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Biomedical subjects

R D Wyatt

Publications and source records attributed to R D Wyatt.

At least 37 records · Page 2Linked to original sources
PubMed1986

The relationship of certain blood parameters to aflatoxin resistance in Japanese quail.

Blood chemistry profiles were obtained for two lines of Japanese quail selected for resistance to aflatoxin, and for a nonselected control line. Nine of the 18 plasma components measured in samples taken at 4 weeks of age changed as a result of selection. Plasma concentrations of total protein, albumin, cholesterol, and potassium, and the activities of lactic dehydrogenase, glutamic-oxalacetic transaminase, and cholinesterase were significantly elevated in aflatoxin-resistant quail compared with the nonselected line. The activities of beta-glucuronidase and alpha-amylase changed most dramatically; both activities were much lower in the resistant lines than in the control line. In another experiment, serum total protein, albumin, alpha-amylase, and beta-glucuronidase were tested as identifiers of aflatoxin-resistant individuals within a nonselected population of quail. Serum samples obtained from 150 nonselected quail immediately before and 24 hr after administration of an oral dose of aflatoxin were analyzed for each of the four components. The acute toxicosis decreased body weight, serum alpha-amylase activity, total protein, and albumin; whereas, serum beta-glucuronidase activity and the coefficients of variation for each parameter were increased. Correlations between measurements made prior to dosing and parameters reflecting aflatoxin susceptibility were not significant. However, postdose determinations of albumin, protein, and beta-glucuronidase were significantly related to susceptibility parameters. These data indicate that the four blood components tested cannot be utilized to identify resistant birds within a nonselected population of quail without an aflatoxin challenge; but albumin, protein, and beta-glucuronidase are correlated with resistance when measured during an aflatoxin stress.

Aflatoxins↗
PubMed1985

Effects of dietary aflatoxin and zinc on enzymes and other blood constituents in dairy calves.

Young male Holstein calves were fed diets containing 40 or 640 ppm zinc with 0 or 5 ppm aflatoxin for 3 wk. The aflatoxin mixture contained 80.5% B1 and the calves consumed 143 mg of B1 over 3 wk. Plasma glutamic-oxaloacetic transaminase and alkaline phosphatase concentrations were increased substantially, and lactic dehydrogenase was reduced in aflatoxin-fed calves. Supplemental zinc partially counteracted the effect of aflatoxin on these enzymes. Hemoglobin, packed cell volume, and total solids in blood plasma were increased in aflatoxin-fed calves, but high dietary zinc had no effect on these blood constituents. Glucose in plasma was reduced in calves receiving aflatoxin. High dietary zinc was only partially effective in protecting against the reduced glucose effect for about 1 wk. Total protein, albumin, globulin, ratio of albumin/globulin in blood plasma, and liver lipid were not affected by aflatoxin. Several enzymes and blood constituents are affected by aflatoxin in calves. The protection of zinc against aflatoxicosis appears to be no more than a partial effect.

Aflatoxins↗
PubMed1985

Effect of mixed organic acid administration on blood levels of chlortetracycline in broiler chicks.

Male broiler chicks, when administered mixed organic acids via the drinking water for 3 days prior to water administration of chlortetracycline (CTC), showed no significant increases in the blood levels of the antibiotic. However, if the organic acids were administered simultaneously with the antibiotic, either via drinking water administration or via oral dosing, significant increases in the blood levels of the antibiotic were noted. With simultaneous administration of the antibiotic and mixed organic acids via the drinking water, a significant decrease in water intake was observed; however, in spite of the decrease in water intake and a concomitant decrease in CTC intake, significant increases in the blood levels of the CTC were still present. These data suggest that mixed organic acids, commonly used in the poultry industry, can be utilized to elicit an increase in CTC blood levels to a greater degree than would be anticipated without the use of the organic acids.

Administration, Oral↗
PubMed1985

Comparative responses of genetically resistant and nonselected Japanese quail to dietary aflatoxin.

