Effects of dietary nickel on survival and growth of mallard ducklings

Mallard (Anas platyrhynchos) ducklings were fed nickel sulphate in their diet from day one to 90 days of age. Ducklings fed 1,200 ppm nickel began to tremor and show signs of paresis after 14 days of dosage (age) and 71% of this group died within 60 days of age. Birds fed 1,200 ppm nickel weighed significantly less (P<0.05) at 28 days of age than birds fed the other diets. Weights of ducklings fed untreated food or dietary dosages of 200 and 800 ppm nickel diets were not significantly different (P>0.05). The weight/length ratio of the humerus (an expression of bone density) from the 800 ppm diet females was significantly lower (P<0.05) than the control fed females at 30 and 60 days and for all ducklings fed 1,200 ppm at 30 days of age. The organ-weight/body-weight ratios for heart, liver, and gizzard did not differ from controls or between any dosage group. Liver nickel residues from ducklings that died during this study ranged between 1.0 to 22.7 ppm and kidney residues ranged between 2.7 to 74.4 ppm. Liver and kidney tissues from all ducklings that survived to 90 days of age contained less than 1.0 ppm nickel.     

Effects of dietary cadmium on mallard ducklings

Mallard (Anas platyrhynchos) ducklings were fed cadmium in the diet at 0, 5, 10, or 20 ppm from 1 day of age until 12 weeks of age. At 4-week intervals six males and six females from each dietary group were randomly selected, bled by jugular venipuncture, and necropsied. Significant decreases in packed cell volume (PCV) and hemoglobin (Hb) concentration and a significant increase in serum glutamic pyruvic transaminase (GPT) were found at 8 weeks of age in ducklings fed 20 ppm cadmium. Mild to severe kidney lesions were evident in ducklings fed 20 ppm cadmium for 12 weeks. No other blood chemistry measurement, hematological parameter, or tissue histopathological measurement indicated a reaction to cadmium ingestion. Body weight, liver weight, and the ratio of the femur weight to length were not affected by dietary cadmium. Femur cadmium concentration in all ducklings 12 weeks of age declined from the values detected at 4 and 8 weeks of age. Liver cadmium concentrations were significantly higher in relation to the increased dietary levels and in relation to the length of time the ducklings were fed the cadmium diets. At 12 weeks of age the cadmium concentration in liver tissue was twice that in the diet.     

Effects of dietary cadmium on mallard ducklings

Mallard (Anas platyrhynchos) ducklings were fed cadmium in the diet at 0, 5, 10, or 20 ppm from 1 day of age until 12 weeks of age. At 4-week intervals six males and six females from each dietary group were randomly selected, bled by jugular venipuncture, and necropsied. Significant decreases in packed cell volume (PCV) and hemoglobin (Hb) concentration and a significant increase in serum glutamic pyruvic transaminase (GPT) were found at 8 weeks of age in ducklings fed 20 ppm cadmium. Mild to severe kidney lesions were evident in ducklings fed 20 ppm cadmium for 12 weeks. No other blood chemistry measurement, hematological parameter, or tissue histopathological measurement indicated a reaction to cadmium ingestion. Body weight, liver weight, and the ratio of the femur weight to length were not affected by dietary cadmium. Femur cadmium concentration in all ducklings 12 weeks of age declined from the values detected at 4 and 8 weeks of age. Liver cadmium concentrations were significantly higher in relation to the increased dietary levels and in relation to the length of time the ducklings were fed the cadmium diets. At 12 weeks of age the cadmium concentration in liver tissue was twice that in the diet.     

Effects of methylmercury on approach and avoidance behavior of mallard ducklings

Summary Mallard ducks were fed a control diet or a diet containing 0.5 or 3 ppm mercury (as methylmercury dicyandiamide) based on the dry feed. These mercury diets are approximately equivalent to 0.1 and 0.6 ppm mercury in a natural succulent diet. I measured for the ducklings the approach behavior in response to a tape-recorded maternal call and the avoidance of a frightening stimulus.There were no significant differences among controls and ducklings from mercury-treated parents in the percentage of ducklings that approached the tape-recorded call. Control ducklings, however, moved back and forth toward the call more than ducklings from mercury-treated parents and also spent more time in the end of the runway near the loudspeaker than ducklings whose parents were fed a diet containing 0.5 ppm mercury.Compared to control ducklings, ducklings from parents fed a diet containing 0.5 or 3 ppm mercury were hyper-responsive in the test of avoidance of a frightening stimulus.Mallard eggs collected in the wild have been found to contain levels of mercury exceeding the 1 ppm (wet-weight) found in the eggs of hens fed a diet containing 0.5 ppm, but there are no reports of mallard eggs collected in the wild that were found to contain as much mercury (6 to 9 ppm) as eggs from hens fed a diet containing 3 ppm mercury. On a dry-weight basis, the concentration of mercury in the eggs was about 6 times as great as that in the feed for ducks fed the 0.5 ppm mercury diet and about 6 to 9 times as great for ducks fed the 3 ppm mercury diet.     

