Search PubMed⌕ Search

Biomedical subjects

C B Ammerman

Publications and source records attributed to C B Ammerman.

At least 37 records · Page 2Linked to original sources
PubMed1988

Estimation of the relative biological availability of inorganic selenium sources for ruminants using tissue uptake of selenium.

An experiment was conducted to estimate the relative bioavailability of inorganic Se sources based on tissue Se deposition following supplementation at high dietary levels. Twenty-eight crossbred wethers averaging 50 kg initial weight were assigned randomly to seven treatments that were fed for 10 d. The basal diet contained .18 mg/kg Se (DM basis). Dietary Se was added at 0, 3, 6 or 9 mg/kg as reagent grade sodium selenite (Na2SeO3) and 6 mg/kg from either calcium selenite (CaSeO3), Na2SeO3 + fumed amorphous carrier or sodium selenate (Na2SeO4). There were four sheep per treatment group, housed in individual, raised pens with slatted floors. Daily feed intake was restricted to 1,200 g and tap water was available ad libitum. The basal diet was fed for a 10-d adjustment period, then sheep were fed experimental diets for 10 d. At the termination of the experiment, blood samples were taken; sheep were stunned and killed, and livers and kidneys were removed and frozen for Se analysis. There was a linear (P less than .001) uptake of Se in liver, kidney and serum. The CaSeO3 and Na2SeO4 sources resulted in greater (P less than .05) Se concentrations in liver and kidney than did Na2SeO3, but these differences were not significant when the analyzed dietary Se concentrations were used as a covariate in the statistical model. Based on linear and multiple linear regression slopes and average increases in serum, liver and kidney Se concentrations, estimated relative bioavailability values corrected for analyzed dietary concentration, were 100, 101, 90 and 133 for Na2SeO3, CaSeO3, Na2SeO3 + carrier and Na2SeO4, respectively.

Animals↗
PubMed1988

Estimation of the relative bioavailability of inorganic selenium sources for poultry. 1. Effect of time and high dietary selenium on tissue selenium uptake.

An experiment was conducted with male broiler-type chicks to study the effect of time and high dietary Se concentration on tissue Se uptake. A basal corn-soybean meal diet (.2 mg/kg Se, DM basis) was supplemented with 0, 3, 6, or 9 mg/kg Se (as-fed basis) as Na2SeO3 and fed ad libitum for 1, 2, or 3 wk. No toxic effect of Se was observed as expressed by mortality; however, there was a reduction in daily feed intake (P less than .01) at 6 and 9 mg/kg added Se, particularly at 3 wk, suggesting developing toxicosis. Selenium concentration in all tissues studied increased linearly (P less than .001) as dietary Se increased, especially in kidney and liver. Coefficients of determination and lambda criterion values were greatest in plasma, followed by liver, muscle, and kidney. It appeared that 1 wk would be an adequate length of time for further Se bioavailability studies based on tissue Se uptake from diets containing 3 to 9 mg/kg added Se.

Animals↗
PubMed1988

Estimation of the relative bioavailability of inorganic selenium sources for poultry. 2. Tissue uptake of selenium from high dietary selenium concentrations.

An experiment was conducted with 192 day-old male Cobb chicks to study tissue uptake of Se as an estimate of the bioavailability of supplemental inorganic Se sources fed at high dietary concentrations. A basal corn-soybean meal diet (.18 mg Se/kg diet, dry matter basis) was supplemented with 0, 3, 6, or 9 mg Se/kg diet (as-fed basis) as either reagent grade Na2SeO3, CaSeO3, or Na2SeO3 plus fumed amorphous carrier or 6 mg Se/kg diet as either Na2SeO4 or Se metal, and fed for 1 wk. No toxic effects were noted as expressed by mortality; however, there was a reduction (P less than .01) in feed intake and daily gain when 9 mg Se/kg diet was fed, suggesting onset of toxicosis. Selenium concentration in liver, kidney, muscle, and plasma increased linearly (P less than .01) as dietary Se increased from all sources. Selenium metal produced lower (P less than .01) Se concentrations in kidney and muscle than other supplemental sources. Multiple regression slope ratios were used to estimate relative bioavailability values of 100, 103, 99, 112, and 83 for Na2SeO3, CaSeO3, Na2SeO3 + carrier, Na2SeO4, and Se metal, respectively. When these ratios were corrected for the analyzed dietary Se concentration, relative values were 100, 96, 94, 109, and 81 for the above sources, respectively.

