Biomedical subjects

P B Hamilton

Publications and source records attributed to P B Hamilton.

At least 37 records · Page 2Linked to original sources

PubMed1990

Comparative toxicity of scirpentriol and its acetylated derivatives.

Scirpentriol (STO) and its seven acetylated derivatives, 3-, 4- and 15-monoacetoxyscirpenol (MAS), 3,4-, 3,15-, and 4,15-diacetoxyscirpenol (DAS), and 3,4,15-triacetoxyscirpenol (TAS) were compared for their acute oral lethality in broiler chicks, lethality in brine shrimp, and dermal toxicity in guinea pigs. Of the eight toxins, 4,15-DAS was the most toxic in the three assays, 3-MAS was the least toxic in brine shrimp and dermal assays, and 3,4-DAS was the least toxic in the chick assay. There was a difference of about a 100-fold and 20-fold, respectively, between 4,15-DAS and 3-MAS in dermal toxicity and brine-shrimp toxicity, as well as a difference of more than 16-fold between 4,15-DAS and 3,4-DAS in chick toxicity. In general, a free hydroxy group at the 3-position was a primary determinant of toxicity. Toxicity in the scirpenol family did not follow precisely the pattern reported earlier for the T-2 toxin family of trichothecene toxins, in which a decrease in the number of acyl groups was accompanied by a decrease in toxicity. At necropsy, the predominant sign in chicks was petechial hemorrhaging, primarily in the gastrointestinal tract and in the vascular beds of the beaks and the toe nails. The 4,15-DAS and 15-MAS were about 3 times more toxic in chicks than aflatoxin. All members of the scirpenol family of trichothecene mycotoxins appeared sufficiently toxic to warrant attention whenever field outbreaks occur. Apparently, brine shrimp and dermal assays are successful predictors of chick lethality by the more toxic trichothecenes and are less suitable for predicting the activity of the less toxic trichothecenes.

Animals↗

PubMed1989

The effect of two applications of atrazine on the water quality of freshwater enclosures.

To simulate runoff from agricultural lands, atrazine was applied to aquatic enclosures (112 m(3)) on 1 June 1983 at a concentration of 0.1 mg litre(-1). Thirty-five days later the nominal concentration was increased to 0.155 mg litre(-1). Treated enclosures became clearer with Secchi disc readings of 3.6 m compared to non-treated controls (2.9 m). Less than 5% of the first atrazine addition disappeared during the first 35 days and little effect on biological activity was observed. However, with the second enrichment the rate of loss of atrazine was rapid (t(1/2) = 150 days), ammonium, calcium, dissolved inorganic carbon and nitrate levels were higher, while oxygen, chlorophyll, dissolved organic carbon and particulate organic carbon concentrations were lower in the treated enclosures. These water quality changes cannot be explained by herbicide-water chemistry interactions alone, thereby suggesting an indirect effect as a consequence of atrazine inhibition on photosynthesis and possibly other microbial processes.

Journal Article↗

PubMed1989

Influence of degree of acetylation of scirpenol mycotoxins on feed refusal by chickens.

The refusal by young chickens of feed containing graded levels (0, 1.25, 2.5, 5.0, 10.0, 20.0, and 40.0 micrograms/g of diet) of the Fusarium mycotoxins scirpentriol (STO), monoacetoxyscirpenol (MAS), diacetoxyscirpenol (DAS), and triacetoxyscirpenol (TAS) was tested in a defined experimental model. The order of activity as measured by minimum effective dose was DAS greater than MAS = STO greater than TAS whereas the order measured by percentage refusal at 10, 20, and 40 micrograms/g was MAS greater than DAS greater than STO greater than TAS. These results imply that feed refusal associated with corn and feed infested with Fusarium sps. might be a multiple toxicosis because the scirpenols, which are not tested for routinely, can occur together naturally.

Acetylation↗

PubMed1988

Factors influencing antifungal activity of gentian violet in poultry feed and ingredients.

