed a rise in hepatic GSH concentration with Pb exposure, the relationship between increased lipid peroxidation and Pb exposure was only significant in geese. Within treatment groups, hepatic GSH concentrations were inversely related to liver Pb concentrations in both species, which may correspond to the role of GSH in Pb excretion. Hepatic GSH was also inversely related to hepatic lipid peroxidation, but only in mallards and in agreement with the species differences observed in GPX and GR activities. The lower resistance to lipid peroxidation of Canada geese may explain why geese can die in the field from Pb poisoning after ingesting fewer shot than found in the gizzards of mallards and with lower liver Pb concentrations than in mallards.

Journal of Toxicology and Environmental Health, Pa↗