Animals↗
PubMed1987

Effect of antibiotics on tissue trace mineral concentration and intestinal tract weight of broiler chicks.

Two experiments were conducted with broiler-type chicks to determine the effect of antibiotics on intestinal weight and kidney, bone, and liver trace mineral concentrations. All antibiotics were in diets at the manufacturers' recommendations. Feed intake of experimental diets (antibiotics or non-treated control) was restricted to 90% of that of an additional group fed the control diet ad libitum. Feed intake, weight gain, and feed efficiency were not affected (P greater than .10) by dietary treatments. Virginiamycin decreased intestinal weight an average of 19% as compared with 14% for bambermycins and oxytetracycline, 6% for Zn bacitracin, and 18% for lincomycin. Except for Zn bacitracin, all antibiotics produced intestinal weights which were lower (P less than .01) than those of controls. Only virginiamycin increased (P less than .01) kidney Mn concentration. Bone Mn concentration was greater (P less than .01) for virginiamycin than bambermycins or oxytetracycline in Experiment 2, and greater (P less than .05) for lincomycin than virginiamycin or Zn bacitracin in Experiment 2. Feeding Zn bacitracin increased (P less than .01) bone Zn concentration whereas feeding virginiamycin caused a decline (P less than .05) in bone Zn concentration in Experiment 1. There were no differences in Cu, Zn, or Fe concentrations in liver or kidney.

Animals↗
PubMed1987

Interaction of dietary nutrient concentration and supplemental copper on chick performance and tissue copper concentrations.

An experiment was conducted with 576 female Cobb feather-sexed chicks to study the influence of methionine (MET) and selected nutrient (SN) supplementation on the performance of chicks fed high Cu levels. Day-old chicks were allotted randomly to pens for the 22-day experiment. A 3 X 2 X 2 factorial arrangement of treatments was used which included Cu at 0, 400, and 800 mg/kg, MET at 0 and .4%, and SN at 0 and 20%. A significant (P less than .001) Cu X MET X SN interaction was found for gain. Supplemental MET reversed the growth depression observed in birds fed 400 but not 800 mg/kg Cu. Additions of 400 and 800 mg/kg Cu to the basal diet depressed (P less than .001) feed consumption by 8.6 and 19.4%, respectively. Hepatic Cu concentrations increased linearly (P less than .001) with increasing dietary Cu and were not influenced (P greater than .10) by supplemental MET or SN. Liver weights increased linearly (P less than .001) with increasing dietary Cu and were higher (P less than .05) for chicks on diets supplemented with SN, but lower (P less than .05) for those with diets supplemented with MET. The interaction of MET X SN was significant (P less than .001) for serum Cu; chicks supplemented with SN in conjunction with MET had the lowest (P less than .05) serum Cu concentrations. Serum glutamic-oxaloacetic transaminase (SGOT) activity was not influenced (P greater than .10) by dietary Cu, but SN supplementation resulted in a 10% elevation (P less than .001) in SGOT activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Kinetic model of whole-body vanadium metabolism: studies in sheep.

A compartmental model for vanadium metabolism in sheep has been proposed. The model is consistent with data obtained from sheep fed a control diet (2.6 ppm vanadium) containing 0 or 200 ppm supplemental vanadium. Sheep were administered 48V dioxovanadium either orally or intravenously. Blood, feces, and urine radioactivity were monitored for 6 days postdosing. Several new insights regarding vanadium metabolism are suggested and tested against the data using the model. Some of these include significant absorption of 48V occurs from the upper gastrointestinal tract; an in vivo process is necessary in order for 48V dioxovanadium to be converted into a more biologically reactive species; at steady state the upper and lower gastrointestinal tracts contain at least 10- and 100-fold more mass of vanadium, respectively, than does blood. No statistically significant differences in transport rate constants were found between animals receiving 0 and 200 ppm supplemental dietary vanadium. The availability of a model will enable the refinement of future studies regarding vanadium metabolism in the ruminant.

Administration, Oral↗
PubMed1986

Vanadium metabolism in sheep. III. Influence of dietary vanadium on kinetics of 48V administered orally or intravenously and comparison of compartmental and graphical models.