The inhibition of fungal activity in poultry feed and ingredients by gentian violet was investigated by measuring respiratory CO2 liberated into the headspace gas above samples of feed and ingredients. Inhibition by gentian violet depended on 1) the lot of corn meal, 2) the concentration of gentian violet, 3) the moisture of the substrate, 4) time of incubation, 5) particle sizes of corn meal and gentian violet, and 6) temperature of a short heating episode mimicking the feed-pelleting process. These same factors were reported earlier to control and limit the activity of organic acid mold inhibitors. These results imply that differences between gentian violet and other mold inhibitors used in poultry feed are quantitative rather than qualitative.

Animal Feed↗

PubMed1988

Carotenoid composition of serum and egg yolks of hens fed diets varying in carotenoid composition.

High performance liquid chromatography of yolks of hens fed a diet based on yellow corn, alfalfa, and soybeans revealed over 20 cartenoids. Lutein, lutein monester, lutein diester, 3'-oxolutein, cryptoxanthin, zeaxanthin, beta-carotene, and zeacarotene were identified by their retention times, visible absorption spectra, behavior on saponification, and their presence or absence when lutein was the primary carotenoid fed. Three weeks after placing the hens on a white corn-soy-based diet supplemented with lutein (20 micrograms/g diet), cryptoxanthin, zeaxanthin, and zeacarotene were undetectable in the yolk and lutein, lutein monoester, lutein diester, and 3'-oxolutein assumed new equilibrium concentrations. The data imply an esterification pathway and an oxidative pathway in laying hens for the metabolism of hydroxycarotenoids. Consideration of the concentrations and ratios of lutein and its metabolites in serum and yolk suggest a nonovarian site for the metabolism of lutein in laying hens.

Animals↗

PubMed1988

Aflatoxin-impaired ability to accumulate oxycarotenoid pigments during restoration in young chickens.

The mechanism by which aflatoxin causes paling in chickens was investigated by measuring its effect on the restoration of pigments in 3-wk-old birds made pale by feeding a white corn-soy diet. Pigment restoration was accomplished by feeding the same diet supplemented with lutein (70 micrograms/g of diet), which is the major oxycarotenoid pigment in chicken diets and tissues. The oxycarotenoids (free, monoester, and diester forms of lutein) in the toe web, liver, serum, and jejunal mucosa of control and aflatoxin-fed (2 micrograms/g of diet) birds were measured by HPLC at 0, 1, 2, 3, 6, and 9 days of repletion. Aflatoxin caused a significant (P less than .05) depression of all forms of lutein in the toe web. In the liver, aflatoxin decreased lutein significantly (P less than .05) but increased lutein monoester and lutein diester. Lutein accumulation in serum and mucosa were inhibited significantly (P less than .05) starting on Days 2 and 3, respectively. These data imply that the normal accumulation of lutein from the diet proceeded into and through the mucosa to the serum to depot sites in the liver and integument, where lutein was acylated to its monoester, which was acylated to its diester. Further, aflatoxin inhibited, apparently independently, the accumulation of lutein by the mucosa, serum, liver, and integument. Pharmacokinetic analysis of the data indicated that both acylation steps in the integument were sensitive to aflatoxin, but the passage of lutein from serum into the integument was not affected.

Aflatoxins↗

PubMed1988

Metabolism of canthaxanthin, a red diketocarotenoid, by chickens.

Canthaxanthin, (4,4'-diketo-beta,beta-carotene), a red carotenoid used to extend the dominant wavelength of the yellow pigments in the skin and egg yolk of chickens, was fed (70 micrograms/g diet) to chicks depleted of normal tissue oxycarotenoids. High performance liquid chromatography analysis of tissues from such chicks revealed that a portion of canthaxanthin was reduced to 4-hydroxyechinenone (4-hydroxy-4'-keto-beta,beta-carotene) that in turn was reduced in part to isozeaxanthin (4,4'-dihydroxy-beta,beta-carotene). The alcohols thus formed were acylated in part to 4-hydroxyechinenone monoester and isozeaxanthin monoester and diester. Individual metabolites were identified by retention times, ratios A470/A430, and stopped-flow spectral analyses, which were identical in each case to authentic standards. Ratios of canthaxanthin to metabolites varied with the tissue, but in general metabolites were concentrated in the integument.