Two lines of Japanese quail (AR2.5 and AR3) selected for resistance to aflatoxin and a nonselected control line (NS) were fed diets containing 0, 10, and 20 micrograms of aflatoxin/g of feed. Line-related reductions in mortality and growth inhibition clearly demonstrated the resistance of the AR lines to dietary aflatoxin. Two-week cumulative mortality percentages for the NS, AR2.5, and AR3 lines fed the 10 micrograms/g diet were 13.9, 7.7, and 2.6%, respectively, and 44.4, 17.9, and 12.8% at 20 micrograms/g. Average growth reduction percentages resulting from feeding the 10 and 20 micrograms/g diets to the NS, AR2.5, and AR3 lines were: 17.3 and 27.5%, 10.7 and 20.1%, and 4.3 and 10.5%, respectively. In addition, AR quail were resistant in varying degrees to the following aflatoxin-induced effects: liver lipid accumulation and enlargement, hepatic protein depletion, elevated hepatic beta-glucuronidase activity, bursal regression, and hypoproteinemia. Comparisons of the AR and NS lines fed the control diet revealed no detrimental physiological or biochemical response to selection for aflatoxin resistance. Genetic resistance to aflatoxin was associated with increased relative liver weight, higher liver protein content, and elevated plasma concentrations of protein and lipid compared with NS quail. One or more of these differences may be related to the mechanism of genetic resistance to aflatoxin in AR quail.

Aflatoxins↗
PubMed1985

The effect of aflatoxin on complement activity in broiler chickens.

Groups of broiler chickens were fed rations containing .625, 1.25, or 2.5 micrograms total aflatoxin/g of feed from one day to 42 days of age. Treatment groups were segregated according to sex and control groups were maintained. The chickens were bled at 14-day intervals, and serum was collected for assay of total complement (C) activity using a radial hemolytic procedure. No significant differences were found in C titers between males and females of the same age group. For the sexes combined, mean C titers of chickens fed aflatoxin were compared to mean titers of controls. For each age group, significant differences in C titers existed only between the control group and those chickens fed 2.5 micrograms/g aflatoxin. Complement is a major component of the humoral immune response and this study adds to the evidence that aflatoxin can be immunosuppressive to chickens.

Aflatoxins↗
PubMed1985

Effect of dietary aflatoxin on the uptake and elimination of chlortetracycline in broiler chicks.

Day-old broiler chicks were fed 0, 1.25, 2.5, and 5.0 micrograms aflatoxin/g of feed for 3 weeks. Chlortetracycline (CTC) was administered in the drinking water at a concentration of 50 mg/liter for 27 hr starting on Day 21. Three hours after initiation of the CTC treatment, birds receiving 2.5 and 5.0 micrograms/g dietary aflatoxin had significantly lower CTC in blood compared with the controls. At 12 and 27 hr after the initiation of CTC treatment, birds receiving any level of aflatoxin had significantly decreased blood levels of CTC compared with the controls. Intravenous injection of CTC of control birds and birds receiving 2.5 micrograms/g aflatoxin revealed a significant decrease in the elimination half-life of CTC and a significant increase in the total systemic clearance of CTC in the birds receiving dietary aflatoxin. Birds receiving 2.5 micrograms/g dietary aflatoxin also had a significant increase in the volume of gall bladder bile; however, this did not result in a greater amount of CTC being eliminated via bile. Studies on protein binding of CTC in the plasma of control birds and the plasma of birds receiving 2.5 micrograms/g dietary aflatoxin demonstrated that 60% more CTC is "free", or unbound, in the plasma of birds receiving no aflatoxin. These results suggest that aflatoxicosis lowers the plasma concentrations of CTC as a result of a decreased binding of CTC to plasma protein. This allows more unbound CTC to be available for elimination from the plasma by a means other than the liver, most likely via the kidney.

Aflatoxins↗
PubMed1984

The effect of diet on performance, digestibility, blood composition and intestinal microflora of weaned pigs.

Good evaluation variables are needed to study postweaning lag in early weaned pigs. In this study, performance, digestibility, concentration of blood components and aerobic fecal microflora under different dietary regimens from weaning at 3 wk of age to 35 d of age are reported. Treatment 1 (T1) consisted of a corn-soybean meal starter diet. Pigs in treatment 2 (T2) received a steamed, rolled oat groats-casein starter diet. Pigs in treatment 1 and 2 were weaned at 3 wk of age while those in treatment 3 remained with the sow. Treatment 1 pigs had lower average daily gains for the 2-wk trial as compared with T2 pigs (P less than .05). Three of the four animals consuming the corn-soybean meal diet were observed to have diarrhea during the experiment as compared with an occasional loose stool from the pigs fed oats-casein. There were no significant differences in digestibility of dry matter, crude protein or ether extract among pigs in T1 and T2. Digestibilities of ash and crude fiber were higher (P less than .05) in T1 pigs, while there was an increase (P less than .05) in digestibility of N-free extract by pigs in T2. Serum protein, Na, CO2 and blood hematocrit were not significantly different among treatments. Blood chloride was higher, whereas glucose was lower for pigs in T1 and T2 than T3 (P less than .05). Blood urea N was higher for pigs in T1 as compared with pigs in T2 or T3. Potassium was higher (P less than .05) for pigs in T1 as compared with those in T2 or T3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1984

Comparative toxicity of Chaetomium contaminated corn and various chemical forms of oosporein in broiler chicks.