Radiotracer techniques were used to investigate the influence of dietary stable V on the excretion, distribution and blood clearance kinetics of 48V in 14 rams averaging 58 kg body weight. Rams were fed a basal diet with added levels of 0, 50 or 200 mg/kg V as NH4 VO3 for 25 wk before either oral or iv administration of the isotope. A three-compartment model was determined by graphical logarithmic analysis of blood disappearance data from iv-dosed rams and compared with a simultaneous multicompartment model, which made it possible to ascribe physiological processes to the components of the graphical model. The principal route of excretion of 48V administered iv was via urine, whereas the isotope given orally was excreted almost entirely by way of feces, resulting in low tissue and urinary 48V levels. Increasing dietary V increased (P less than .05) the percentage of dose excreted in urine regardless of dosing route, but dietary V had no effect on 48V excreted in feces. Stable dietary V had no effect on blood clearance rates of orally or iv-dosed rams. Dietary V addition decreased 48V concentration in kidney (P less than .01), liver, spleen, testes and muscle (P less than .05) of iv-dosed rams, but had no effect in rams dosed orally. Kidney, bone, liver and spleen retained the highest levels of 48V activity 144 h after dosing. Dietary V appeared to have a minimal effect on V kinetics in rams.

Administration, Oral↗
PubMed1986

Influence of virginiamycin and dietary manganese on performance, manganese utilization, and intestinal tract weight of broilers.

An experiment was conducted with day-old Cobb feather-sexed chicks for 21 days to study the effect of virginiamycin and dietary manganese on tissue uptake of manganese and intestinal tract weight. The 2 X 2 factorial arrangement of dietary treatments included 0 or 12 ppm virginiamycin and 0 or 1000 ppm added manganese as MnSO4 X H2O. Ad libitum intake was determined with four pens of five birds fed the basal corn-soybean meal diet. To eliminate the possibility that tissue manganese concentration of virginiamycin-fed birds could be attributed to increased dietary manganese intake, chicks fed experimental diets were restricted to 90% of the previous day's intake of ad libitum-fed birds. Feed intake, average daily gain, and feed efficiency were not affected by treatments. Virginiamycin decreased (P less than .001) relative intestinal tract weight from 3.34 to 2.68 g/100 g body weight. Kidney and bone manganese increased (P less than .05) when virginiamycin was fed (14.0 vs. 15.4 ppm dry basis and 21.8 vs. 24.6 ppm ash basis, respectively), indicating that virginiamycin increased absorption of manganese.

Animals↗
PubMed1986

Bioavailability of manganese sulfate and manganese monoxide in chicks as measured by tissue uptake of manganese from conventional dietary levels.

The biological availability of reagent grade manganese sulfate and manganese monoxide was determined in broiler chicks fed conventional dietary Mn levels. A basal corn-soybean meal diet (35 ppm Mn) was supplemented with 40, 80, or 120 ppm Mn from the two sources and fed ad libitum for 21 days. There were no differences in average daily feed intake, daily gain, or feed conversion among treatments. There was a linear (P less than .001) increase in bone, kidney, and liver Mn as dietary Mn increased. Manganese monoxide averaged 66% of the availability of manganese sulfate as determined by a combination of linear regression, multiple linear regression and tissue Mn increase. Bioavailability was similar to that obtained when sources were fed at high dietary levels in a previous study.

Animals↗
PubMed1985

Effects of high dietary manganese as manganese oxide or manganese carbonate in sheep.

Twenty-four crossbred Florida native wether lambs, 28 kg initially, were assigned randomly to a basal diet (31 ppm Mn dry matter basis) supplemented with either 0, 500, 1,000, 2,000 or 4,000 ppm Mn from feed grade MnO or 2,000, 4,000 or 8,000 ppm Mn from reagent grade MnCO3. There were three sheep/treatment, with ad libitum access to feed and tap water. After 84 d, all animals were slaughtered and tissues removed for analysis. Dietary Mn at the highest levels from either source reduced (P less than .05) average daily feed intake and average daily gain. Hemoglobin and hematocrit were not affected by dietary Mn. Manganese concentration in kidney, spleen, heart, skeletal muscle, bone, serum (P less than .01) and liver (P less than .05) increased as dietary Mn increased. Kidney P was reduced (P less than .05) as dietary Mn increased; however, no other tissue minerals were affected. At comparable levels of supplementation, sheep fed feed-grade MnO exhibited numerically greater tissue Mn concentration than did those fed reagent-grade MnCO3 and regression analysis indicated higher rates of tissue uptake in MnO-supplemented sheep. Reduced feed intake and gain and apparent Mn homeostatic failure in liver were the only observed effects that may have been related to Mn toxicosis.