Animals↗

PubMed1988

Depletion of oxycarotenoid pigments in chickens and the failure of aflatoxin to alter it.

Aflatoxin, a demonstrated cause of pale bird syndrome in chickens, was investigated for its effects on the depigmentation of chickens placed on a diet low in carotenoids. Chickens were pigmented by feeding for 3 wk a white corn-soy diet supplemented with 50 micrograms free lutein and 0 or 4 micrograms aflatoxin/g diet. Then birds were switched to the same diets unsupplemented with lutein. At 0, 1, 2, 3, 6, and 9 days after switching, jejunal contents and mucosa, serum, liver, and toe web of 4 groups of 10 birds were removed for analysis of their carotenoids by high performance liquid chromatography. In control birds the order of decrease in total lutein was jejunal contents greater than jejunal mucosa greater than serum greater than liver greater than toe web. Aflatoxin did not alter the depletion process, except for minor retardation of lutein depletion in the mucosa and liver. Pharmacokinetic analysis of the data indicated that lutein depletion in the integument was accomplished through three sequential reactions (lutein diester----lutein monoester----lutein----serum lutein) and that aflatoxin had no effect on the reactions. These results imply that aflatoxin induces pale bird syndrome by interfering with the accumulation of pigment by chickens rather than by enhancing the depletion of pigment.

Aflatoxins↗

PubMed1987

The impact of atrazine on lake periphyton communities, including carbon uptake dynamics using track autoradiography.

Chlorophyll a, freshweight biomass, ash-free dry weight, cell numbers, species richness, community carbon uptake and species-specific carbon uptake were used to monitor the impact of atrazine (2 chloro-4-ethylamino-6-isopropylamino-s-triazine) on an in situ, enclosed periphyton community. Atrazine concentrations ranging from 0.08 to 1.56 mg litre(-1) were used during the 2 years of study. In both 1982 and 1983, there was a shift from a chlorophyte- to a diatom-dominated community. In 1982 the cyanobacterium Cylindrospermum stagnale and the chlorophyte Tetraspora cylindrica developed isolated colonies in the 1.56 mg litre(-1) treatment, indicating resistance to atrazine at this concentration. After atrazine exposure, community productivity was reduced by 21% to 82% in the low to high exposures, respectively. After day 21 productivity returned to control levels. It was shown, using track autoradiography, that the productivities of the larger algae Mougeotia sp., Oedogonium sp., Tolypothrix limbata and Epithemia turgida were the most affected, with reductions of 74.3% to 93.1% that of the controls. All the biotic measures indicated reduced growth after herbicide exposure.

Journal Article↗

PubMed1987

Preparation of scirpentriol and triacetoxyscirpenol in good yield from cultures of Fusarium sambucinum NRRL 13495.

Crude extracts of filtrates of cultures of Fusarium sambucinum NRRL 13495 were acetylated or hydrolyzed. After chromatography on cartridge columns of silica gel and recrystallization three times from mixtures of ethyl acetate and hexane, 3,4,15-triacetoxyscirpenol (435 +/- 10 mg/liter of filtrate; mean +/- standard error [n = 3]) and the parent alcohol scirpentriol were isolated (261 +/- 29 mg/liter of filtrate; mean +/- standard error [n = 3]) in 68 and 53% yield for a 130- and 14-fold improvement, respectively, over prior reports.

Acetates↗

PubMed1987

Preparation of 4,15-diacetoxyscirpenol from cultures of Fusarium sambucinum NRRL 13495.

Filtrates of Fusarium sambucinum NRRL 13495 grown in a stagnant culture for 9 days contained up to 458 +/- 60 (mean +/- standard error; n = 3) mg of 4,15-diacetoxyscirpenol per liter depending on culture conditions. Extraction with ethyl acetate, chromatography on a column of silica gel, and crystallization from mixtures of ethyl acetate and hexane provided pure material in 96% yield.

Acetates↗

PubMed1987

Alterations in carotenoid metabolism during ochratoxicosis in young broiler chickens.

