Biomedical subjects

P B Hamilton

Publications and source records attributed to P B Hamilton.

At least 19 recordsLinked to original sources

PubMed1992

The use of high-performance liquid chromatography for studying pigmentation.

The use of HPLC has established that chickens possess unexpected metabolic abilities to acylate, deacylate, reduce, and oxidize carotenoids. The use of HPLC permits more consistent and more economic pigmentation of carcasses and of egg yolks. Hopefully, the use of HPLC will raise pigmentation from an art to a science. Apparently, HPLC will be an essential tool in terms of future efforts to understand and master the process of poultry pigmentation.

Animal Feed↗

PubMed1992

Abnormal feathering of chicks caused by scirpenol mycotoxins differing in degree of acetylation.

Graded levels of the Fusarium mycotoxins, scirpentriol (STO), 15-monoacetoxyscirpenol (15-MAS), 4,15-diacetoxyscirpenol (4,15-DAS), and 3,4,15-triacetoxyscirpenol (TAS), were fed to chicks until 3 wk of age. The primary wing feathers, which were scored visually on a scale of 1 to 5 using a newly created scoring scheme, were altered in a dose-related fashion by 15-MAS [minimum effective dose (MED) = .5 microgram/g diet], 4,15-DAS (MED = 2 micrograms/g), and STO (MED = 4 micrograms/g) but not by TAS (MED greater than 8 micrograms/g). The minimum growth inhibitory doses were 2 micrograms/g for STO, 15-MAS, and 4,15-DAS and 8 micrograms/g for TAS. The main alteration of the feathers was a frayed and missing web on the medial side of the distal half of the feather. The shafts of the feathers tended to have an accentuated medial curve. These results imply that the feather alterations associated with corn and feed infested with Fusarium spp. might be caused by trichothecene mycotoxins such as the scirpenols.

Acetylation↗

PubMed1991

Altered metabolism of carotenoids during pale-bird syndrome in chickens infected with Eimeria acervulina.

The progression of changes in carotenoid metabolism during pale-bird syndrome caused by a coccidial infection was investigated. Male broiler chickens 15 days of age on a yellow corn and soybean meal-based diet were infected with Eimeria acervulina oocysts and their serum, liver, and toe webs were sampled at 0, 4, 6, and 10 days postinfection for HPLC analysis of carotenoids. At 4 days postinfection a drastic reduction (71%) in serum lutein, the main body carotenoid, and smaller reductions in liver (58%) and toe webs (38%) occurred. Derivative forms of lutein, mainly esters, continued to be lost from tissues for 10 days postinfection. These carotenoids were apparently lost via the intestinal tract because birds placed on a white corn and soybean meal-based diet at time of infection had lutein in their jejunal contents even at 7 days postinfection. The loss of carotenoids from the body was accompanied by a decreasing ability to absorb canthaxanthin, a red carotenoid, from the intestinal contents. The absorption of canthaxanthin measured at 0, 3, 4, 5, 6, and 7 days reached its low point of 1% of preinfection ability on Day 5 before a slow recovery commenced. Thus, the pale-bird syndrome caused by E. acervulina appeared to be the result of a loss of previously absorbed carotenoids coupled with drastic malabsorption of dietary carotenoids.

Animals↗

PubMed1991

Mouth lesions in broiler chickens caused by scirpenol mycotoxins.

Dietary scirpentriol (STO), triacetoxyscirpenol (TAS), monoacetoxyscirpenol (MAS), and diacetoxyscirpenol (DAS), mycotoxins produced by Fusarium species, were compared for their ability to cause mouth lesions when graded dietary levels (0, 1, 2, 4, and 8 micrograms STO or TAS/g; 0, .5, 1, 2, and 4 micrograms MAS or DAS/g) were fed to male broiler chickens for 21 days after hatching. The mouth lesions provoked by each scirpenol were dose-related. The minimum effective doses (MED) were 4, 2, 1, and .5 micrograms/g for TAS, STO, DAS, and MAS, respectively, whether the number of affected birds or the number of affected mouth parts (angles, upper beak, lower beak, and tongue) was the measured response. Lesion sites in the mouth varied with the toxin. The rank orders from greatest to least affected sites were angles, upper beak, lower beak, and tongue for TAS and STO, upper beak, lower beak, angles, and tongue for MAS, and upper beak, lower beak, tongue, and angles for DAS. Mouth lesions were clearly visible with each toxin after feeding for 1 wk and the numbers of affected mouth parts almost tripled after 2 wk exposure. During Week 3 of exposure, only the increase caused by MAS was significant (P less than .05). The MED for growth inhibition were 2, 2, 2, and 8 micrograms/g for STO, MAS, DAS, and TAS, respectively. Thus, mouth lesions were of equal or greater sensitivity than growth inhibition as an indicator of scirpenol toxicity. It would appear that the discovery of mouth lesions in birds justifies a mold and mycotoxin control program.

Acetylation↗

PubMed1991

Scirpentriol toxicity in young broiler chickens.

