Effects of a silica-based feed supplement on performance, health, and litter quality of growing turkeys.

Poor litter quality is a potential challenge to footpad health as well as the primary cause of ammonia volatilization. High ambient ammonia concentration is one of the most significant factors negatively affecting poultry production today. Some minerals have been reported to reduce ammonia release from poultry litter. Silicon dioxide, a highly pure and natural mineral, shows promise in decreasing ammonia volatilization and improving litter quality. The objective of the current study was to investigate the effects of feed-borne silicon dioxide on litter quality and how this impacts bird performance, general health and footpad health throughout a 12-wk posthatching turkey study. Supplementing the diet with silicon dioxide was found to significantly improve turkey BW gain and the efficiency of feed conversion. The severity of footpad dermatitis was monitored throughout the experimental period but no significant effect of diet was seen. The feeding of silicon dioxide reduced litter pH which decreased the conversion of NH4⁺ to NH3 thereby reducing nitrogen losses from litter. It was concluded that, under our study conditions, the feeding of 0.02% silicon dioxide offers potential economic benefits to turkey producers.

Effects of feeding grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of laying hens, turkey poults, and broiler breeder hens.

Three experiments were conducted to compare the effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of laying hens, turkey poults, and broiler breeder hens. In Experiment 1, thirty-six 45-wk-old laying hens were fed diets including the following for 4 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent (GMA). Concentrations of brain neurotransmitters and metabolites were analyzed in pons, hypothalamus, and cortex by HPLC with electrochemical detection. Neurotransmitters and the metabolites measured included dopamine, 3,4-dihydroxylphenyacetic acid, homovanillic acid, serotonin [5-hydroxytryptamine (5-HT)], 5-hydroxyindolacetic acid, epinephrine, and norepinephrine. The feeding of contaminated grains significantly increased concentrations of 5-HT and decreased the 5-hydroxyindolacetic acid:5-HT in the pons region in the brain stem. Dietary supplementation with GMA prevented these effects. There was no effect of diet on concentrations of other neurotransmitters or metabolites in the pons, hypothalamus, or cortex. In Experiment 2, thirty-six 1-d-old turkey poults were fed diets including the following for 4 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA. Hypothalamic, pons, and cortex neurotransmitter concentrations were not affected by diet. In Experiment 3, forty-two 26-wk-old broiler breeder hens were fed diets including the following for 15 wk: 1) control, 2) contaminated grains, and 3) contaminated grains + 0.2% GMA. There was no effect of diet on neurotransmitter concentrations in the pons, hypothalamus, or cortex. It was concluded that differences in intraspecies effects of these mycotoxins on brain neurotransmitter concentrations might explain the intraspecies differences in the severity of Fusarium mycotoxin-induced reductions in feed intake.

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on feed intake, metabolism, and indices of athletic performance of exercised horses.

An experiment was conducted to determine the effect of feeding blends of grains naturally contaminated with Fusarium mycotoxins to mature, exercised horses, and to test the efficacy of a polymeric glucomannan mycotoxin adsorbent (GM polymer) in preventing Fusarium mycotoxicoses. Six mature, mixed-breed mares with an average BW of 530 kg were assigned to one of three dietary treatments for 21 d in a replicated 3 x 3 Latin square design. Feed consumed each day was a combination of up to 3.5 kg of concentrates and 5.0 kg of mixed timothy/alfalfa hay (as-fed basis). The concentrates fed included 1) manage; 2) blend of contaminated grains; and 3) contaminated grains + 0.2% GM polymer (MTB-100, Alltech Inc., Nicholasville, KY). Concentrates containing contaminated grains averaged 11.0 ppm deoxynivalenol, 0.7 ppm 15-acetyldeoxynivalenol, and 0.8 ppm zearalenone (as-fed basis). Feed intake and BW were monitored over a 21-d period. Horses were maintained on a fixed exercise schedule throughout the experiment. At the end of the experiment, each horse completed a time-to-fatigue treadmill step test. Variables measured during pretest, each step of the test, and 5 and 10 min posttest were as follows: 1) time-to-fatigue, 2) heart rate, 3) hematological variables, and 4) serum lactate concentration. Each step consisted of 2 min of fast trot with a 2% increase in incline after each 2 min. Feed intake by horses fed contaminated grains was decreased compared with controls throughout the experiment (P < 0.05). Supplementation of 0.2% GM polymer to the contaminated diet did not alter feed intake by horses compared with those fed the unsupplemented contaminated diet. All hay was consumed regardless of concentrate fed. Weight loss from 0 to 21 d was observed in horses fed contaminated grains compared with controls (P < 0.05). No effect of diet was seen on variables used to measure athletic ability, although the results showed an expected response to exercise for a fit horse. We conclude that exercised horses are susceptible to Fusarium mycotoxicoses as indicated by appetite suppression and weight loss.

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological measurements of starter pigs, and the efficacy of a polymeric glucomannan mycotoxin adsorbent.