The mechanism by which ochratoxin impairs the ability of chickens to utilize dietary carotenoids for carcass pigmentation was investigated. Graded doses of pure ochratoxin A (0, .5, 1.0, 2.0, and 4.0 micrograms of toxin/g of feed) were incorporated into a white corn-soy diet supplemented with an efficiently used oxycarotenoid (110 micrograms free lutein/g) and fed to broiler chicks from day of hatch to 3 weeks of age. Concentrations of free lutein and its metabolites, lutein diester, lutein monoester, and oxolutein, in the jejunal contents, jejunal mucosa, serum, liver, and toe web from these birds were measured by high performance liquid chromatography. Based on the threshold level of ochratoxin required for an effect on the concentrations of carotenoids and on the severity of the effect, five separate loci for the action of ochratoxin on carotenoid metabolism were detected: dilution of carotenoids in intestinal contents, depressed uptake by intestinal mucosa, depressed transport in serum, altered accumulation in liver, and altered acylation steps in the integument.

Animals↗

PubMed1987

Enhanced production of pancreatic digestive enzymes during aflatoxicosis in egg-type chickens.

As aflatoxin causes malabsorption and its toxicity is enhanced by a low protein diet, digestive enzymes formed in the pancreas apparently are influenced by aflatoxin. This hypothesis was investigated in a 2 X 2 factorial experiment. Six groups of 10 egg-type chickens per treatment were analyzed for the absence and presence of aflatoxin (0 and 4 micrograms/g diet) and for normal (12.75%) and low (10.00%) protein in soy-dextrose diets. The specific activities of pancreatic chymotrypsin, amylase, and lipase, but not trypsin, were increased significantly (P less than .01) by aflatoxin. Lowering dietary protein had no effect by itself except to increase amylase activity. Low protein and aflatoxin interacted to lessen but not prevent the effect of aflatoxin on chymotrypsin and amylase. Calculation of total pancreatic activities revealed that aflatoxin increased trypsin, chymotrypsin, amylase, and lipase to 107, 169, 113, and 119%, respectively, of control values on the low protein diet, whereas values were 99, 175, 115, and 115%, respectively, on the normal protein diet. Neither aflatoxin nor low protein altered significantly (P less than .05) the lipid content of fecal material. Thus, aflatoxicosis in egg-type chickens is characterized by a surplus of some digestive enzymes and by normal fecal lipids in contrast to the specific deficiency of amylase and lipase and steatorrhea reported earlier in meat-type chickens. Whereas malabsorption caused by aflatoxin in broilers can be accounted for in part by impaired digestion, this mechanism apparently does not occur in egg-type chickens.

Animals↗

PubMed1987

Interaction of dietary protein level on dose response relationships during aflatoxicosis in young chickens.

It is well known that the effect of aflatoxin is enhanced by a low protein diet, but whether this is associated with a lower apparent minimum effective dose, increased slope of response curves, or both has not been investigated previously. Aflatoxin at 12 dosages ranging from 0 to 2.34 micrograms/g of feed was fed to eight groups of 10 young chickens per treatment consuming a 10.00 or 12.75% protein diet for 3 weeks. The body weights, liver weights relative to body weights, and total lipid content of the livers were determined. Mathematical models were fitted to the data and from the appropriate equations the dose-response curves were predicted as continuous functions of aflatoxin concentration. A quadratic polynomial fit body weight data on the 12.75% protein diet whereas a plateau-linear model fit body weight data on the 10.00% protein diet. This implies that in a low protein diet aflatoxin affects only one of the factors controlling growth. Plateau-linear models fit liver relative weight and liver lipid content data on both 10.00 and 12.75% diets. For both variables the lower protein diet decreased the apparent minimum effective dose and increased the positive slope of the linear response. The apparent minimum effective doses (micrograms of aflatoxin per gram of feed) in this experimental system were calculated from the modeling approach to be 1.21 and 2.00 for body weight, 1.08 and 1.65 for liver lipids, and 1.45 and 2.34 for liver relative weight in 10.00 and 12.75% protein diets, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMed1987

Altered metabolism of carotenoids during aflatoxicosis in young chickens.

