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Biomedical subjects

W E Donaldson

Publications and source records attributed to W E Donaldson.

At least 55 records · Page 3Linked to original sources
PubMed1987

Effect of lead toxicity on the organ concentration of glutathione and glutathione-related free amino acids in the chick.

Total non-protein sulfhydryl (NPSH) and glutathione (GSH) concentrations in liver and kidney and GSH-related free amino acid concentrations in liver, kidney and plasma were examined in the chick following intoxication with 2000 ppm dietary lead (Pb). After 3 weeks, NPSH content was significantly (P less than 0.05) increased by Pb in both liver and kidney while only liver GSH was increased by Pb treatment. The concentrations of glutamate, glycine and methionine were elevated in liver by Pb while glycine, cysteine and cystathionine concentrations were increased in the kidney. In plasma, Pb significantly decreased cysteine, taurine and cystathionine concentrations.

Amino Acids↗
PubMed1987

Lead effects in the chick during selenium deficiency.

1. Growing chicks (Gallus domesticus) were fed a selenium-deficient diet supplemented with 0 or 2000 ppm lead (Pb) and 0 or 0.1 ppm selenium (Se). 2. Selenium addition stimulated growth at 0 but not at 2000 ppm Pb, while Pb depressed growth at both levels of Se. 3. Selenium addition stimulated Se-dependent glutathione peroxidase (GSH-Px) activity in liver, but Pb was without effect on GSH-Px activity. 4. Lead addition increased non-protein sulfhydryl (NPSH) concentrations in liver, kidney and thigh muscle. NPSH levels were not altered by Se. 5. The reported antagonism between Pb and Se does not appear to be mediated through effects on GSH-Px or NPSH metabolism.

Aging↗
PubMed1987

Chromium and vanadium effects on glucose metabolism and lipid synthesis in the chick.

The effects of 20 ppm chromium (CrCl3.6H2O) and/or 20 ppm vanadium (NaVO3.nH2O) on growth, glucose metabolism, and lipid synthesis in chicks were studied in a 2 X 2 factorial experiment. Chicks were fed experimental diets from day-old to 3 weeks of age. At 3 weeks, four chicks per treatment were injected intraperitoneally (i.p.) with 250 mu Ci 3H2O and 4 mu Ci [U-14C]glucose. Chicks were bled by cardiac puncture and killed 30 min postinjection. Dietary vanadium reduced body and liver weights and liver cholesterol while serum cholesterol was increased. Chromium had no effect on these parameters and there was no significant interaction of chromium with vanadium. Chromium and vanadium each increased 14C incorporation into liver fatty acids over that of controls. However, the combination of chromium and vanadium was without effect so that the interaction was significant. Incorporation of 3H from H2O into liver fatty acids paralleled that of 14C from glucose for all treatments. In vitro studies on the uptake and oxidation of glucose by liver slices from chicks fed the basal diet were conducted. Chromium increased the rate of glucose utilization 16% over control and vanadium increased the rate by 33%. The combination of chromium and vanadium was no different from vanadium alone. A chromium vanadium antagonism was observed in some metabolic processes but not on body or organ weight.

Animals↗
PubMed1986

Interaction of lead toxicity and riboflavin status in chicks (Gallus domesticus).

Chicks (Gallus domesticus) were fed diets containing 0 or 2000 ppm lead (Pb) and adequate, marginal or deficient levels of riboflavin. In comparison to adequate, marginal riboflavin depressed growth at 2000 ppm Pb but not at 0 ppm Pb. Deficient riboflavin depressed growth at both Pb levels, and Pb depressed growth at all riboflavin levels. Hepatic glutathione reductase activity was reduced by riboflavin deficiency, but Pb was without effect. Hepatic non-protein sulfhydryl concentrations were increased by Pb, and the increases were greater at the lower riboflavin levels. Dietary Pb appears to increase the level of riboflavin required in chick diets.

Animals↗
PubMed1986

Modification of lead toxicity and organ distribution by dietary sulfur amino acids in chicks (Gallus domesticus).

Chicks (Gallus domesticus) were fed a basal diet deficient in methionine and total sulfur amino acids with 0 or 1000 ppm added lead for 21 days. Methionine or methionine and cystine addition improved growth regardless of dietary lead level. Cystine addition alone improved growth only when lead was present. Relative inhibition of growth by lead was greater with diets containing no added methionine. Hepatic non-protein sulfhydryl concentration was increased by lead and all amino acid additions. Organ lead concentrations were generally lower with added amino acids. Dietary methionine appears to counteract lead toxicity more effectively than cystine.

Animals↗
PubMed1986

Lead toxicity in chicks: interactions with dietary methionine and choline.