Animals↗
PubMed1985

Effect of quantity and route of administration of manganese monoxide on feed intake and serum manganese in ruminants.

The experiment investigated effects of high quantities of manganese and route of administration (diet versus capsule-dosed) on feed intake and blood characteristics in sheep. Twenty-four Florida native or Florida native by St. Croix crossbred wethers, 47 kg initially, were assigned randomly to eight treatments including basal diet supplemented with 0, 3000, 6000, or 9000 ppm manganese as a reagent grade manganese monoxide or basal diet plus gelatin capsules containing the equivalent of 0, 3000, 6000, or 9000 ppm manganese based on intake of the previous day. Three sheep per treatment were provided feed and tap water for ad libitum intake. Sheep were fed basal diet for 7 days followed by a 21-day experimental period, then placed back on the basal diet for 7 days. Average daily feed intake was reduced by increasing supplemental manganese, regardless of route. Animals dosed by capsule consumed less feed than those administered manganese in the diet. Serum manganese increased as manganese supplementation increased, but route of administration had no effect.

Administration, Oral↗
PubMed1985

Effect of dietary manganese and age on tissue trace mineral composition of broiler-type chicks as a bioassay of manganese sources.

An experiment was conducted with 144 Cobb broiler-type chicks in a 4 X 3 factorial arrangement of treatments to investigate the effects of dietary manganese (Mn) and age on trace mineral composition in tissues. Day-old chicks were fed a basal corn-soybean meal diet (112 ppm Mn) supplemented with 0, 1000, 2000, or 3000 ppm Mn as manganese sulfate monohydrate (MnSO4 X H2O) for 1, 2, or 3 weeks. There were two pen replications per treatment combination and six chicks per pen. Liver, kidney, pancreas, skeletal muscle, and bone were excised from 4 chicks per replication. Plasma was pooled from the remaining 2 chicks, and all samples were frozen for subsequent mineral analysis. There was a reduction in average daily feed intake (P less than .05) at the 3000 ppm dietary level accompanied by a nonsignificant decrease in average daily gain and an increase in feed per unit gain. Tissue Mn increased (P less than .001) for all tissues as dietary Mn increased. Tissue Mn concentration was reduced with age in kidney, pancreas, muscle (P less than .001), and plasma (P less than .05). Manganese in bone was lowest (P less than .01) at 1 week of age. Of those ages tested, the optimum for bioassay based on lambda criterion values appeared to be 3 weeks. The highest lambda criterion values were obtained at 3 weeks of age in kidney followed by bone at 2 weeks. High dietary Mn increased copper (Cu) concentration in liver (P less than .05) and plasma (P less than .05) and reduced iron (Fe) in pancreas (P less than .001). Liver Fe was lower (P less than .001) at 3000 ppm than at 1000 or 2000 ppm dietary Mn. Plasma zinc (Zn) was higher (P less than .05) at all supplemental Mn levels than the unsupplemented control, and kidney Zn increased (P less than .001) at 3000 ppm dietary Mn.

Age Factors↗
PubMed1984

Biological availability of manganese sources and effects of high dietary manganese on tissue mineral composition of broiler-type chicks.

An experiment was conducted with male broiler-type chicks to study tissue uptake of Mn as a measure of biological availability of Mn sources. A basal corn-soybean meal diet (116 ppm Mn) was supplemented with 0, 1000, 2000, or 4000 ppm Mn as either reagent grade sulfate, carbonate, or monoxide and fed ad libitum for 26 days. No toxic effects were noted as expressed by feed intake, weight gain, feed conversion, hematocrit, hemoglobin, or mortality. Analysis of Mn in tissues revealed a highly linear relationship between liver or bone Mn concentration and dietary Mn for all three sources. Manganese concentration in all tissues increased (P less than .01) as dietary Mn increased. Liver and bone Mn accumulation appeared to be excellent indicators of relative biological availability. On the basis of tissue uptake and solubility tests, MnSO4 X H2O was the most available, followed by MnO and MnCO3, respectively. There were no effects of Mn source or level on concentration of Ca, P, Mg, Cu, Zn, or Fe in tissues studied.

