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Biomedical subjects

J A Doerr

Publications and source records attributed to J A Doerr.

29 records · Page 2Linked to original sources
PubMed1980

Evaluation of bone strength during aflatoxicosis and ochratoxicosis.

Young chickens were fed graded levels of aflatoxin (0, 0.625, 1.25, 2.5, 5.0, and 10.0 mug/g of diet) or ochratoxin (0, 0.5, 1.0, 2.0, 4.0, and 8.0 mug/g of diet), and the breaking strength, displacement before failure, and diameter of their tibias were determined. Breaking strength was decreased at growth inhibitory levels of aflatoxin (2.5 mug/g) and ochratoxin (2 mug/g), whereas a reduction in diameter required higher levels (5.0 and 4.0 mug/g, respectively). Bones from birds with ochratoxicosis selected to have diameters equal to control bones had lower breaking strength. In an attempt to negate mathematically the effect of decreased diameter and bias in any selection process, stress at time of failure of the bones was calculated and found to be decreased by feeding aflatoxin but not ochratoxin. Total displacement of bones before breaking was increased significantly (P < 0.05) by both toxins at the highest levels administered, but this increase was primarily the result of an increase in displacement from the start of failure to complete failure. Increased displacement associated with both toxicoses was equal in bones selected to be of equal diameter or in bones from the same treatment but of different diameters. However, calculation of modulus of elasticity which is corrected for diameter revealed aflatoxin had no effect whereas ochratoxin tripled the effect. These data indicate that the material properties of bones can be altered during mycotoxicoses and suggest yet another way in which mycotoxins are detrimental to animal health.

Aflatoxins↗
PubMed1980

The early influence of aflatoxin upon sexual maturation in the male Japanese quail.

The effects of early exposure to aflatoxin on sexual maturation were investigated in young male Japanese quail. Quail in Treatment A were fed a soy-corn starter mash with 10 micrograms aflatoxin/g added from 7 to 21 days of age. Treatment B quail were fed this from 14 to 28 days of age. Animals from each treatment were sampled at intervals from 25 days to 70 days of age. Both behavioral and physiological indicators of sexual maturation were monitored including measurements of sexual behavior, cloacal gland area, testes weight, and peripheral concentrations of testosterone. Statistical estimation was conducted to determine the age at which occurred rapid increase in hormone concentrations and morphological variables indicative of sexual maturation. Control animals showed increased testosterone concentration at 26 days and increased testes weight at 27 days. The cloacal gland area enlarged by 34 days and sexual behavior was first observed at 31 days. Animals in the A treatment had rapid testicular growth at 29 days and testosterone concentrations rose after 27 days. Concentrations were depressed compared to those of controls. Cloacal gland hypertrophy occurred after 37 days; initial sexual activity began at 35 days. The B treatment animals began showing evidence of sexual maturation significantly later with increasing testes weight by 36 days, testosterone concentrations by 37 days, cloacal gland area by 37 days, and initial sexual activity at 35 days. This experiment indicates that exposure to aflatoxin at an early age results in a delay in physiological and behavioral sexual maturation. Animals exposed between 7 and 21 days recovered slightly earlier than those treated between 14 and 28 days.

Aflatoxins↗
PubMed1980

Delayed reproductive development resulting from aflatoxicosis in juvenile Japanese quail.

Aflatoxicosis was induced in young Japanese quail. In the first experiment five replicates of 30 birds per treatment were fed a soy-corn basal ration containing 0, 5, or 10 microgram aflatoxin per gram of feed from 1 to 3 weeks of age. At 3 weeks, the animals were sacrificed and mesurements taken. In the second experiment, 0 to 10 microgram aflatoxin per gram of diet were fed from either 1 to 3 weeks of age or 2 to 4 weeks of age. At 3 weeks of age body weights were significantly (P < .05) reduced and relative liver weights were significantly (P < .05) increased. Testicular weights relative to body weight were depressed by up to 50%. Ovary wet weights, but not relative weights, were reduced. Testicular development (weight) was impaired through 6 weeks of age. Ovarian development, determined both by weight and number of developing follicles, was delayed as long as 3 weeks following withdrawal of aflatoxin from the diet. Radioimmunoassay for circulating androgens revealed that aflatoxin suppressed both the onset of production and the final concentratin of male hormone. The data demonstrate that aflatoxin can exert a deleterious inhibition of sexual development in quail with subsequent impairment of reproductive capacity. These findings raise the implication of potential reproductive failure in economically important species such as broiler breeders.

