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Biomedical subjects

T D Phillips

Publications and source records attributed to T D Phillips.

At least 73 records · Page 4Linked to original sources
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

Effect of peanut tannin extracts on growth of Aspergillus parasiticus and aflatoxin production.

Twenty-three peanut (Arachis hypogaea L.) genotypes were evaluated for kernel resistance to Aspergillus parasiticus Spear. colonization and aflatoxin contamination when incubated under high relative humidity. Also, tannin-containing extracts from kernel coats (testae) and cotyledons of these genotypes were prepared and tested for their effect on A. parasiticus growth and aflatoxin production in vitro. The lowest degree of colonization, less than 30%, was noted in kernels from the genotypes, Toalson x UF 73-4022 (selections TX-798731 and TX-798736), A72118, SN 55-437, PI337409, and Florunner. Genotypes with low levels of colonization also had the lowest aflatoxin contamination. The coefficient of correlation between infection frequency and aflatoxin contamination was 0.66. Higher levels of tannins were detected in the testae (23.9-97.2 mg g tissue) compared to the cotyledons (0.17-0.82 mg g tissue). Some of the methanol-extracted and water-soluble tannin extracts from testae and cotyledons, when incorporated in yeast extract sucrose liquid medium (100 mg l), significantly inhibited A. parasiticus growth and reduced the levels of aflatoxin produced. There was no overall correlation between the peanut genotypes and the influence of tannin extracts on A parasiticus growth and aflatoxin production. However, correlations were higher for specific genotypes. For example, the coefficient of correlation between the ability of tannin extracts from testae of genotypes PI337409 and TX-798736 to inhibit aflatoxin production was 0.93 and 0.85 respectively.

Aflatoxins↗
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

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↗
PubMed1990

Detection and detoxification of aflatoxins: prevention of aflatoxicosis and aflatoxin residues with hydrated sodium calcium aluminosilicate.

Our recent findings demonstrate that HSCAS can prevent aflatoxicosis in chickens and swine and significantly decreases the level of aflatoxin M1 residues in the milk of lactating dairy cattle. The basic mechanism for this action appears to involve sequestration of aflatoxin in the gastrointestinal tract and chemisorption (i.e., tight binding) to HSCAS which results in a reduction in aflatoxin bioavailability. Research is in progress to elucidate the specificity of HSCAS action and to construct a series of selective chemisorbents for mycotoxin control in livestock and poultry.

Aflatoxins↗
PubMed1990

Effects of treatment of growing swine with aflatoxin and T-2 toxin.

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1989

Individual and combined toxicity of deoxynivalenol and T-2 toxin in broiler chicks.

Effects of feeding diets containing deoxynivalenol (DON)-contaminated wheat (16 mg DON/kg) and purified T-2 toxin at 4 mg/kg singly and in combination were characterized in male broiler chicks from 1 day to 3 wk of age. Total body weight gains and final body weights were significantly reduced by the DON/T-2 toxin combination but were not significantly affected by the toxins singly. The efficiency of feed utilization was reduced in chicks fed either of the diets containing DON-contaminated wheat. The incidence and severity of oral lesions induced by T-2 toxin was increased in the DON/T-2 toxin combination. Several parameters not altered by DON or T-2 toxin singly were significantly affected by the combination, indicating that the combination may pose a potentially greater problem to the poultry industry than either of the mycotoxins individually.

Animal Feed↗
PubMed1989

Prevention of aflatoxicosis by addition of hydrated sodium calcium aluminosilicate to the diets of growing barrows.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCAS/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Silicates↗
PubMed1989

Effects of aflatoxin, deoxynivalenol, and their combinations in the diets of growing pigs.

In 2 studies, the effects of dietary aflatoxin (AF) and deoxynivalenol (DON) were evaluated in growing crossbred barrows. The first study consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 2.5 mg of DON/kg of feed, 0.75 mg of AF/kg of feed, and 2.5 mg of DON + 0.75 mg of AF/kg of feed. Pigs were fed their respective diets for 21 days. Treatment with DON caused decreases in weight gains, but no other treatment-related differences could be attributed to diets. In a second study, the experimental design consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 3 mg of DON/kg of feed, 3 mg of AF/kg of feed, and 3 mg of DON + 3 mg of AF/kg of feed fed ad libitum for 28 days. The pigs were observed twice daily for clinical signs, hematologic and serum biochemical measurements were made weekly, and body weights and feed consumption were determined weekly. Body weight gains were significantly depressed by the AF and the AF + DON treatments for days 7, 14, 21, and 28. Body weights and body weight gains were only slightly reduced in the DON treatment. Changes in serum enzymatic activities of alkaline phosphatase, aspartate transaminase, creatine kinase, and gamma-glutamyl transferase were noticed in pigs given treatments with AF alone and those given AF + DON.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1989

Evaluation of diets contaminated with aflatoxin and ochratoxin fed to growing pigs.