The toxicity to broiler chicks of Chaetomium contaminated corn and various chemical forms of oosporein were compared by feeding diets containing 60% Chaetomium contaminated corn (300 micrograms oosporein/g diet), and 300 or 150 micrograms/g of purified oosporein in either the K salt, Na salt, or organic acid form from hatching to 3 weeks of age. The Chaetomium contaminated corn diet caused 100% mortality during the first week of feeding. Necropsies revealed extensive visceral and articular gout, enlarged pale kidneys, dehydration, proventricular enlargement with mucosal necrosis, and a dark green discoloration of the gizzard lining. When the mortality percentages of the two experiments conducted were considered collectively, the K and Na salts of oosporein caused significantly higher mortality than the organic acid form of oosporein. The K salt caused the most severe lesions and the organic acid caused the least severe lesions. No mortality occurred at the 150 micrograms/g K salt or 150 micrograms/g organic acid levels. Relative kidney weights were increased by all forms of oosporein at 300 micrograms/g, but at 150 micrograms/g only the K salt caused an increase in kidney weight. The LD50 values, based on mortality from 1 to 10 days, were 5.77, 5.00, and 4.56 mg/kg for oosporein acid, oosporein Na salt, and oosporein K salt, respectively. These results suggest that the salts of oosporein (particularly the K salt) are more toxic than the organic acid, and the natural occurrence of oosporein in a salt form could contribute to the increased toxicity of the Chaetomium contaminated corn.

Animals↗
PubMed1984

Toxicity of Aspergillus ochraceus contaminated wheat and different chemical forms of ochratoxin A in broiler chicks.

The toxicity of Aspergillus ochraceus contaminated wheat and various chemical forms of ochratoxin A (OA) were compared by feeding diets containing A. ochraceus contaminated wheat (3.0 micrograms OA/g diet) and 3.0 micrograms/g of purified OA in the K salt, Na salt, or organic acid form to broiler chicks from hatching to 4 weeks of age. All OA diets caused listlessness, emaciation, dehydration, and occasional diarrhea. Cumulative mortalities were 0, 13, 17, and 10% for the control, contaminated wheat, OA Na salt, OA K salt, and OA acid, respectively. Necropsies at the end of the experiment revealed pale friable livers, enlarged pale kidneys, and enlarged gall bladders in all OA treatments. Body weights and gain were significantly depressed throughout the experiment, and cumulative feed conversion ratios were significantly increased by all forms of OA. Relative kidney and liver weights were also significantly increased by all forms of OA. Serum analysis revealed significant decreases in total protein, albumin, globulin, cholesterol, and phosphorus concentrations and significant increases in uric acid concentrations in chicks fed all forms of OA. Determinations of median lethal dose (LD50) were conducted by dosing day-old chicks and recording mortality for 10 days. LD50 values were 4.41, 3.95, and 2.69 mg/kg for OA acid, Na salt, and K salt, respectively. These results indicated that the K salt of OA was more toxic than the Na salt in acute oral dosing. During the feeding study, results also suggested that chemical form of OA affected its toxicity, but after feeding 3.0 micrograms/g OA for 4 weeks, no significant differences in toxicity were caused by the various chemical forms of OA or the A. ochraceus contaminated diet.

Animal Feed↗
PubMed1983

Effect of dietary aflatoxin concentration on the assessment of genetic variability of response in a randombred population of chickens.