Two factorial experiments were conducted to study the effects of dietary methionine and choline on lead toxicity in chicks. Dietary variables were 0.3 or 0.63% (experiment 1) or 0.23 or 0.75% methionine (experiment 2); 0 or 1000 ppm lead (as Pb acetate X 3H2O); and 1130 or 3300 mg/kg (experiment 1) or 396 or 1266 mg/kg choline (experiment 2). In both experiments, lead depressed growth while methionine stimulated growth. Growth depression by lead was less with methionine-adequate than with methionine-inadequate diets. There were no differences in growth with the choline-marginal or choline-excess diets. In experiment 2, the methionine x lead interaction for growth was observed with choline-adequate but not with choline-inadequate diets. Lead-induced depression of growth was exacerbated by added choline when methionine-inadequate diets were fed. With methionine-adequate diets, choline level had no effect on the lead-induced depression of growth. Hepatic nonprotein sulfhydryl (NPSH) concentrations were increased by both supplemental methionine and lead with no interaction. Choline levels had no effect on NPSH. Dietary methionine significantly lowered Pb concentration of kidney and muscle but not of bone, liver or blood. Choline had no effect on organ Pb concentrations. Methionine, either dietary or in the dosing solution, had no effect on in situ intestinal absorption or 203PbCl2. These results suggest that lead lowers the chick's choline requirement and that the methyl moiety of methionine does not participate directly in lead detoxication. The amelioration of Pb toxicity by methionine appears to be related to increased excretion of Pb.

Animals↗
PubMed1985

Biotin effects on fatty acid synthesis in chicks.

Data are summarized from several papers on the effects of biotin deficiency on lipid metabolism, especially fatty acid synthesis, in chicks. Biotin deficiency inhibits in vivo lipogenesis and hepatic acetyl-CoA carboxylase (ACC) activity. Although acetate incorporation into fatty acids is inhibited in biotin-deficient chicks, malonate incorporation is not inhibited. In fact, dietary malonic acid stimulates lipogenesis during biotin deficiency as measured by total carcass fatty acid content. Biotin-deficient chicks exhibit altered hepatic and whole body fatty acid composition in comparison with control chicks. The deficiency results in an increased proportion of the 16-carbon to 18-carbon fatty acids, and the most striking increase is for palmitoleic (16:1) acid. Biotin deficiency increases the relative incorporation of palmitate and stearate into phospholipids and decreases the relative incorporation of these fatty acids into triglycerides. Finally, mercury stimulates lipogenesis in biotin-deficient, but not in control, chicks by an unknown mechanism.

Acetates↗
PubMed1985

Lipogenesis and body fat in chicks: effects of calorie-protein ratio and dietary fat.

Two experiments were conducted with battery-reared, broiler chicks from day-old through 19 or 20 days of age. In each experiment, body weight, feed consumption, liver weight, liver fat, body fat, in vivo lipogenesis, and the hepatic activities of the lipogenic enzymes, acetyl-Coenzyme A carboxylase (ACC) and fatty acid synthetase (FAS), were measured. In Experiment 1, four diets having calorie-protein (C/P) ratios expressed as kilocalories of metabolizable energy per kilogram of diet per percent crude protein of 120, 139, 158, or 177 were used. Growth was decreased with ratios above 139. The C/P ratio had no significant effect on feed conversion, liver weight, liver fat, or FAS activity. In vivo lipogenesis and ACC activity were increased by C/P ratios above 120. Body fat increased with increasing C/P ratios, but only the C/P 177 diet produced significantly fatter chicks. In Experiment 2, four diets containing total fat 2.0, 4.1, 6.3, or 8.6% at a constant C/P ratio of 139 were used. All fat levels above 2.0% improved growth and feed conversion. Fat levels had no effect on liver weight, liver fat, or body fat. In vivo lipogenesis and ACC and FAS activities decreased with increasing dietary fat. The data indicate that C/P ratio affects body fat by increasing lipogenic activity as the ratio is increased. Although dietary fat depressed lipogenesis, the depression appears to be offset by increased availability of fatty acids from the diet for deposition in adipose tissue. Hence, added dietary fat does not change body fat content.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1984

Dietary lead: effects on hepatic fatty acid composition in chicks.

