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Biomedical subjects

W E Huff

Publications and source records attributed to W E Huff.

At least 19 recordsLinked to original sources
PubMed1992

Aflatoxin and glutathione in domestic fowl (Gallus domesticus)--II. Effects on hepatic blood flow.

1. The effect of aflatoxin on plasma aspartate aminotransferase (AST), protein, and hepatic glutathione (GSH) and hepatic blood flow (perfusion), were determined in 3-week-old male chickens. 2. Daily aflatoxin gavage (2 mg/kg body wt, in corn oil) for 5 and 10 days elevated plasma AST and hepatic GSH, and depressed plasma protein and hepatic perfusion. Also, renal GSH was elevated after 10 days of aflatoxin treatment. 3. Birds given aflatoxin for 10 days followed by a 10-day recovery period exhibited tissue GSH, plasma AST and protein levels that were not different from control, but hepatic perfusion remained depressed.

Aflatoxins↗
PubMed1992

Efficacy of hydrated sodium calcium aluminosilicate to reduce the individual and combined toxicity of aflatoxin and ochratoxin A.

A 2 x 2 x 2 factorial arrangement of treatments consisting of dietary aflatoxin (3.5 micrograms/g), ochratoxin A (2.0 micrograms/g), and hydrated sodium calcium aluminosilicate (HSCAS, .5%) was used to evaluate the individual and combined effects of these treatments. There were six replicate pens of 10 broilers per pen for each of the eight treatments. The broilers were maintained on these treatments from 1 day to 3 wk of age with feed and water available for ad libitum intake. Aflatoxin and ochratoxin A each significantly decreased body weight, serum protein, albumin, and cholesterol and increased the relative weight of the liver, kidney, and proventriculus. Aflatoxin increased the relative weight of the heart and decreased serum aspartate aminotransferase activity and ochratoxin A increased serum uric acid. The toxicity resulting from the combination of aflatoxin and ochratoxin A was more severe than when either of these mycotoxins were present alone. Addition of HSCAS alone did not alter any of the parameters evaluated. The HSCAS reduced the toxicity of aflatoxin, but had little effect on either the toxicity of ochratoxin A alone or the toxicity resulting from the combination of aflatoxin and ochratoxin A.

Aluminum Silicates↗
PubMed1991

Aflatoxicosis alters avian renal function, calcium, and vitamin D metabolism.

Experiments were designed to determine the effects of aflatoxicosis on avian renal function, calcium (CA), inorganic phosphorous (Pi), and vitamin D metabolism, and to determine if the effects of aflatoxin are reversible upon discontinuation of toxin administration. Three-week-old male broiler chickens (n = 12 per treatment) received aflatoxin (AF; 2 mg/kg po) or an equal volume of corn oil, the AF carrier vehicle, for 10 consecutive days. After 10 d of treatment, half of the birds from each treatment group were anesthetized and prepared for renal function analysis, which included a 2-h phosphate loading period. Ten days after discontinuation of AF treatment, the remaining birds in each treatment group were anesthetized and prepared for renal function analysis. AF decreased plasma 25-hydroxy vitamin D [25(OH)D] and 1,25-dihydroxy vitamin D [1,25(OH)2D] levels after 5 d of treatment. After 10 d of treatment, urine flow rate (V), fractional sodium excretion (FENa), and fractional potassium excretion (FEK) were lower in AF-treated birds. In addition, total plasma Ca tended to be lower (p = .10) and fractional Ca excretion (FECa) tended to be higher (p = .10) in the AF-treated birds. Intravenous phosphate loading produced a sharp increase in urine hydrogen ion concentration ([H+]) in the AF-treated birds. Glomerular filtration rate (GFR) was reduced and plasma osmolality was increased in AF-treated birds 10 d after discontinuation of toxin administration. The results indicate that AF directly or indirectly affects Ca and Pi metabolism in avians. At the present time, the effects may be related to altered vitamin D and parathyroid hormone (PTH) metabolism. Aflatoxicosis may decrease endogenous PTH synthesis and the renal sensitivity to PTH. The AF-related increase in urine [H+] during phosphate loading is probably due to increased Na+/H+ counterport, suggesting that AF stimulates sodium reabsorption. Also, the decrease in GFR exhibited 10 d after toxin removal indicates that AF may cause prolonged alteration in renal function.