The effect of graded levels of dietary aflatoxin on the assessment of genetic variability of body weight and gain and plasma protein response was tested utilizing the Athens-Canadian randombred population of chickens. Dietary aflatoxin was administered at levels of either 0, 1.25, 2.50 or 5.0 microg/g of diet ad libitum from 7 to 21 days of age to progeny from 58 sire families. Twenty-one-day body weights, gain and plasma protein concentration were used to assess the variation in response.-The administration of increasing levels of aflatoxin resulted in a dose-related decrease of gains and plasma protein concentrations. Plasma protein concentrations were significantly higher among males than females within the control group; however, this difference was reversed as the severity of the aflatoxin challenge increased. Heritability estimates for all responses increased as the level of aflatoxin administered increased. This change was most notable for total plasma protein concentration. Phenotypic correlations for plasma protein concentration and growth measurements tended to diminish with increasing levels of aflatoxin. A similar trend was noted for the genetic correlations; however, a moderate correlation between growth responses and plasma protein response was detected in the 5.0-microg/g aflatoxin treatment group. Genetic correlations were calculated for the same characters between the different levels of aflatoxin. Regardless of which aflatoxin challenges were compared, a very high genetic correlation for 21-day body weight and 7- to 21-day gain was estimated. This variation in growth potential in the toxic environment paralleled that observed in the control environment but at a lower plane. Genetic correlations for plasma protein response across aflatoxin levels diminished as the difference between the levels of aflatoxin administered increased. Plasma protein concentration in the control environment was positively correlated with plasma protein response in groups fed a low level of aflatoxin, but negatively correlated when an aflatoxin challenge of 2.5 microg/g or more was given, suggesting that selection for aflatoxin resistance using plasma protein response as a selection criterion should be made under an aflatoxin stress environment.

Aflatoxins↗
PubMed1983

Aflatoxicol and aflatoxins B1 and M1 in eggs and tissues of laying hens consuming aflatoxin-contaminated feed.

This study was undertaken to relate quantitatively the aflatoxin residue found in eggs and tissues to the aflatoxin intake via feed. Eighteen hens were fed an aflatoxin B1 (B1)-contaminated feed (8 micrograms/g) for 7 days, after which half the group was sacrificed; the remainder were sacrificed after an additional 7 days on an aflatoxin-free diet. Eggs were collected over the entire 14-day period. Aflatoxicol (R0), B1, or both were found in eggs and tissues (kidneys, liver, muscle, blood, and ova). Aflatoxin M1 (M1) (.04 to .1 ng/g) was found only in the kidneys. Levels of R0 and B1 were approximately the same in eggs, ova, kidneys, and liver. In eggs, the levels of R0 and B1 (.02 to .2 ng/g) increased steadily for 4 or 5 days, after which time the levels plateaued and then decreased after B1 withdrawal at the same rate as they had increased. At 7 days after withdrawal, only trace amounts of R0 (.01 ng/g) remained in eggs. All tissues, except blood, from hens sacrificed immediately before aflatoxin withdrawal contained R0 (.04 to .4 ng/g) or R0 and B1 (.04 to .8 ng/g). The R0 (.03 to .11 ng/g) was the only aflatoxin detected in muscle, and B1 (.05 to .07 ng/g) was the only aflatoxin in blood. Seven days after aflatoxin withdrawal, B1 (.08 ng/g) was found in one of nine livers and R0 (.01 to .04 ng/g) in eight of nine muscles analyzed, but no aflatoxins were found in any other tissues.

Aflatoxin B1↗
PubMed1982

Some effects of phenobarbital dosing of dairy cattle on aflatoxin M1 and fat in milk.

Eight Holstein cows were selected randomly to determine effects of phenobarbital on the fate of orally administered aflatoxin B1, milk fatty acid profiles, total milk fat, and milk production. Animals were grouped in pairs for one of four treatments: 1) control, 2) oral dosing with sodium phenobarbital for 5 days, 3) dosing with sodium phenobarbital followed by oral dosing with aflatoxin B1, and 4) oral dosing with aflatoxin B1 for 5 days. Daily composite raw milk samples were taken and assayed for aflatoxin M1 by thin-layer chromatography, and milk fatty acid profiles were measured by gas-liquid chromatography. Milk production for all treatments was less than that of controls. Total milk fat was not affected. Both aflatoxin B1 and phenobarbital affected fatty acid distribution, suppressing the amount of fatty acids carbons 8 through 14 while increasing the amount of 16-carbon fatty acids. No treatment effect was significant for the short chain fatty acids of 4 and 6 carbons and the 18-carbon acids oleic, stearic, and linoleic. Pretreatment with phenobarbital resulted in a significant difference between treated and untreated difference between treated and untreated animals. A greater than 50% reduction in the amount of aflatoxin B1 excreted as M1 in the milk was realized.

Aflatoxin M1↗
PubMed1982

Relationship between Eimeria adenoeides infection and aflatoxicosis in turkey poults.