Arbor Acre broiler chicks were fed diets containing 0, 500, 750, 1000, 2000, or 4000 ppm lead (as Pb acetate X 3 H2O) from day-old through 21 days of age. There were 8 groups of 10 male chicks per lead level. Eight chicks from each dietary lead level were killed at 21 days, and hepatic fatty acid composition was determined for each chick by gas-liquid chromatography. Increasing dietary lead levels decreased the concentrations of 16:1 and 18:1 fatty acids (first No. = No. carbons; second No. = No. double bonds) and increased the concentrations of 18:0 and 20:4. The concentration of 18:2 fatty acids did not differ significantly from control values for any level of lead. However, the ratio 18:2/20:4 declined from a control value of 3.3 to approximately 2 for all lead treatments. The ratio of saturated/monoenoic fatty acids increased with dietary lead levels above 1000 ppm. In a second experiment 10 male broiler chicks per treatment were fed either a control diet or the control diet plus 2000 ppm lead, 60 ppm cadmium, 500 ppm mercury, or 10 ppm selenium (as Pb acetate X 3 H2O, CdSO4, HgCl2, or Na2SeO3, respectively) for 21 days. Six chicks from each group were killed at 21 days, and hepatic fatty acid composition was determined for each chick. In comparison to control, the ratio 18:2/20:4 was lowered by lead but unaffected by cadmium, mercury, and selenium. The data suggest that lead may increase tissue peroxidation (as noted by other workers) via a relative increase of 20:4 fatty acid and that a decrease of hepatic ratio 18:2/20:4 may be a specific sign of lead toxicity.

Animals↗
PubMed1984

Effect of dietary methionine and lysine on the toxicity of ingested lead acetate in the chick.

The interaction of methionine or lysine with lead in the diet of chicks was studied. In experiment 1, lead acetate to supply 0 or 1000 ppm lead was added to a diet that was either deficient in the total sulfur-containing amino acid (TSAA) content (62% of the requirement) or supplemented with DL-methionine to provide 100% of the requirement (NRC, 1977). Supplementing the 0 ppm lead diet with methionine improved body weight gain. Dietary addition of 1000 ppm lead significantly decreased body weight gain; however, supplemental methionine partially alleviated the lead-induced growth depression (methionine X lead interaction was significant). Liver glutathione levels were markedly increased by supplemental methionine and also by lead but no methionine X lead interaction was detected. In experiment 2, the interaction between an essential non-sulfur-containing amino acid, lysine, and dietary lead was investigated. Two levels of lead, 0 or 1000 ppm, were fed in diets either deficient or adequate in lysine (85 or 100% of the requirement, respectively). Addition of lysine to the lysine-deficient basal diet increased growth. The magnitude of the lead-induced growth depression was not affected by dietary lysine content. The lysine level of the diet did not influence the liver glutathione concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

The effects of ethylene chlorohydrin on fatty acid synthesis.

Male chicks weighing 700 to 900 g. received an acute or eight doses IG of 60 or 40 mg/kg ethylene chlorohydrin (ECH) respectively and were sacrificed eighteen hours after the last dose. Mitochondrial elongation of fatty acids was decreased significantly while fatty acid synthetase activity was not significantly affected by ECH treatment. Cytochrome c oxidase activity in fresh whole liver homogenate was significantly higher in chicks subjected to acute exposure with ECH when compared to the controls. Upon freezing and thawing of homogenates, cytochrome c oxidase activity increased significantly in the control group but was unchanged in the ECH group which suggests that the mitochondrial membrane integrity is compromised by the ECH treatment. Serum and liver triglyceride levels were significantly elevated in both the single and multiple ECH dose groups. Liver to body weight ratios were significantly higher in both treatment groups when compared to their controls. Histological examination of the liver of ECH-treated chicks showed cytoplasmic clearing of the cells but no vacuolization or centrilobular necrosis. Serum isocitrate dehydrogenase levels were significantly higher in the multiple treatment ECH group than in the control group.

Animals↗
PubMed1982

Atherosclerosis in cholesterol-fed Japanese quail: evidence for amelioration by dietary vitamin E.

Three experiments were conducted with adult, male Japanese quail (Coturnix coturnix japonica) from 5 through 14 weeks of age. In Experiment 1, quail fed a cholesterol-free diet were compared with quail fed .5% of United States Pharmacopoeias (USP), recrystallized (RCR), or oxidized (OXI) cholesterol preparations. In Experiment 2, .5% OXI cholesterol was fed alone and with .1% butylated hydroxytoluene (BHT) or 100 mg d-alpha-tocopherol acetate/kg of diet and compared with .5% RCR cholesterol. Experiment 3 was the same as Experiment 2 except the BHT treatment was deleted. In comparison to RCR-treated quail, OXI-treated quail exhibited significantly increased serum (P less than .05) and liver (P less than .01) cholesterol concentrations and increased severity of atherosclerotic lesions (P less than .05). Addition of vitamin E to the OXI cholesterol diet appeared to reduce severity of atherosclerotic lesions. Vitamin E did not completely prevent atherosclerosis nor did it change the proportion of the quail population that exhibited lesions.

Animals↗
PubMed1982

Separation of serum lipoproteins of Japanese quail by disc polyacrylamide gel electrophoresis and single discontinuous density gradient ultracentrifugation.