Aflatoxins↗
PubMed1991

Cocontamination of swine diets by aflatoxin and diacetoxyscirpenol.

The effects of dietary aflatoxin (AF) and diacetoxyscirpenol (DAS), singly and in combination, were evaluated in growing crossbred barrows. The experimental design consisted of 4 treatments of 9 barrows each fed diets containing 1) 0 mg AF and 0 mg DAS/kg feed (control), 2) 2.5 mg AF/kg feed, 3) 2.0 mg DAS/kg feed, or 4) 2.5 mg AF + 2.0 mg DAS/kg feed for 28 days (10-14 weeks of age). Production performance, serum biochemical, hematologic, and pathologic measurements were made. Body weight and body weight gain were significantly decreased by each toxin but more so by the combination treatment. The effects were additive in nature. Liver and spleen weights, as percentages of body weight, were increased by the AF and AF + DAS treatments, and AF or AF + DAS treatments induced diffuse hepatocellular vacuolar change, early portal fibrosis, and early bile duct hyperplasia. Aflatoxin increased serum values of creatinine and gamma glutamyl transferase, cholinesterase, and alkaline phosphatase activities; increased packed cell volume and hemoglobin; and decreased urea nitrogen and total iron binding capacity. DAS reduced serum iron binding capacity. The AF + DAS treatment increased serum gamma glutamyl transferase and alkaline phosphatase activities, increased hemoglobin, and decreased serum iron binding capacity. Generally, the combination treatment could be described as additive or less than additive, with most of the effects attributable to AF. Under the conditions and parameters monitored in this study, AF and DAS had no synergistic toxic effects when incorporated into diets of growing barrows.

Aflatoxins↗
PubMed1991

Toxic effects of kojic acid in the diet of male broilers.

The toxicological effects induced by the administration of kojic acid were characterized in young male broiler chickens (Hubbard x Peterson). The experimental design consisted of six dietary treatments of kojic acid (0, .5, 1, 2, 4, and 8 g/kg feed) and four replicates of 10 broilers per replicate. Kojic acid significantly (P less than .05) decreased growth rates at concentrations greater than 2 g basic acid/kg feed. Kojic acid in higher concentrations also significantly increased the relative weights of the proventriculus, gizzard, pancreas, and liver, and significantly decreased the relative weight of the bursa of Fabricius at necropsy (Day 21). Hematological changes included a significant increase in the number of red blood cells, a significant increase in packed-cell volume, and a significant decrease in mean corpuscular volume. Also occurring was a significant increase in the serum concentrations of total protein, albumin, cholesterol, and triglycerides. Hepatotoxicity of dietary kojic acid was evident through a significant increase in the activities of serum glutamic oxalacetic transaminase and creatine kinase and a significant decrease in the activity of alkaline phosphatase. A significant increase in serum uric acid concentration was indicative of nephrotoxicity, and a significant increase in serum glucose concentration was indicative of pancreatic toxicity. A significant decrease in colonic temperature was also observed. Because the toxic effects of kojic acid were only observed at concentrations greater than 2 g kojic acid/kg feed, this mycotoxin alone does not appear to pose a serious economic threat to the poultry industry.

Animal Feed↗
PubMed1991

Comparative fate of the tritiated trichothecene mycotoxin, T-2 toxin, in chickens and ducks.

A tritiated preparation of the trichothecene mycotoxin, T-2 toxin, was administered as a single oral dose to 21-day-old male broiler (Hubbard x Hubbard) chickens and White Pekin ducks. There were few significant differences between the two species in metabolism, tissue retention, and excretion of T-2 toxin and its metabolites. On the basis of the data obtained, the differences in toxicological sensitivity to T-2 toxin known to exist between these two species cannot likely be attributed to differences in the metabolism or elimination of T-2 toxin from the body.

Animals↗
PubMed1991

The individual and combined toxicity of kojic acid and aflatoxin in broiler chickens.