Three-week-old turkey poults receiving 250 micrograms/kg of dietary aflatoxin displayed prolonged prothrombin times due to decreased fibrinogen levels and depressed activity of factor II. Decreased body weights and increased mortality were also evident. Poults experiencing an Eimeria adenoeides infection had slightly increased prothrombin times that were not corrected by the addition of specific clotting factors. These birds exhibited significant reductions in total plasma protein levels. The combination of E. adenoeides and aflatoxicosis resulted in a significant depression in body weight, altered prothrombin time, and decreased levels of plasma calcium, protein, and fibrinogen. Increased mortality was also observed. E. adenoeides did not affect the hemostatic system of the turkey as severely as does aflatoxin. Turkeys were shown to be highly susceptible to aflatoxin when compared to chickens.

Animals↗
PubMed1982

Natural occurrences of ochratoxicosis in poultry.

Five independent episodes of ochratoxicosis in about 970,000 turkeys, two episodes in about 70,000 laying hens, and two episodes in about 12,000,000 broiler chickens were investigated. Ochratoxin A concentrations in suspect feed and ingredients ranged from less than .2 to 16 ppm. Feed samples tested for T-2 toxin, F-2 toxin, heavy metals, and polychlorinated biphenyls were negative. Minor amounts of aflatoxin (less than 60 ppb) were found in suspect feed from two episodes. The main symptoms in turkeys were mortality (up to 59%), nephrotoxicity (pale, swollen kidneys that became tan colored in the sequel to acute toxicity), decreased feed consumption (as little as 20% of the normal feed intake) prior to death, and secondary air sacculitis. Histopathology revealed edema and necrosis of the proximal tubules of the kidneys and no changes in the liver or other organs. Suspect feed containing 2 ppm ochratoxin A increased uric acid levels in serum when fed to poults in the laboratory. The episodes in laying hens were characterized by reduced egg production, poor egg shell quality, and nephropathy. The episodes in broiler chickens were characterized by poor growth rate, poor feed conversion efficiency, poor pigmentation, nephropathy, and increased incidence of air sacculitis. Obtaining feed and ingredients free of ochratoxin, cleaning the feed and ingredient handling equipment, and adding antifungal agents to the feed proved beneficial. Eight of the 9 episodes were traced to the corn supply and the ninth episode was traced to corn gluten meal that became contaminated during storage after manufacture. Evidence was obtained that the ochratoxin was unstable and declined in concentration during storage. Aqueous acetone was a better solvent for extracting ochratoxin than was the recommended phosphoric acid: chloroform. The ochratoxin extracted from high potency samples consisted of ochratoxins A, B, and C in ratios of about 90:8:2.

Animals↗
PubMed1982

High performance liquid chromatographic determination and clearance time of aflatoxin residues in swine tissues.

Liver, kidney, and muscle tissues from swine given a single oral dose of 1.2 mg aflatoxins/kg body weight and from young pigs fed an aflatoxin-contaminated diet (0,400, or 800 ng/g feed) for 10 weeks were analyzed for aflatoxin residues. Extraction was performed according to the method of Stubblefield and Shotwell. Aflatoxin residues were detected by high performance liquid chromatography (HPLC), and residue levels were correlated with withdrawal times. Residues were present in liver and kidney but not muscle by 12 h post-dosing; residues were detected in muscle by after 24 h. Residue levels decreased over the 72 h period in all tissues. No aflatoxin residues were detected in the muscle from any pig 72 h post-dosing or in those pigs fed the 400 ng/g diet, but were present in the muscle of pigs fed the 800 ng/g diet.

Aflatoxins↗
PubMed1982

Enzyme studies in tardive dyskinesia. I. One-year biochemical follow-up.

Over a 1-year period we followed 12 female in-patients with and 13 without persistent tardive dyskinesia. Clinical signs of tardive dyskinesia as well as plasma dopamine-beta-hydroxylase and platelet monoamine oxidase activities remained stable over time in spite of medication changes. Tardive dyskinesia was associated with higher plasma dopamine-beta-hydroxylase and lower monoamine oxidase activities, both initially and at follow-up. In two patients, an apparent elevation in dopamine-beta-hydroxylase activity preceded the onset of clinical dyskinesia, suggesting that elevated plasma dopamine-beta-hydroxylase activity might be a potential risk marker for the development of tardive dyskinesia.

Aged↗