A method based on disc polyacrylamide gel electrophoresis (disc PAGE) for the separation of serum lipoproteins of Japanese quail (Coturnix coturnix japonica) prestained with Sudan Black B is described and evaluated. Good separation was obtained by using 3% separating gel and decreasing the concentration of buffer solution A used for preparation of separating gel solution to one-half that recommended by Narayan (1975). Best resolution of the high density lipoproteins was achieved by using 7 to 10% of separating gel, which separated the high density lipoproteins into three bands. Clear lipoprotein bands were obtained after ultracentrifugation of prestained serum. For corresponding positions, the bands of unstained serum after staining had the same mobility in the disc (PAGE) as prestained lipoprotein bands. In quail, density smaller than 1.006 g/ml contains chylomicrons and very low density lipoproteins (VLDL); density from 1.018 to 1.05 g/ml contains the low density lipoprotein (LDL); and density more than 1.05 g/ml and less than 1.16 g/ml contains the high density lipoproteins (HDL). In the profile of serum lipoproteins after ultracentrifugation, two peaks were observed in the density range of HDL. There was one small peak with density 1.05 to 1.09 g/ml and one large peak with density 1.09 to 1.16 g/ml. Based on the lipoprotein profiles from both disc PAGE and ultracentrifugation, HDL is the predominant form, LDL is intermediate, and VLDL and chylomicrons are smallest in amount.

Animals↗
PubMed1982

Effect of cholesterol feeding on serum lipoproteins and atherosclerosis in atherosclerosis-susceptible and atherosclerosis-resistant Japanese quail.

Male and female Japanese quail from two strains bred for differing susceptibility to induction of atherosclerosis by dietary cholesterol (RES = resistant, SUS = susceptible) were fed a control diet or control diet + .5% USP cholesterol. The diets were fed for 20 weeks beginning when the quail were 7 weeks old. Only quail fed cholesterol developed atherosclerosis. Atherosclerosis (incidence and severity) was higher in males than females and higher in SUS than RES. Cholesterol feeding increased aortic, liver, and serum cholesterol concentrations and liver total fat content. There were high positive correlations between serum cholesterol and liver cholesterol in all cholesterol-fed groups but not in control groups. Diet, sex, and strain differences in cholesterol distribution among the various serum lipoproteins and ratios of beta/alpha lipoproteins were observed. These differences are discussed in terms of their usefulness in predicting atherosclerosis in quail as compared with humans.

Animals↗
PubMed1979

Regulation of fatty acid synthesis.

Acetyl-CoA carboxylase and fatty acid synthetase are the two major enzymes involved in the synthesis of fatty acids in animals. The activities of both enzymes are affected by nutritional manipulations. Although acetyl-CoA carboxylase is considered generally to be the rate-limiting step in lipogenesis, there is evidence that suggests that fatty acid synthetase may become rate limiting under certain conditions. The principal support for the view that acetyl-CoA carboxylase is the rate-limiting enzyme for lipogenesis is that the activity of the enzyme is controlled by allosteric effectors that change the catalytic efficiency of the enzyme. Until recently, the only known control of fatty acid synthetase was through changes in rate of enzyme synthesis. Data are reviewed that show that fatty acid synthetase can exist in forms possessing different catalytic activities. Thus fatty acid synthetase appears to be subject to the type of control necessary for an enzyme to serve as a regulator of the rate of a biological process over a short term.

Acetyl-CoA Carboxylase↗
PubMed1979

Cholesteremia in Japanese quail: response to a mixture of vitamins C and E and choline chloride.

Five-week old, male, Japanese quail (Coturnix coturnix japonica) were given ad libitum access to glucose- soybean meal-10% fat diets containing 0, 0.25, 0.5, or 1% cholesterol, with or without the addition of a vitamin supplement (vitamin C--1 g/kg of diet, vitamin E--30 I.U./kg of diet and choline chloride--5.5 g/kg of diet). After 12 weeks, 9 quail from the 24 quail fed each diet were killed and the total cholesterol concentration of serum, liver, kidney, and aorta was determined. Cholesterol concentrations of these organs increased with increasing levels of dietary cholesterol. The vitamin supplementation enhanced the increase in the cholesterol concentration of serum and kidney, lessened the elevation of the liver cholesterol concentration and had no effect on the aorta cholesterol concentration. The remaining quail were fed the same diets, for a subsequent 12 week period, except that cholesterol was deleted. At the termination of the experiment, the total cholesterol concentration of serum, liver, and kidney returned to control level for all treatments in which organ cholesterol concentrations had been increased previously. Aortic cholesterol concentration decreased during the second 12 week period (0.5 and 1% cholesterol diets fed for the first 12 weeks), however, the aortic cholesterol concentration remained higher than those of the control at 24 weeks. No significant effect of vitamin supplementation on organ cholesterol concentration was noted at 24 weeks although serum cholesterol concentration was significantly lower for the vitamin- fed groups at all levels of dietary cholesterol. Aortic ahteromata were observed at both 12 and 24 weeks in all groups fed 0.5 and 1% cholesterol.

Animals↗