The individual and combined effects of kojic acid and aflatoxin were studied in male broiler chicks (Peterson x Hubbard). The experiment had a two by two factorial arrangement of treatments with dietary treatments of 0 and 2,500 mg kojic acid/kg feed and 0 and 2.5 mg aflatoxin/kg feed. The broilers were obtained at 1 day of age and housed in electrically heated batteries with feed and water available for ad libitum intake until they reached 3 wk of age. The toxicity of kojic acid was characterized by significant (P less than .05) reductions in body weight, the relative weight of the bursa of Fabricius, serum cholesterol concentration, and serum alkaline phosphatase activity, and by significant (P less than .05) increases in the relative weight of the pancreas, proventriculus, and gizzard, and serum concentrations of uric acid and triglycerides. Aflatoxicosis was characterized by significant (P less than .05) reductions in body weight, serum concentrations of total protein, albumin, cholesterol, and inorganic phosphorus, serum glutamic oxalacetic transaminase activity, and mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. Significant (P less than .05) increases in the relative weight of the liver, kidney, spleen, pancreas, proventriculus, and heart, and the serum pyruvic transaminase activity were also caused by aflatoxin alone. The only significant (P less than .05) interaction between kojic acid and aflatoxin, which can best be described as antagonistic, was seen through an increase in mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration. These data indicate that kojic acid is not an aflatoxin synergist at the levels used in the present study.

Aflatoxins↗
PubMed1991

Effects of a hydrated sodium calcium aluminosilicate on growing turkey poults during aflatoxicosis.

Effects of adding .5% of a hydrated sodium calcium aluminosilicate (HSCAS) to diets containing 1 or .5 mg aflatoxin (AF)/kg were determined in male turkey poults from 1 day to 3 wk of age. Body weight gains were significantly reduced by 51 and 19% in turkey poults fed 1 and .5 mg AF/kg, respectively; efficiency of feed utilization was not affected. There were no deaths in poults fed .5 mg AF/kg; however, the mortality rate was 88% in poults fed 1 mg AF/kg. The addition of .5% dietary HSCAS resulted in a 68% decrease in mortality to 28% for the 3-wk experimental period. Treatment-related changes in relative organ weights, hematological values, serum biochemical values, and enzyme activities were observed. The HSCAS in the absence of AF did not alter any of the parameters measured. The HSCAS diminished the adverse effects of AF on body weight gains, most relative organ weights, hematological values, serum biochemical values, and enzyme activities associated with .5 mg AF/kg, but not 1 mg AF/kg. These findings indicate that HSCAS may diminish many of the adverse effects of AF in an AF-sensitive species, the turkey.

Aluminum Silicates↗
PubMed1991

Effects on aflatoxin M1 residues in milk by addition of hydrated sodium calcium aluminosilicate to aflatoxin-contaminated diets of dairy cows.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for agricultural feeds, was added to aflatoxin (AF)-contaminated diets of 3 lactating dairy cows and evaluated for its potential to reduce aflatoxin M1 (AFM1) residues in milk. During phase I, cows were fed alternating diets that consisted of 200 micrograms of AF/kg of feed for 7 days, 0.5% HSCAS plus 200 micrograms of AF/kg of feed for 7 days, and feed with the HSCAS removed for a final 7 days. The AFM1 milk concentrations from the intervals with HSCAS added to diets were compared with those times when HSCAS was absent. The presence of 0.5% HSCAS in feed containing 200 micrograms of AF/kg reduced AFM1 secretion into the milk by an average of 0.44 micrograms/L (from pretreatment of 1.85 micrograms/L to 1.41 micrograms/L with HSCAS, a 24% reduction). Following a 10-day period of noncontaminated feed consumption and no AFM1 residues in the milk, phase II of the study was begun. The same experimental design as phase I was used, but the dosages of HSCAS and AF were changed to 1.0% and 100 micrograms/kg of feed, respectively. The addition of 1.0% HSCAS in feed containing 100 micrograms of AF/kg decreased AFM1 content in the milk by an average of 0.40 micrograms/L (from a pretreatment of 0.91 micrograms/L to 0.51 micrograms/L when HSCAS was present, a 44% reduction). These findings suggest that HSCAS, a high-affinity sorbent compound for AF in vitro, is capable of reducing the secretion of AFM1 into milk.

