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L. J. LeCaptain

Publications and source records attributed to L. J. LeCaptain.

13 recordsLinked to original sources
USGS2009

Developmental toxicity of diphenyl ether herbicides in nestling American kestrels

Beginning the day after hatching, American kestrel (Falco sparverius) nestlings were orally dosed for 10 consecutive days with 5 microliters/g of corn oil (controls) or one of the diphenyl ether herbicides (nitrofen, bifenox, or oxyfluorfen) at concentrations of 10, 50, 250, or 500 mg/kg in corn oil. At 500 mg/kg, nitrofen resulted in complete nestling mortality, bifenox in high (66%) mortality, and oxyfluorfen in no mortality. Nitrofen at 250 mg/kg reduced nestling growth as reflected by decreased body weight, crownrump length, and bone lengths including humerus, radiusulna, femur, and tibiotarsus. Bifenox at 250 mg/kg had less effect on growth than nitrofen, but crownrump, humerus, radiusulna, and femur were significantly shorter than controls. Liver weight as a percent of body weight increased with 50 and 250 mg/kg nitrofen. Other manifestations of impending hepatotoxicity following nitrofen ingestion included increased hepatic GSH peroxidase activity in all nitrofentreated groups, and increased plasma enzyme activities for ALT, AST, and LDHL in the 250mg/kg group. Bifenox ingestion resulted in increased hepatic GSH peroxidase activity in the 50and 250mg/kg groups. Nitrofen exposure also resulted in an increase in total plasma thyroxine (T4) concentration. These findings suggest that altricial nestlings are more sensitive to diphenyl ether herbicides than young or adult birds of precocial species.

Journal of Toxicology and Environmental Health↗
USGS2000

Developmental toxicity of lead-contaminated sediment to mallard ducklings

Sediment ingestion has been identified as an important exposure route for toxicants in waterfowl. The toxicity of lead-contaminated sediment from the Coeur d'Alene River Basin (CDARB) in Idaho was examined on posthatching development of mallard ( Anas platyrhynchos ) ducklings for 6 weeks. Day-old ducklings received either untreated control diet, clean sediment (24%) supplemented control diet, CDARB sediment (3,449 μg/g lead) supplemented diets at 12% or 24%, or a positive control diet containing lead acetate equivalent to that found in 24% CDARB. The 12% CDARB diet resulted in a geometric mean blood lead concentration of 1.41 ppm (WW) with over 90% depression of red blood cell ALAD activity and over threefold elevation of free erythrocyte protoporphyrin concentration. The 24% CDARB diet resulted in blood lead of 2.56 ppm with over sixfold elevation of protoporphyrin and lower brain weight. In this group the liver lead concentration was 7.92 ppm (WW), and there was a 40% increase in hepatic reduced glutathione concentration. The kidney lead concentration in this group was 7.97 ppm, and acid-fast inclusion bodies were present in the kidneys of four of nine ducklings. The lead acetate positive control group was more adversely affected in most respects than the 24% CDARB group. With a less optimal diet (mixture of two thirds corn and one third standard diet), CDARB sediment was more toxic; blood lead levels were higher, body growth and liver biochemistry (TBARS) were more affected, and prevalence of acid-fast inclusion bodies increased. Lead from CDARB sediment accumulated more readily in duckling blood and liver than reported in goslings, but at given concentrations was generally less toxic to ducklings. Many of these effects are similar to ones reported in wild mallards and geese within the CDARB.