Effects of lead nitrate ingestion on open-field behavior of mallard ducklings

Summary Mallard ducklings were fed a control diet or a diet containing 5, 50, or 500 ppm lead as lead nitrate,ad libitum, and their open-field behavior was tested after either 3 or 8 days on treatments. Differences in open-field performances among treatments were not significant. Percentage weight gain differed significantly among treatment groups over an 8 day period, with the least growth occurring in the 5 ppm treatment group.     

Effects of chronic ingestion of south Louisiana crude oil on mallard ducklings.

South Louisiana crude oil was fed to duckling mallards (Anas platyrhynchos) in concentrations of 0.025, 0.25, 2.5, and 5.0% of the diet from hatching to 8 weeks of age to assess the effects of chronic oil ingestion during early development. Growth was depressed in birds receiving a diet containing 5% oil but there was no oil-related mortality. Diets containing 0.25, 2.5, and 5.0% oil impaired avoidance behavior of 6-day-old mallard ducklings when compared with controls or ducklings fed 0.025% oil, but had no effect on open-field behavior of 7-day-old ducklings. Liver hypertrophy and splenic atrophy were gross evidence of the pathological effects of oil in birds on the 2.5 and 5.0% oil diets. Biochemical lesions that occurred included elevation of plasma alanine aminotransferase and ornithine carbamyl transferase activity. Hepatocyte hypertrophy and bile duct proliferation in the liver were noted in birds fed the 2.5 and 5.0% oil diets and tubular inflammation and degeneration in the kidney were noted in birds fed the 5.0% oil diet.     

Impact of oil-sands based wetlands on the growth of mallard (Anas platyrhynchos) ducklings

Identifying the potential effects of industrially formed wetlands on waterfowl populations is important for assessing the suitability of such wetlands in industrial reclamation strategies. Mallard ducklings were held in situ on two industrially formed wetlands and one reference wetland in northern Alberta, Canada. Duckling mass and skeletal size were measured at regular intervals over 33 d, and blood was collected to investigate the analysis of plasma metabolites (triglyceride and glycerol) as an indicator of physiological condition. In repeated-measures analysis of variance (ANOVA), multivariate ANOVA, and subsequent multiple-comparisons tests, body mass and skeletal size were significantly lower in ducklings maintained on the industrial wetland after 2, 5, 9, and 13 d of exposure. In this situation, plasma metabolite analysis did not provide additional information on mass-independent condition. We conclude that if the observed differences in growth and size translate into a decreased survival of juvenile waterfowl inhabiting these wetlands, then populations of these birds in the area could be negatively affected. We emphasize the importance of field-based ecological research in toxicological studies of wildlife.     

Toxicity of organic and inorganic selenium to mallard ducklings

The toxicity of selenomethionine and sodium selenite to mallard ducklings (Anas platyrhynchos) was measured by feeding each form from hatching to six weeks of age at dietary concentrations of 0, 10, 20, 40, and 80 ppm selenium. At 80 ppm selenium, sodium selenite caused 97.5% mortality by six weeks and selenomethionine caused 100% mortality. At 40 ppm, these two forms of selenium caused 25 and 12.5% mortality. No mortality occurred at 10 or 20 ppm. Diets containing 20, 40, or 80 ppm selenium in both forms caused decreases in food consumption and growth. The only statistically significant effect of 10 ppm selenium was with sodium selenite, which resulted in larger livers than controls. Selenomethionine was more readily stored in the liver than sodium selenite at levels above 10 ppm selenium in the diet. Based on comparisons of residues of selenium in livers of surviving and dead ducklings, concentrations in the liver were not diagnostic of death due to selenium poisoning. Because both forms of selenium resulted in severe reductions in food consumption, selenium-induced starvation may have been related to duckling mortality. It was not clear whether either form of selenium at 10 ppm in the diet resulted in a leveling off of selenium concentrations in the liver within six weeks.     