Aflatoxin M1↗
PubMed1991

Diminution of aflatoxin toxicity to growing lambs by dietary supplementation with hydrated sodium calcium aluminosilicate.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing wethers (mean body weight, 34.0 kg) and was evaluated for its ability to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 4 treatment groups of 5 wethers each, consuming concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control; group 1); 20 g of HSCAS/kg (2.0%; group 2), 2.6 mg of AF/kg (group 3); or 20 g of HSCAS (2.0%) plus 2.6 mg of AF/kg (group 4). Wethers were maintained in indoor pens, with feed and water available ad libitum for 42 days. Lambs were observed twice daily and weighed weekly, and blood samples were obtained every 2 weeks for hematologic and serum biochemical analyses and for measurement of mitogen-induced lymphocyte-stimulation index. At the termination of the study, wethers were euthanatized and necropsied. Body weight gain was diminished significantly (P less than 0.05) by consumption of 2.6 mg of AF/kg of feed, whereas body weight of lambs consuming HSCAS plus AF did not differ from that of control wethers. The AF-alone treatment increased serum aspartate transaminase and gamma-glutamyltransferase activities, prothrombin time, and cholesterol, uric acid, and triglyceride values and decreased albumin, glucose, and urea nitrogen values, and urea-to-creatine ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1990

Impact of L-phenylalanine supplementation on the performance of three-week-old broilers fed diets containing ochratoxin A. 1. Effects on body weight, feed conversion, relative organ weight, and mortality.

An experiment with a completely randomized 2-by-3 factorial design was used to study the effects of ochratoxin A (OA; 0 and 4 mg of OA per kg) and supplemental L-phenylalanine (Phe; .0%, .8%, and 2.4% of Phe) in the diets of 3-wk-old broilers. Diets based on ground yellow corn and dehulled soybean meal were fed from Day 1 to 3 wk of age. A total of 240 male Hubbard-by-Hubbard broilers were randomly placed in battery brooders with 10 birds per pen. Each treatment was replicated 4 times. The parameters measured included mortality, BW, feed conversion, and relative organ weight. Broilers receiving OA weighed less and had poorer feed conversions than birds not receiving OA. For broilers receiving OA, the relative weights (grams of organ weight per 100 g of BW) of the liver, proventriculus, gizzard, and heart increased, while the relative weight of the bursa decreased. Supplemental Phe decreased the relative weight of the liver and increased the relative weight of the gizzard and heart. The regression slopes for Phe at 4 mg of OA per kg of diet were significantly different from 0 for BW, the relative weights of the kidney, spleen, and pancreas and approached significance for mortality (P = .065). In the absence of supplemental Phe, 42.5% of the birds died during the study when the dose level was 4 mg of OA per kg of diet. However, when Phe was supplemented at .8 and 2.4%, only 12.5 and 15.0% of the birds died, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Impact of L-phenylalanine supplementation on the performance of three-week-old broilers fed diets containing ochratoxin A. 2. Effects on hematology and clinical chemistry.

Phenylalanine was evaluated for its ability to protect broiler chickens from the toxic effects of ochratoxin A (OA). A completely randomized 2-by-3 factorial design was utilized consisting of 0, .8, and 2.4% supplemental L-phenylalanine (Phe) and of 0 and 4 mg of OA per kg of diet. The basal diet contained 14% protein. Broilers were raised in battery brooders to 3 wk of age, when blood was collected and various hematological parameters were determined. The health status of the broilers was evaluated by assaying serum for various enzyme activities and metabolites using an automated, clinical chemistry analyzer. Adding OA to the broiler diets resulted in an increased concentration of serum hemoglobin as well as increased activity for cholinesterase and gamma glutamyl transferase but in decreased activity for aspartate amino transferase, lactate dehydrogenase, and alkaline-phosphatase activity as well as decreased concentrations of total triglyceride and of inorganic phosphorus. Supplemental Phe decreased the concentrations of hemoglobin and serum glucose. The regression slopes for Phe at 4 mg of OA per kg of diet were significant for uric acid, creatinine, total protein, albumin, and cholesterol suggesting that supplemental Phe improved the health status of the broilers fed diets containing OA with respect to these parameters.

Alkaline Phosphatase↗
PubMed1990

Diminution of aflatoxicosis in growing chickens by the dietary addition of a hydrated, sodium calcium aluminosilicate.