Idaho↗
USGS1999

Lead exposure in passerines inhabiting lead-contaminated floodplains in the Coeur d'Alene River Basin, Idaho, USA

Blood collected from song sparrows ( Melospiza melodia ) and American robins ( Turdus migratorius ) captured with mist nets in a lead-contaminated (assessment) area and nearby uncontaminated (reference) areas within the Coeur d'Alene Basin in northern Idaho was analyzed for δ-aminolevulinic acid dehydratase activity (ALAD) and hematocrit levels, and livers were analyzed for lead. Mean ALAD inhibition in the assessment area was 51% in song sparrows and 75% in American robins. The proportion of the sampled population with ALAD inhibition >50% was calculated to be 43% for song sparrows and 83% for American robins. Assessment area hematocrit values for song sparrows ( x = 39.9) and American robins ( x = 39.5) were lower than in reference areas ( x = 42.4 for song sparrows and 40.2 for American robins); however, differences were not statistically significant ( p > 0.05). Significantly higher levels of lead (wet weight) were found in livers from song sparrows captured on the assessment area ( x = 1.93 ppm) than on reference areas ( x = 0.10 ppm) ( p = 0.0079). Study results indicate that 43% (95% confidence interval [CI] = 12.9-77.5%) of the song sparrows and 83% (95% CI = 41.8-99.2%) of the American robins inhabiting the floodplain along the Coeur d'Alene River in the assessment area are being exposed to lead at levels sufficient to inhibit ALAD by > 50%. Variability in lead exposure indicators was attributed to high variability in environmental lead concentrations in the Coeur d'Alene River Basin.

Environmental Toxicology and Chemistry↗
USGS1999

Toxicity of lead-contaminated sediment to mallards

Because consumption of lead-contaminated sediment has been suspected as the cause of waterfowl mortality in the Coeur d?Alene River basin in Idaho, we studied the bioavailability and toxicity of this sediment to mallards (Anas platyrhynchos). In experiment 1, one of 10 adult male mallards died when fed a pelleted commercial duck diet that contained 24% lead-contaminated sediment (with 3,400 μg/g lead in the sediment). Protoporphyrin levels in the blood increased as the percentage of lead-contaminated sediment in the diet increased. Birds fed 24% lead-contaminated sediment exhibited atrophy of the breast muscles, green staining of the feathers around the vent, viscous bile, green staining of the gizzard lining, and renal tubular intranuclear inclusion bodies. Mallards fed 24% lead-contaminated sediment had means of 6.1 μg/g of lead in the blood and 28 μg/g in the liver (wet-weight basis) and 1,660 μg/g in the feces (dry-weight basis). In experiment 2, we raised the dietary concentration of the lead-contaminated sediment to 48%, but only about 20% sediment was actually ingested due to food washing by the birds. Protoporphyrin levels were elevated in the lead-exposed birds, and all of the mallards fed 48% lead-contaminated sediment had renal tubular intranuclear inclusion bodies. The concentrations of lead in the liver were 9.1 μg/g for mallards fed 24% lead-contaminated sediment and 16 μg/g for mallards fed 48% lead-contaminated sediment. In experiment 3, four of five mallards died when fed a ground corn diet containing 24% lead-contaminated sediment (with 4,000 μg/g lead in this sample of sediment), but none died when the 24% lead-contaminated sediment was mixed into a nutritionally balanced commercial duck diet; estimated actual ingestion rates for sediment were 14% and 17% for the corn and commercial diets. Lead exposure caused elevations in protoporphyrin, and four of the five mallards fed 24% lead-contaminated sediment in a commercial diet and all five fed the contaminated sediment in a corn diet had renal intranuclear inclusion bodies. Lead was higher in the livers of mallards fed 24% lead-contaminated sediment in the corn diet (38 μg/g) than in the commercial diet (13 μg/g).

Idaho↗
USGS1996

Toxicity of seleno-l-methionine, seleno-dl-methionine, high selenium wheat, and selenized yeast to mallard ducklings