Scirpentriol (STO) (3 alpha,4 beta,15-trihydroxy-12,13-epoxytrichothec-9- ene), the parent alcohol of the family of acetylated scirpenol mycotoxins produced by several Fusarium species, has been implicated in mixed toxicoses of animals, but there is not a general description of its toxicity in chickens. Dietary STO (0, 2, 4, 8, 16, and 32 micrograms/g feed) was fed to four groups of 10 male day-old broiler chickens for 3 wk. The minimum effective dose (MED) for reducing growth rate significantly (P less than .05) was 4 micrograms/g. The same MED was found for increased serum alkaline phosphatase and relative weight of the gizzard. Unlike literature reports for two other trichothecene mycotoxins, T-2 toxin and diacetoxyscirpenol (DAS), STO impaired feed conversion efficiency but did not alter spleen or pancreas size. The MED of STO for decreases in serum lactic dehydrogenase and aspartate aminotransferase was 8 micrograms/g, but the MED for decreased serum albumin and total proteins and regression of the bursa of Fabricius was 16 micrograms/g. Serum sodium, potassium, and calcium were not altered at the highest dose, 32 micrograms/g, but serum phosphate, uric acid, and cholesterol were decreased by 32 micrograms/g. Serum chloride was increased slightly but significantly (P less than .05) at 16 and 32 micrograms/g. Based on these results, STO toxicosis of chickens can be differentiated from those of T-2 toxin and DAS and its toxicity appears sufficient to warrant further attention.

Alkaline Phosphatase↗

PubMed1991

High dietary fat increases toxicity of diacetoxyscirpenol in chickens.

The influence of high dietary fat on the toxicity of diacetoxyscirpenol (DAS) was investigated in a 2 x 5 factorial arrangement of treatments (6 and 12% fat, and 0, 1, 2, 4, and 8 micrograms DAS/g diet). The 3-wk body weight was decreased (P less than .0001) by DAS, but fat had no significant (P less than .05) effect. There was a highly significant (P less than .0059) interaction manifested at the higher levels of DAS by a greater decrease in body weight in the high-fat diet than in the low-fat diet. Neither feed conversion nor percentage of fat in fecal material were affected significantly (P less than .05) by DAS. These data were consistent with the high-fat diet promoting lipid micellar absorption of DAS and with DAS, once absorbed, inhibiting protein synthesis at the ribosomal level, a well established mechanism of action for trichothecene toxins such as DAS.

Animals↗

PubMed1991

Measurement of malabsorption of carotenoids in chickens with pale-bird syndrome.

Because pale-bird syndrome (PBS), defined as the failure of birds to realize the color potential of their diet, has been demonstrated to be caused by malabsorption or by hyperexcretion of carotenoids, a method for measuring malabsorption of carotenoids would be useful. The absorption of dietary canthaxanthin, a red diketocarotenoid, into serum during aflatoxicosis was measured in an experiment with a 2 x 9 factorial arrangement of treatments (0 and 5 micrograms of aflatoxin/g of diet; serum collected at 0, 2, 4, 6, 8, 10, 12, 14, and 24 h after a standard meal fed to four groups of 10 3-wk-old birds). Serum canthaxanthin levels determined by HPLC attained plateau values between 8 and 14 h after the meal. The absorption of canthaxanthin was depressed significantly (P less than .05) in birds with aflatoxicosis from 4 to 24 h after feeding the standard meal. Four field flocks diagnosed as having PBS were tested for malabsorption by intubating 10 birds with a standard amount of canthaxanthin and measuring serum canthaxanthin 12 h later. One flock had about 85% normally pigmented birds and 15% extremely pale birds, the second flock had a coccidiosis history, the third had a Newcastle disease history, and the fourth had a history of both coccidiosis and Newcastle disease. The flocks were 5- to 6-wk-old, received feed of the same manufacture, and their disease outbreaks had occurred 2 wk earlier.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMed1990

Effect of dietary lipid on lutein metabolism during aflatoxicosis in young broiler chickens.

The effect of concentration of dietary fat on pigmentation of broiler chickens was investigated in diets containing: 1) 0 or 1.4 micrograms of aflatoxin and 35 micrograms of lutein/kcal of diet; and 2) different levels of dietary fat (0, 2, 4, 6, 8, or 10% cottonseed oil). Serum lutein and its metabolite, 3'-oxolutein, increased with increasing dietary fat until it reached a plateau at 6% fat. Aflatoxin significantly (P less than .05) lowered serum lutein and 3'-oxolutein at all levels of fat. Dietary fat and aflatoxin interacted significantly (P less than .05), with the effect of aflatoxin being greater at the low levels of fat than at the high fat levels. In the toe webs of the birds, the concentrations of lutein and its metabolites, lutein monoester, lutein diester, and 3'-oxolutein responded similarly to aflatoxin and to dietary fat, except that increasing the amount of dietary fat did not spare the effect of aflatoxin on 3'-oxolutein. The effect of chain length and the saturation of fatty acids on the absorption of lutein during aflatoxicosis was investigated in a factorial design for aflatoxin (0 and 4 micrograms/g of diet) and seven fatty acids at 5% of the diet. In control birds, lutein absorption was promoted by lauric = oleic greater than capric = linoleic greater than myristic greater than palmitic = stearic acids. Aflatoxin significantly (P less than .05) depressed the absorption of lutein regardless of the fatty acid present.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

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

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

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↗