Effect of dietary acid or aluminum on growth and growth-related hormones in mallard ducklings (Anas platyrhynchos)

Acid precipitation may exert negative effects on growth and survival of birds whether by the acid itself (H⁺ ions) or by aluminum consumption due to increased solubility at low pHs. The effects of aluminum or acid on growth-related hormones were compared in mallard ducklings: growth hormone, insulin-like growth factor, and insulin-like growth factor binding proteins (IGFBPs). Birds received two levels of acid: sulfuric acid (0.056 or 0.277 moles sulfate per kg) or aluminum sulfate (0.1 or 0.5% aluminum; 0.056 or 0.277 moles sulfate per kg). Two sodium sulfate (0.056 or 0.277 moles sulfate per kg) treatment groups were added as additional controls, and a group was given control diet ad libitum. Ducklings were fed the test diets for 15 days. In addition, there were pair-fed controls to the acid and aluminum diets. Growth as indicated by body weight, average daily gain, and tibiotarsus length was reduced (p<0.05) in ducklings on the high aluminum diet compared to those receiving the control diet ad libitum. Moreover, ducklings on the high aluminum diet had a reduced (p<0.05) growth (average daily gain) compared to the pair-fed controls. No effects of the aluminum diets on plasma concentrations of growth hormone, insulin-like growth factor-I, or IGFBPs were observed (IGFBPs being observed in the duck for the first time). Diets containing acid had no effects on growth or circulating hormone levels. It is concluded that aluminum influences growth in ducks directly and by reducing feed consumption.     

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 (g/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.     

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.     

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. Day-old 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 protein-restricted (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.     

Behavior of mallard ducklings from parents fed 3 ppm DDE

Summary Mallard ducks fed a diet containing 3 ppm DDE (equal to about 0.6 ppm in a natural succulent diet) laid eggs that contained an average of 5.8 ppm DDE; ducklings that hatched from these eggs differed from controls in behavioral tests designed to measure responses to a maternal call and to a frightening stimulus. In response to the maternal call, ducklings from parents fed DDE were hyper-responsive; compared to controls, a greater percentage approached the call and a greater percentage of those that approached remained near the call for the remainder of the test. In a test of avoidance behavior, ducklings whose parents were fed DDE traveled shorter distances from the frightening stimulus than did controls.     

Toxic,neurochemical and behavioral effects of dieldrin exposure in mallard ducks

Toxic, neurochemical and behavioral alterations were evaluated in ducks fed various dietary levels of dieldrin. Increasing amounts of dieldrin in the diet caused an appreciable decrease in the levels of three biogenic amines in whole brain,i.e. serotonin, norepinephrine and dopamine. No effect was noted in whole brain gamma aminobutyric acid contents. Hepatic microsomal enzymes were assayed in these birds usingp-nitroanisol andO-ethyl-O-p-nitrophenyl benzenethionophosphate as substrates. Sublethal amounts of dieldrin caused an increase in hepatic drug metabolizing enzymes. Similar alterations were noted in liver protein, deoxyribonucleic acid and ribonucleic acid contents. Studies involving encounters between mallard drakes indicated a decline in the tendency for dieldrin exposed drakes to take the initiative and establish rights of access in approach confrontations. Although many of these changes are compatible with life processes, their significance is not well understood, especially in terms of lifelong exposure to persistent pesticides. The possible relationship between neurochemical alterations and the mechanisms of insecticide neurotoxicity is discussed.Supported in part by contract No. 14-16-008-1020 between the U.S. Fish and Wildlife Service and Utah State University, and USPHS Grant No. MH 18589-01. Wildlife Management Institute, Utah Division of Wildlife Resources, and the Bureau of Sport Fisheries and Wildlife, cooperating.     

Failure of dieldrin to affect color vision in juvenile mallard ducks

Nine mallard ducks were raised artificially from eggs and fed the same long-term doses of dieldrin as their parents (0, 4, or 10 ppm); in addition, three ducks from 10 ppm parents were raised on 50 ppm. The parents had been on dieldrin-treated feed for two years. The juvenile ducks were tested at approximately two months of age. Each duck was trained to respond (key peck) differentially to light wavelengths of 552 mµ (S⁺) and 610 mµ (S^–) and, subsequently, was presented 13 different wavelengths, in random order. Differential responding was analyzed for stimulus generalization. No significant differences (p<.05) were found between the control and treated groups' mean stimulus generalization gradients. Only the group receiving 50 ppm in their feed had a mean whole-brain dieldrin residue significantly larger (p<.05) than that of the control group. These results indicate that the ingestion of dieldrin, under the test conditions used, does not have a measurable effect on light wavelength discrimination in mallard ducks.     