The toxicity of four chemical forms of selenium (seleno-L-methionine, seleno-DL-methionine, selenized yeast, and high selenium wheat) was compared in day-old mallard ducklings ( Anas platyrhynchos ). In the first experiment, in which the basal diet was 75% wheat, survival after 2 weeks was lower for ducklings fed 30 μg/g selenium as seleno-L-methionine (36%) than for ducklings fed 30 μg/g selenium as seleno-DL-methionine (100%) or 30 μg/g selenium from high selenium yeast (88%). The concentration of selenium at 2 weeks in the livers of survivors was similar for ducklings fed 15 μg/g selenium as seleno-DL-methionine (12 μg/g, wet weight), seleno-L-methionine (11 μg/g), and high selenium wheat (11 μg/g), but was lower when the selenium came from selenized yeast (6.2 μg/g). When fed 30 μg/g selenium from the various sources, the selenium concentrations in liver were 20 μg/g for seleno-DL-methionine, 19 μg/g for seleno-L-methionine, and 9.9 μg/g for selenized yeast. In a second experiment, in which the basal diet was a commercial duck feed, survival after 2 weeks was 100% in ducklings fed 30 μg/g selenium as seleno-DL-methionine, seleno-L-methionine, or selenized yeast. Selenium concentrations in liver were similar for ducklings fed the 30-μg/g selenium diets as the DL or L forms of selenomethionine (27 and 25 μg/g), but lower for ducklings fed selenized yeast (13 μg/g). The greater toxicity of the L form of selenomethionine was probably related to the palatability or nutritional nature of the wheat-based diet used in experiment 1, but the exact reason for the difference between the DL and L forms is unknown. Biologically incorporated selenium, derived from high selenium wheat, was no more toxic than selenium derived from the two purified forms of selenomethionine, and the selenium in selenized yeast was not as toxic as that in the two forms of selenomethionine.

Archives of Environmental Contamination and Toxico↗
USGS1993

Biomonitoring environmental contamination with pipping black-crowned night heron embryos: Induction of cytochrome P450

Cytochrome P450-associated monooxygenase activities and cytochrome P450 proteins were measured in pipping black-crowned night heron ( Nycticorax nycticorax ) embryos collected from a reference site (next to the Chincoteague National Wildlife Refuge, VA) and three polluted sites (Cat Island, Green Bay, Lake Michigan, WI; Bair Island, San Francisco Bay, CA; West Marin Island, San Francisco Bay, CA). In a laboratory study, artificially incubated night heron embryos from the reference site were treated with 3-methylcholanthrene (200 μg administered into the air cell 2 d before pipping) or phenobarbital (2 mg daily for 2 d before pipping). Compared to controls (untreated + vehicle-treated embryos), 3-methylcholanthrene induced a greater than fivefold increase in activities of several monooxygenases (arylhydrocarbon hydroxylase, AHH; benzyloxyresorufin- O -dealkylase, BROD; ethoxyresorufin- O -dealkylase, EROD; pentoxyresorufin- O -dealkylase, PROD) and a greater than 100-fold increase in the concentration of immunodetected cytochrome P450 1A (CYP1A). Phenobarbital treatment resulted in only a slight increase in BROD activity but induced proteins recognized by antibodies to cytochrome P450 2B (CYP2B) by 2,000-fold. In a field study, activities of AHH, BROD, EROD, and ethoxycoumarin- O -dealkylase (ECOD) were up to 85-fold higher in pipping black-crowned night herons collected from Cat Island compared to other sites. Hepatic CYP1A and CYP2B cross-reactive proteins were detected in significantly more individuals from Cat Island than from the reference site. Greatest burdens of total PCBs and p,p ′-DDE were detected in embryos from Cat Island. Cytochrome P450-associated monooxygenase activities and cytochrome P450 proteins (AHH, BROD, EROD, ECOD, CYP1A, CYP2B) were significantly associated with total PCB burdens ( r = 0.50-0.72). These data indicate that cytochrome P450 may be a useful biomarker of exposure to some PCB mixtures in black-crowned night heron embryos.