The effects of dietary aflatoxin and ochratoxin, fed singly and in combination, were evaluated in growing crossbred pigs. Five barrows (7 weeks old at beginning of study) per group were fed either control feed, 2.0 mg of aflatoxin (AF)/kg of feed, 2.0 mg of ochratoxin (OA/kg of feed, or 2.0 mg of AF and 2.0 mg of OA/kg of feed for 28 days. Production performance, serum biochemical, hematologic, and pathologic evaluations were made. Body weights were reduced by the combination treatment, whereas body weight gain was decreased by all toxin treatments. The effect of AF and OA in combination on body weight gain was additive. Liver weights were increased by the combination treatment, whereas kidney weights were increased only in the OA group. Aflatoxin caused decreases in serum calcium, sodium, phosphorus, urea nitrogen, cholesterol, and glucose concentrations, whereas OA alone caused decreases in serum phosphorus, cholesterol, and hematologic values. The AF-OA treatment induced decreases in mean corpuscular volume, packed cell volume, and in serum concentrations of phosphorus, cholesterol, and urea nitrogen. The AF-OA treatment increased serum alkaline phosphatase activities and triglycerides. It was concluded that AF and OA, singly or in combination, can affect clinical performance, serum biochemical and hematologic values, and organ weights of barrows. Although values of some measurements were affected more by the combination than by either toxin alone and suggested synergism or antagonism, the toxic interactions could best be described as additive.

Aflatoxins↗
PubMed1988

Aflatoxin B1 hydroxylation by the pregnenolone-16 alpha-carbonitrile-inducible form of rat liver microsomal cytochrome P-450.

The effects of treating rats with various pregnenolone-16 alpha-carbonitrile (PCN)-type inducers of cytochrome P-450p on the liver microsomal metabolism of aflatoxin B1 (AFB1) were investigated. Treatment of male rats with PCN resulted in a 6-fold increase in the 9-hydroxylation of AFB1 to aflatoxin Q1 (AFQ1). Treatment of female rats with PCN resulted in a 16-fold increase in the formation of AFQ1. The age-dependent decline in constitutive cytochrome P-450p levels in female but not male rats resulted in a sex difference in the formation of AFQ1 in liver microsomes from untreated rats (male:female approximately 3:1). The formation of AFQ1 was stimulated up to 5.4-fold when liver microsomes from triacetyloleandomycin (TAO)-treated rats were treated with potassium ferricyanide, which dissociates the complex between cytochrome P-450p and TAO. Treatment of male rats with the cytochrome P-450p inducer, dexamethasone, increased (approximately 7-fold) the 9-hydroxylation of AFB1 to AFQ1 by liver microsomes, and also enhanced (approximately 2-fold) the microsomal activation of AFB1 to metabolites that were mutagenic to Salmonella typhimurium TA98 and TA100. These results indicate that the 9-hydroxylation of AFB1 to AFQ1 is catalyzed by rat liver microsomal cytochrome P-450p.

Aflatoxin B1↗
PubMed1988

Hydrated sodium calcium aluminosilicate: a high affinity sorbent for aflatoxin.

Aluminas, silicas and aluminosilicates were evaluated for their ability to sorb radiolabeled aflatoxin B1 (AFB1) from aqueous solution (in vitro). Hydrated sodium calcium aluminosilicate (HSCAS) was selected for testing in vivo due to its high affinity for AFB1, because of its stable association with AFB1, and its GRAS (generally recognized as safe) status as an anticaking agent. The HSCAS, when added to the diet of Leghorn and broiler chicks at a level of .5%, significantly diminished the adverse effects of feeding 7.5 mg AFB1/kg of feed. Thus, this agent (and other aluminosilicate congeners) may prove effective in the preventive management of aflatoxicosis.

Absorption↗
PubMed1988

Influence of ochratoxin A and deoxynivalenol on growing broiler chicks.

The effects of feeding diets containing ochratoxin A (OA) (2.0 mg/kg) and deoxynivalenol (DON) (16 mg/kg) singly and in combination were characterized in male broiler chicks from 1 to 3 wk of age. Body weight gains and efficiency of feed utilization were significantly reduced by feeding OA singly, DON singly, and the OA/DON combination. Increased relative liver, kidney, and proventriculus weights were observed in the OA and OA-DON groups and blood urea nitrogen (BUN) was increased in the DON group. Serum uric acid, creatinine, and triglycerides were significantly elevated, and total protein, albumin, cholesterol, and aspartate amino transferase (AST) activity were decreased in the OA group. Histopathological examination of the liver, kidney, spleen, proventriculus, gizzard, and bursa revealed that lesions were confined primarily to mild hepatocellular degeneration, with milk diffuse lipidosis of the liver and mild swelling of the renal tubular epithelium of the OA and OA/DON combination groups. For a few parameters such as efficiency of utilization and relative liver, gizzard, and spleen weights. OA and DON appear to interact additively. However, many of the parameters such as body weights, body weight gains, BUN, total protein, and AST show significant interactions that can best be described as less than additive or in some cases antagonistic.