Toxic, neurochemical and behavioral effects of dieldrin exposure in mallard ducks.

Toxic, neurochemical and behavioral alterations were evaluated in ducks fed various dietary levels of dieldrin. Increasing amounts of dieldrin in the diet caused an appreciable decrease in the levels of three biogenic amines in whole brain, i.e. serotonin, norepinephrine and dopamine. No effect was noted in whole brain gamma aminobutyric acid contents. Hepatic microsomal enzymes were assayed in these birds using p-nitroanisol and O-ethyl-O-p-nitrophenyl benzenethionophosphate as substrates. Sublethal amounts of dieldrin caused an increase in hepatic drug metabolizing enzymes. Similar alterations were noted in liver protein, deoxyribonucleic acid and ribonucleic acid contents. Studies involving encounters between mallard drakes indicated a decline in the tendency for dieldrin exposed drakes to take the initiative and establish rights of access in approach confrontations. Although many of these changes are compatible with life processes, their significance is not well understood, especially in terms of lifelong exposure to persistent pesticides. The possible relationship between neurochemical alterations and the mechanisms of insecticide neurotoxicity is discussed.     

Toxicity and estimated water quality criteria values in mallard ducklings exposed to pentachlorophenol

Tests were conducted to determine the effects of pentachlorophenol (PCP) in feed on growth and bioaccumulation in mallard ducklings (Anas platyrhynchos). Significant effects of PCP on growth (LOAEL) were observed after 11 days at 961 g/g PCP. The NOAEL value (no significant growth effects) was 423 g/g PCP. Concentrations of PCP in tissues at the NOAEL were 20.7 (liver), 12.2 (lipid), 3.3 (muscle), and 2.6 (brain) g/g (wet wt); no bioaccumulation was observed. Using a toxicity threshold model, it was estimated that about 1.1 mg/L of waterborne PCP was a threshold for adverse effects for mallard ducks.     

Effects of pentachlorophenol-contaminated food organisms on toxicity and bioaccumulation in the frogXenopus laevis

Sub-adult African clawed frogs (Xenopus laevis) were fed pentachlorophenol (PCP)-injected mealworms containing 64.8 to 2604 ug of PCP per gram of worm for 27 days. There was no mortality and no significant bioaccumulation of PCP in the frogs. After three weeks, frogs fed 2,604 Rg/g of PCP ceased eating. The no observed adverse effects level (NOAEL) based on significantly reduced food consumption (PCP-injected mealworms) was 638 g/g. This corresponded to a NOAEL based on PCP intake of about 8 g PCP/ g frog/day. A toxicity threshold model estimated that about 800 g/L of waterborne PCP may be a threshold for adverse effects in Xenopus or similar amphibians. Further study is needed to verify threshold estimates.     

Toxicity and oxidative stress of different forms of organic selenium and dietary protein in mallard ducklings

Concentrations of over 100 ppm (mg/kg) selenium (Se) have been found in aquatic plants and insects associated with irrigation drainwater and toxicity to fish and wildlife. Composition of diet for wild ducklings can vary in selenium-contaminated environments. Earlier studies have compared toxicities and oxidative stress of Se as selenite to those of seleno-DL-methionine (DL) in mallards (Anas platyrhynchos). This study compares DL, seleno-L-methionine (L), selenized yeast (Y) and selenized wheat (W). Day-old mallard ducklings received an untreated diet (controls) containing 75% wheat (22% protein) or the same diet containing 15 or 30 ppm Se in the above forms except for 30 ppm Se as W. After 2 weeks, blood and liver samples were collected for biochemical assays and Se analysis. All forms of selenium caused significant increases in plasma and hepatic glutathione peroxidase activities. Se as L at 30 ppm in the diet was the most toxic form, resulting in high mortality (64%) and impaired growth (>50%) in survivors and the greatest increase in ratio of oxidized to reduced hepatic glutathione (GSH). Se as both L and DL decreased the concentrations of hepatic GSH and total thiols. Se as Y accumulated the least in liver (approximately 50% of other forms) and had less effect on GSH and total thiols. In a second experiment, in which the basal diet was a commercial duck feed (22% protein), survival was not affected by 30 ppm Se as DL, L, or Y and oxidative effects on GSH metabolism were less pronounced than with the wheat diet.