Environmental Toxicology and Chemistry↗
USGS1992

Interactive effects of selenium, methionine, and dietary protein on survival, growth, and physiology in mallard ducklings

Concentrations of over 100 ppm (100 mg/kg) selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Both quantity and composition of dietary protein for wild ducklings may vary in selenium-contaminated environments. Day-old mallard (Anas platyrhynchos) ducklings received one of the following diets containing 22% protein: unsupplemented (controls), 15 ppm Se (as selenomethionine), 60 ppm Se, methionine supplemented, 15 ppm Se with methionine supplement, or 60 ppm Se with methionine supplement. In a second concurrent experiment the above sequence was repeated with a protein-restricted (11%) but isocaloric diet. In a third concurrent experiment all ducklings received 44% protein with 0, 15, or 60 ppm Se added. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and histopathological lesions of the liver occurred. Antagonistic interactive effects occurred between supplementary methionine and Se, including complete to partial alleviation of the following Se effects by methionine: mortality, hepatic lesions, and altered glutathione and thiol status. With 11% protein, growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and methionine supplementation, although protective afforded less protection than it did with 22% protein. With 44% protein, ducklings experienced physiological stress, and Se was more toxic than with methionine-supplemented 22% protein. These findings suggest the potential for antagonistic effects of Se, methionine, and protein on duckling survival and physiology.

Archives of Environmental Contamination and Toxico↗
USGS1992

Interactive effects of arsenate, selenium, and dietary protein on survival, growth, and physiology in mallard ducklings

High concentrations of arsenic (As) and selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Total biomass of invertebrates, a maJor source of protein for wild ducklings, may vary in environments that are contaminated with selenium. Dayold mallard (Anas platyrhynchos) ducklings received an untreated diet (controls) containing 22% protein or diets containing 15 ppm Se (as selenomethionine), 60 ppm Se, 200 ppm As (as sodium arsenate), 15 ppm Se with 200 ppm As, or 60 ppm Se with 200 ppm As. In a concurrent experiment, the same sequence was repeated with a proteinrestricted (7%) but isocaloric diet. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and livers had histopathological lesions. Arsenic alone caused some reduction in growth. Antagonistic interactive effects occurred between As and Se, including complete to partial alleviation of the following Se effects: mortality, impaired growth, hepatic lesions and lipid peroxidation, and altered glutathione and thiol status. With 7% protein, survival and growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and As (200 ppm) caused mortality, decreased growth, and liver histopathology. These findings suggest the potential for antagonistic effects of Se and As on duckling survival, growth, and physiology with adequate dietary protein but more severe toxicological effects when dietary protein is diminished.

Archives of Environmental Contamination and Toxico↗
USGS1991

Interactive effects of boron, selenium, and dietary protein on survival, growth and physiology in mallard ducklings

High concentrations of boron (B) and selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Total biomass of invertebrates, a major source of protein for wild ducklings, is sometimes diminished in agricultural drainwater ponds contaminated with Se and B. Day-old mallard ( Anas platyrhynchos ) ducklings received an untreated diet (controls) containing 22% protein or diets containing 15 ppm (μg/g) Se (as selenomethionine), 60 ppm Se, 1,000 ppm B (as boric acid), 15 ppm Se with 1,000 ppm B, or 60 ppm Se with 1,000 ppm B. In a concurrent experiment, the above sequence was repeated with a protein-restricted (7%) but isocaloric diet. After four weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and histopathological lesions of the liver occurred. Boron alone caused some reduction in growth. Several interactive effects occurred between B and Se, including further reduction in growth, and increases in plasma glutathione reductase activity, hematocrit, hemoglobin and plasma protein concentrations. With 7% protein, the growth of controls was less than that with 22% protein, 60 ppm Se caused 100% mortality, and growth effects of 15 ppm Se and 1,000 ppm B alone were more pronounced than with 22% protein. Selenium accumulation increased in the liver with 7% protein. Interactive effects were greater for Se and B with 7% protein than with 22% protein and included significant mortality and enhanced accumulation of Se in the liver. These findings suggest the potential for more severe toxicological effects of Se and B independently and interactively on duckling survival and development when dietary protein is diminished.