Aflatoxins↗
PubMed1979

Decreased glycogen mobilization during ochratoxicosis in broiler chickens.

Graded doses of pure ochratoxin A (0, 0.5, 1.0, 2.0, 4.0, and 8.0 microgram of toxin per g of feed) were incorporated into a commercial diet which was fed to chickens from hatching to 3 weeks of age, at which time the experiments were terminated. Liver glycogen levels were elevated significantly (P less than 0.05) by 4.0 and 8.0 microgram/g but not lower doses. Glucagon stimulation of glycogen mobilization was inhibited at the same concentrations. Histopathological examination revealed cytoplasmic but not nuclear deposits of glycogen in cells at the periphery of liver lobes. These data demonstrated that ochratoxin inhibited glycogenolysis. Impaired ability to generate glucose from glycogen could account for the increased susceptibility to cold stress previously reported to occur in ochratoxicosis. Based on present and prior observations, it seems possible that ochratoxin induces a syndrome which mimics the glycogen storage disease of type X which is caused by a deficiency in the cyclic AMP-dependent enzyme of the glycogenolytic enzymatic cascade.

Animals↗
PubMed1975

Egg production, shell thickness, and other physiological parameters of laying hens affected by T-2 toxin.

T-2 toxin has been reported to cause severe oral lesions and neural disturbances in young broiler chickens. T-2 toxin, when added at a level of 20 mug per g of feed, caused oral lesions but no abnormal neural disturbances in young broiler chickens. T-2 toxin, when added at a level of 20 mug per g of feed, caused oral lesions but no abnormal neural symptoms in laying hens. T-2 toxin had no effect on either hemoglobin, hematocrit values, erythrocyte count, plasma glucose, prothrombin times, or the sizes of the liver, spleen, pancreas, and heart. Lipid content of the liver was not altered. Feed consumption, however, was reduced, as were the total plasma protein and lipid concentrations and the total leukocyte count. Most important economically was the lowered egg production and a thinner egg shell. The timing and severity of the symptoms suggest that T-2 toxin causes primary oral lesions that reduce feed consumption with a consequent reduction in serum proteins and lipids, which culminate in decreased egg production. The leucopenia and thinner egg shell may be independent systemic effects of T-2 toxin in laying hens.

Animals↗
PubMed1975

Investigation and standardization of prothrombin times in chickens.

This investigation was undertaken to standardize the determination of the one-stage prothrombin time for use with chickens. Homologous thromboplastin was essential and the most active thromboplastin was obtained from chickens four-weeks old or younger. Acetone-dried brain powder could be stored for at least 4 months at -15 degrees C. without loss of activity. Extraction of brain powder with 0.025 M CaCl2 at 42 degrees C. gave better thromboplastic activity than the standard extraction with physiological saline at room temperature. Thromboplastin solutions could be stored in ice water for only 6 hours without loss of activity. Citrate concentration had to be increased from the usual 0.10 M to 0.18 M to prevent premature clotting of plasma. Plasma donor age had no effect on the prothrombin times. Freezing and thawing as well as storage of plasma in the frozen state increased the prothrombin times. Using the best conditions, the mean prothrombin time for 1200 birds determined over a 6-month period was 9.4 sec. with an individual range of 7.18-11.4 sec. This represents a significantly lower prothrombin time with lower variability than that reported in the literature.

Age Factors↗