The amelioration of aflatoxicosis in broiler and Leghorn chickens was examined by feeding a hydrated, sodium calcium aluminosilicate (HSCAS) or activated charcoal. In three experiments, HSCAS or activated charcoal at a concentration of .5% of the total diet were incorporated into diets for broiler and Leghorn chicks containing either no added, purified aflatoxin B1 (AFB1), 7.5 mg of AFB1 per kg, or 5 mg of aflatoxin (AF) per kg (produced by Aspergillus parasiticus on rice). Compared to the controls, the AFB1 reduced BW gains at 0 to 3 wk by 21 to 38% in broilers; and the AF reduced BW gains at 0 to 4 wk in Leghorns by 20 percent. The HSCAS significantly diminished the growth-inhibitory effects of AFB1 or of AF on growing chicks by 50 to 67 percent. Feeding 5 mg of AF per kg of diet with or without charcoal to Leghorn chicks caused a significant increase in the relative weights of the liver, kidney, proventriculus, and gizzard as well as significant increases in activity of serum gamma glutamyltransferase; also, significant decreases in the relative bursa weights as well as the concentrations of serum total protein and albumin. With the exception of the relative bursa weights, the toxic effects caused by aflatoxin were prevented or were reduced by adding hydrated, sodium calcium aluminosilicate. These data suggest that HSCAS can modulate the toxicity of AFB1 and AF in the chicken; however, adding activated charcoal to the diet did not appear to have protective properties against the effects of aflatoxin B1 or of aflatoxin.

Aflatoxin B1↗
PubMed1990

Ascites in growing broilers: a research model.

A method was developed to experimentally produce ascites in broiler chickens. High-altitude simulation (treatment group) was conducted to study the development of ascites in broiler chickens. In each of three experiments, 15 male broiler chicks (1 wk old) were placed in a hypobaric chamber (principal groups) for 5 wk and 15 other chicks were reared in batteries (control groups). Ascites occurred among chicks in the principal groups recorded at 13, 27, and 80% at simulated altitudes of 1,980, 2,438, and 2,896 m, respectively. No ascites were observed in the controls at 100 m (the altitude at College Station, Texas). Body weight was significantly (P less than .05) reduced for broilers in the principal groups versus the controls-especially at 2,896 m, where the principals weighed 500 g less than the controls. The counts for hematocrit, hemoglobin, and red blood cells were significantly (P less than .05) increased in all treatment groups; while at 2,438 and 2,896 m, corticosterone was significantly reduced. Histopathology indicated consistent, mild, cardiopulmonary lesions similar to those observed in the spontaneous ascites of broiler chickens. The high-altitude simulation model will be useful in studying the etiological factors and interactions causing ascites.

Altitude↗
PubMed1990

Single and combination effects of administering salinomycin and aflatoxin to broiler chicks.

A factorial design (2 by 3) was used to evaluate the interaction between aflatoxin (0, 2.5, and 5 mg per kg) and salinomycin [0, 60 g per ton (909 kg)]. There were four replicates of 10 chicks per treatment. The chicks were maintained in batteries from 0 to 3 wk of age, with feed and water available for ad libitum intake. Aflatoxin at both levels (2.5 and 5 mg per kg) with and without salinomycin decreased body weight. The efficiency of feed utilization was affected only at the 5 mg per kg level of aflatoxin. Feeding 5 mg per kg of aflatoxin alone decreased the hemoglobin level. The inclusion of salinomycin (60 g per ton) in the diet with 2.5 or 5 mg per kg of aflatoxin initiated no significant change in body weight or feed efficiency. No significant interaction was observed between aflatoxin and salinomycin on any of the parameters measured.

Aflatoxins↗
PubMed1990

Efficacy of a hydrated sodium calcium aluminosilicate to reduce the toxicity of aflatoxin and T-2 toxin.

A hydrated sodium calcium aluminosilicate (HSCAS) was incorporated into diets (.5%) containing 3.5 mg of aflatoxin (AF) per kg and 8.0 mg of T-2 toxin (T-2) per kg, singly, and in combination. Male broiler chicks (n = 480) were provided with feed and water for ad libitum consumption from 1 to 21 days of age. Body weight gains were significantly depressed by AF and T-2, singly, and further decreased by the combination of the two toxins. Efficiency of feed utilization was not affected. The AF alone and the AF plus T-2 combination caused increases in relative liver, kidney, proventriculus, gizzard, spleen, and pancreas weights. Treatment-related changes in hematological and serum biochemical values and enzyme activities were observed. Oral lesions were observed only in chicks receiving the T-2 diets. The HSCAS fed singly did not alter any of the parameters measured but it did diminish the toxicity of AF for many parameters but did not appear to alter the toxicity of T-2. Addition of HSCAS to the AF plus T-2 combination diet diminished some of the effects of the toxin combination. These findings indicate that HSCAS can diminish many of the adverse effects of dietary AF in the chicken, but it has no effect on T-2 toxicity.

Aflatoxins↗