Young chickens were fed from hatching until 3 weeks of age with a white corn-soy diet (containing 1.36 micrograms total carotenoids per gram of diet) amended with a commercial preparation of lutein, a dihydroxycarotenoid, to supply 25 micrograms free lutein per gram diet. The diet which also contained 0, 1, 2, 4, or 8 micrograms aflatoxin per gram of diet was fed to four groups of ten chickens per aflatoxin treatment until they were 3 weeks old. Aflatoxin had no effect on the partial acylation of free lutein to lutein monoester that occurs in the jejunal contents of normal birds but it decreased significantly (P less than .05) the conversion of free lutein to lutein diester. Aflatoxin reduced up to 35% the lutein (94% free alcohol) content of the jejunal mucosa and the serum lutein (99% free alcohol) was reduced by up to 70%. Aflatoxin caused a slight (25%) decrease in the free lutein content of liver while increasing the monoester content 3.5-fold and the diester content 10-fold. This sequestering of lutein in the liver in esterified forms poorly transported to the integument presumably contributes to the poor pigmentation during aflatoxicosis. The forms of lutein in the toe web were diester (66%0, free alcohol (26%), and monoester (8%) and their sensitivity to aflatoxin followed the same order. These data offer clear, unequivocal proof that aflatoxin can cause poor pigmentation in birds, presumably by interfering with the absorption, transport, and deposition of carotenoids.

Aflatoxins↗

PubMed1987

Effect of dietary fat level on dose response relationships during aflatoxicosis in young chickens.

The effect of aflatoxin in poultry is greater on birds fed a low fat diet, but it is not known whether this effect is associated with a lower apparent minimum effective dose (MED), altered slope of the response curve, or both. Aflatoxin at 16 dosages ranging from 0 to 3.797 micrograms/g of feed was fed to six groups of 15 young chickens per treatment ingesting a 2 or 4% fat diet for 3 wk. The weights of the body, liver, bursa of Fabricius, and spleen and the total lipid content of the liver were measured. Mathematical models were fitted to the data and dose-response curves were predicted as continuous functions of aflatoxin concentration. Quadratic polynomials fit body weight and spleen weight whereas plateau-linear models fit liver weight and liver lipid content in both 2 and 4% fat diets. The weight of the bursa of Fabricius was fit equally well by quadratic and linear plateau models. Dietary fat had negligible effects on the apparent MED (micrograms of aflatoxin per gram of feed) for body, liver and spleen weights, which were calculated from the modeling approach to be 1.37 and 1.41, 1.68 and 1.69, and 1.49 and 1.46 on 2 and 4% fat diets, respectively. The apparent MED for liver lipid content was appreciably lower for birds fed the 2% fat diet than those fed the 4% fat diet (.88 and 1.62, respectively). Similarly, the apparent MED for the bursa was 1.48 and 1.74 for birds fed the 2 and 4% fat diets, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMed1987

Relationship of feed surface area to fungal activity in poultry feeds.

Weekly composite feed samples were collected from three farms that had manually filled tube type feeders and three that had automatic pan type feeders. Feed from pan type feeders had four-fold higher fungal activity than did feed from tube type feeders. The data suggest that the ratio of surface area to feed weight was associated with this difference.

Animal Feed↗

PubMed1987

Increased sensitivity to staphylococcal beta hemolysins of erythrocytes from chickens during aflatoxicosis.

The size of the zones of beta-hemolysis surrounding staphylococcal colonies on blood agar was found to be related to the level of dietary aflatoxin consumed by the chickens donating the blood. Zone sizes on blood from chickens fed the highest level of aflatoxin (10 micrograms/g of diet) were about six-fold larger than those on blood from control birds. The percentage of staphylococcal isolates displaying beta-hemolysis was increased from about 15% in normal blood to about 90% in blood from chickens fed aflatoxin (10 micrograms/g) whereas the time required for detection of beta-hemolysis was decreased by about one-half. The hemolytic activity of purified staphylococcal beta-hemolysin against suspensions of washed erythrocytes increased as the level of aflatoxin consumed by the donor chickens increased. These data imply a new mechanism for enhanced susceptibility of animals to infectious agents during mycotoxicoses whereby the animal is made more sensitive to the virulence factors of pathogens.

Animals↗