Archives of Environmental Contamination and Toxico↗
USGS1991

Subchronic hepatotoxicity of selenomethionine ingestion in mallard ducks

Twoyearold male mallards (Anas platyrhynchos) received a control diet (0.2 ppm Se) or diets containing 1, 2, 4, 8, 16, or 32 ppm Se as selenomethionine for 14 wk. Se accumulated readily in the liver in a dosedependent manner, reaching a mean concentration of 29 ppm (wet weight) in the 32 ppm group. Dietary Se of 2 ppm or greater increased plasma glutathione peroxidase activity. Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. These histopathological effects were accompanied by lower hemoglobin concentrations (16 and 32 ppm groups) and hematocrit (32 ppm group), and elevated plasma alkaline phosphatase activity (32 ppm group) indicative of cholestatic liver inJury. Other manifestations of hepatotoxicity included significant linear dose responses for hepatic oxidized glutathione (GSSG) concentrations and ratio of GSSG to reduced glutathione (GSH). Means for both of these responses differed from controls in groups receiving 832 ppm Se. Mean hepatic GSH and malondialdehyde (a measure of lipid peroxidation) concentrations were significantly elevated in the 16 and 32 ppm groups. Subchronic effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

Journal of Toxicology and Environmental Health↗
USGS1990

Effects of arsenate on growth and physiology in mallard ducklings

Arsenic (As) has been found at elevated concentrations in irrigation drainwater and in aquatic plants utilized by waterfowl. Mallard ( Anas platyrhynchos ) ducklings received an untreated diet (controls) or diets containing 30, 100 or 300 ppm As added as sodium arsenate. After 10 weeks blood and tissue samples were collected for biochemical and histological examination. Arsenic accumulated significantly in brain and liver of ducklings fed 100 or 300 ppm but did not result in histopathological lesions. The 300-ppm dietary As concentration decreased overall growth (weight gain) in males, whereas all concentrations of As decreased overall growth and rate of growth in females. Food consumption was less during the first three weeks in the 300-ppm group and during the second week for the 100-ppm group compared to controls. Plasma sorbitol dehydrogenase activity and plasma glucose concentration were higher in the 300-ppm group compared to controls. Plasma triglyceride concentration increased in all As-treated groups. Brain ATP was lower in the 300-ppm group and sodium/potassium-dependent ATPase activity was higher in the 30- and 100-ppm groups. Hepatic glutathione peroxidase activity was lower in the 300-ppm group and malondialdehyde lower in all treatment groups. All treatment levels caused elevation in hepatic glutathione and ATP concentrations. These findings, in combination with altered duckling behavior (increased resting time), suggest that concentrations of As that have been found in aquatic plants (up to 430 ppm dry weight) could adversely affect normal duckling development.

Environmental Toxicology and Chemistry↗
USGS1990

Effects of boron on growth and physiology in mallard ducklings

High concentrations of boron (B) have been associated with irrigation drainwater and aquatic plants consumed by waterfowl. Day-old mallard ( Anas platyrhynchos ) ducklings received an untreated diet (controls) or diets containing 100, 400 or 1,600 ppm B as boric acid. Survival, growth and food consumption were measured for 10 weeks. At termination, blood and tissue samples were collected for biochemical assays and histological examination. The highest dietary concentration of B caused 10% mortality, decreased overall growth and the rate of growth (sexes combined), whereas lower concentrations of B altered growth only in females. Food consumption was lower during the first 3 weeks in the 1,600-ppm group and during the second week in all B-treated groups compared to controls. Hematocrit and hemoglobin were lower and plasma calcium concentration higher in the 1,600-ppm group compared to controls. Plasma triglyceride concentration was elevated in all B-treated groups. Brain B concentration increased to 25 times that of controls in the 1,600-ppm group. Brain ATP decreased with increasing dietary B. Brain acetylcholinesterase activity and total ATPase activity (in males) were elevated and protein concentration lowered in the 1,600-ppm group. Boron accumulated less in the liver than in the brain but resulted in an initial elevation of hepatic glutathione. These findings, in combination with altered duckling behavior, suggest that concentrations of B occurring in aquatic plants could adversely affect normal duckling development.

Environmental Toxicology and Chemistry↗