Animals↗
PubMed1983

Influence of dietary lead and calcium on tissue lead accumulation and depletion, lead metabolism and tissue mineral composition in sheep.

Two experiments were conducted to study the metabolism and tissue accumulation and depletion of dietary Pb in sheep. In Exp. 1, a feeding trial, 33 wethers, 56 kg initially, were assigned randomly to two dietary treatments: .25% Ca plus 1,000 ppm Pb or .50% Ca plus 1,000 ppm Pb. Supplemental Ca and Pb were supplied as reagent grade calcium carbonate or reagent grade lead acetate. The experiment was divided into two phases of 75 and 180 d; during the first phase, diets contained 1,000 ppm supplemental Pb and during the second phase, diets contained 3 ppm Pb. Calcium level remained constant within treatments throughout both phases. Sheep were slaughtered at various intervals during both phases and tissue samples taken. Lead increased in all tissues during the accumulation period and decreased during the depletion period; however, kidney was the only tissue in which Pb concentration declined to control values by 180 d. Dietary Ca reduced (P less than .05) the concentration of Pb deposited in liver, but not in other tissues. Interactions of dietary Ca and Pb on tissue concentration of various minerals occurred. In Exp. 2, a balance trial, 27 wethers, 53 kg initially, were allotted randomly to four treatments in a 2 X 2 factorial arrangement. Diets contained either 0 or 1,000 ppm supplemental Pb as reagent grade lead acetate and .25 or .50% total Ca with supplemental Ca from calcium carbonate. Increasing dietary Pb increased (P less than .05) percentage of Pb retained and increased (P less than .01) whole blood Pb concentration (1.0 vs 1.42 micrograms/ml).

Animals↗
PubMed1982

Vanadium metabolism in sheep. I. Comparative and acute toxicity of vanadium compounds in sheep.

Twelve Florida native wethers were given ammonium metavandate, calcium orthovanadate and calcium pyrovanadate by capsule in a study to examine the toxicity of the compounds. The initial daily dosage of 100 mg elemental vanadium was increased by 50 mg at 2-d intervals for an assessment not only of the toxic effects, but also to determined the amount that caused a decline in feed intake to 25% of that of control animals. The initial decline in feed intake was observed at 400 to 500 mg vanadium/d (9.6 to 12 mg/kg body weight, 310 to 350 ppm); a rapid decline in feed intake was accompanied by diarrhea. One sheep fed 550 mg vanadium as calcium orthovanadate died 3 d after dosing. One animal on each of the other three treatments was killed and necropsied for immediate comparison. Extensive mucosal hemorrhage of the small intestine and diffuse or petechial subcapsular hemorrhages of the kidneys were observed for sheep fed all compounds. The three vanadium compounds appeared to be similar in toxicity, as determined by abrupt declines in feed intake and pathological changes of the intestine and kidney. For a determination of acute toxicosis, three sheep were given 40 mg/kg body weight of vanadium as NH4VO3 in gelatin capsules and two sheep were included as controls. Two of the treated animals died within 80 h after administration and the other three were killed at 96 h. Vanadium content of kidney, liver, bone, spleen, lung and muscle was elevated by treatment.

Acute Disease↗
PubMed1982

Vanadium metabolism in sheep. II. Effect of dietary vanadium on performance, vanadium excretion and bone deposition in sheep.

Sixteen ram lambs were fed 0, 50 or 200 ppm supplemental vanadium daily as NH4VO3 for 90 d and coccygeal vertebrae were sampled at 0, 15, 30, 60 and 90 d after the imposition of dietary treatments. Vertebral vanadium content was elevated (P less than .05) after exposure to 200 ppm added vanadium in the diet of 15 d, but nonsignificant increases occurred thereafter. Increasing dietary vanadium increased bone ash vanadium concentration from .4 to 1.7 and 3.8 ppm in sheep fed 0, 50 and 200 ppm supplemental vanadium, respectively. In a balance study, urinary concentrations of the element also were related directly to dietary intake. A trend toward elevated urine volume with increased intake of vanadium was also observed.

Absorption↗