Animals↗
PubMed1988

Progression of aflatoxicosis in growing barrows.

The progression of aflatoxicosis was evaluated in growing crossbred barrows given 0, 1, 2, 3, or 4 mg of aflatoxin (AF)/kg of feed for 28 days (6 to 10 weeks of age). On day 28, pigs were euthanatized and necropsied, and tissues were removed for histologic examination. Body weight gains were decreased in barrows fed 2 mg of AF/kg after 7 days and in barrows fed 1 mg of AF/Kg after 14 days. By 28 days, all barrows fed AF had decreased body weights and weight gains. Compared with decreased in all barrows fed AF. Neither liver weights nor bone ash values were altered, although liver lipid values were increased in barrows fed AF. Serum aspartate transaminase, gamma-glutamyl transferase, and alkaline phosphatase activities were increased in barrows fed AF, whereas creatine kinase activity was decreased. Aflatoxin diets resulted in decreases in serum concentrations of urea nitrogen, phosphorus, cholesterol, albumin, and total protein. Histologic alterations in liver included interlobular fibrosis, periportal lipidosis, bile duct hyperplasia, and periportal lymphocytic infiltration. Lymphocytes in the thymus were depleted, and numbers of granulocytic cells in the bone marrow were reduced. The frequency and severity of lesions increased with increased doses of AF.

Aflatoxins↗
PubMed1987

Feed refusal in swine fed ochratoxin-contaminated grain sorghum: evaluation of toxicity in chicks.

In an episode of feed refusal in a swine herd, feed specimens were found to be contaminated with mycotoxin. Grain sorghum, the chief ingredient of the swine diet, was found to be the source of contamination and contained 5 mg of ochratoxin/kg of feed. Incorporation of the grain into poultry diets induced renal and hepatic lesions, reduced weight gains, decreased feed utilization, and altered serum uric acid, blood urea nitrogen, and serum creatinine concentrations in chicks.

Animal Feed↗
PubMed1987

Developmental toxicity of diacetoxyscirpenol in the mouse.

Mycotoxins (frequently referred to as secondary metabolites of toxigenic fungi) are commonly found in foodstuffs and are important because of their association with disease. The mycotoxin diacetoxyscirpenol, or 3-hydroxy-4,15-diacetoxy-12,13-epoxytrichothec-9-ene (DAS), is produced by numerous species of Fusarium and is reportedly toxic to humans and animals. The teratogenic potential of DAS was determined in time-mated ICR mice. DAS (dissolved in a 1:9 mixture of propylene glycol/saline) was administered intraperitoneally to pregnant mice at levels of 1.0, 1.5, 2.0, 3.0 and 6.0 mg/kg body weight in a single dose on one of gestation days 7-11 during the period of organogenesis. Term fetuses were examined for anomalies by routine teratologic procedures. Reabsorption frequency was dose-related and occurred as follows: 100% at 6.0 mg/kg on all gestation days tested; 90-99% at 3.0 mg/kg on days 7-9 and 100% on days 10 and 11; 26-51% at 2.0 mg/kg on days 7-9 and 100% on days 10 and 11; 9-77% at 1.5 mg/kg on days 7-10 and 100% on day 11; 7-34% at 1.0 mg/kg on days 7-11. A significant reduction in mean fetal body weight and a variety of fetal malformations (i.e. external and skeletal) were observed following maternal exposure to DAS. This is the first report to implicate this mycotoxin as a teratogen.

Abnormalities, Drug-Induced↗
PubMed1987

Aroclor 1254 as an antagonist of the teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 20 micrograms/kg) to pregnant C57BL/6J mice (on day 10) resulted in 62% fetuses with cleft palate per litter without any observable maternal toxicity. In contrast, Aroclor 1254 administered at a dose of 750 mumol/kg was not teratogenic. Cotreatment of the pregnant mice with both Aroclor 1254 (244 mg/kg) and 2,3,7,8-TCDD (20 micrograms/kg) resulted in an 8.2% incidence of cleft palate per litter. In contrast, Aroclor 1254 did not afford any protection from the teratogenicity of dexamethasone in C57BL/6J mice. Previous studies have shown that Aroclor 1254 can act as a partial antagonist of the microsomal enzyme induction and immunotoxic effects of 2,3,7,8-TCDD in C57BL/6J mice and this paper demonstrates that the commercial polychlorinated biphenyl mixture also antagonizes 2,3,7,8-TCDD-mediated teratogenicity in this strain of mice.

Abnormalities, Drug-Induced↗