An experiment was conducted to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological parameters of starter pigs. A polymeric glucomannan mycotoxin adsorbent (GM polymer, Alltech Inc., Nicholasville, KY) was also tested for its efficacy in preventing Fusarium mycotoxicoses. A total of 150 starter pigs (initial weight of 9.3 +/- 1.1 kg) were fed one of five treatment diets (six pens of five pigs per diet) for 21 d. Diets included control, low level of contaminated grains, high level of contaminated grains, high level of contaminated grains + 0.20% GM polymer, and pair-fed control for comparison with pigs receiving the high level of contaminated grains. Feed intake and cumulative weight gain of pigs decreased linearly with the inclusion of contaminated grains in the diet throughout the experiment (P < 0.0001). Weight gains recovered, however, during wk 3 (P > 0.05). There was no difference between the pair-fed group and the pigs fed the diet containing the high level of contaminated grains in terms of weight gain or feed efficiency (P > 0.05). Feeding contaminated grains linearly increased the serum albumin:globulin ratio (P = 0.01), whereas serum urea concentrations and gamma-glutamyltransferase activities responded in a quadratic fashion (P = 0.02). When compared with the pair-fed pigs, serum concentrations of total protein (P = 0.01) and globulin (P = 0.02) were decreased in pigs fed the diet containing the high level of contaminated grains. The feeding of contaminated diets did not significantly alter organ weights expressed as a percentage of BW, serum immunoglobulin concentrations, percentages of peripheral blood lymphocyte subsets, contact hypersensitivity to dinitrochlorobenzene, or primary antibody response to sheep red blood cells (P > 0.05). It was concluded that most of the adverse effects of feeding Fusarium mycotoxin-contaminated grains to starter pigs were caused by reduced feed intake. Although supplementation of GM polymer to the contaminated diet prevented some toxin-induced changes in metabolism, it did not prevent the mycotoxin-induced growth depression under the current experimental conditions.

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on feed intake, serum chemistry, and hematology of horses, and the efficacy of a polymeric glucomannan mycotoxin adsorbent.

The feeding of Fusarium mycotoxin-contaminated grains adversely affects the performance of swine and poultry. Very little information is available, however, on adverse effects associated with feeding these mycotoxin-contaminated grains on the performance of horses. An experiment was conducted to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on feed intake, serum immunoglobulin (Ig) concentrations, serum chemistry, and hematology of horses. A polymeric glucomannan mycotoxin adsorbent (GM polymer) was also tested for efficacy in preventing Fusarium mycotoxicoses. Nine mature, nonexercising, light, mixed-breed mares were assigned randomly to one of three dietary treatments for 21 d. The horses were randomly reassigned and the experiment was subsequently replicated in time following a 14-d washout interval. Feed consumed each day was a combination of up to 2.8 kg of concentrates and 5 kg of mixed timothy/alfalfa hay. The concentrates fed included the following: 1) control, 2) blend of contaminated grains (36% contaminated wheat and 53% contaminated corn), and 3) blend of contaminated grains + 0.2% GM polymer. Diets containing contaminated grains averaged 15.0 ppm of deoxynivalenol, 0.8 ppm of 15-acetyldeoxynivalenol, 9.7 ppm of fusaric acid, and 2.0 ppm of zearalenone. Feed intake by all horses fed contaminated grains was reduced (P < 0.001) compared with controls throughout the experiment. Supplementation of 0.2% GM polymer to the contaminated diet increased (P = 0.004) feed intake of horses compared with those fed the unsupplemented contaminated diet. Serum activities of gamma-glutamyltransferase were higher (P = 0.047 and 0.027) in horses fed the diet containing contaminated grain compared with those fed the control diet on d 7 and 14, but not on d 21 (P = 0.273). Supplementation of GM polymer to the contaminated diet decreased (P < 0.05) serum gamma-glutamyltransferase activities of horses compared with those fed unsupplemented contaminated diet on d 7 and 14. Other hematology and serum chemistry measurements including serum IgM, IgG, and IgA, were not affected by diet. It was concluded that the feeding of grains naturally contaminated with Fusarium mycotoxins caused a decrease in feed intake and altered serum gamma glutamyltransferase activities. The supplementation of GM polymer prevented these mycotoxin-induced adverse effects.

Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on production and metabolism in broilers.

Three hundred sixty, 1-d-old male broiler chicks were fed diets containing grains naturally contaminated with Fusarium mycotoxins for 56 d. The four diets included control (0.14 mg/kg deoxynivalenol, 18 mg/ kg fusaric acid, < 0.1 mg/kg zearalenone), low level of contaminated grains (4.7 mg/kg deoxynivalenol, 20.6 mg/kg fusaric acid, 0.2 mg/kg zearalenone), and high level of contaminated grains without (8.2 mg/kg deoxynivalenol, 20.3 mg/kg fusaric acid, 0.56 mg/kg zearalenone) and with (9.7 mg/kg deoxynivalenol, 21.6 mg/kg fusaric acid, 0.8 mg/kg zearalenone) 0.2% esterified-glucomannan polymer derived from Saccharomyces cerevisiae1026 (E-GM). Body weight gain and feed consumption responded in a significant quadratic fashion to the inclusion of contaminated grains during the finisher period. Efficiency of feed utilization, however, was not affected by diets. The feeding of contaminated grains in the finisher period also caused significant linear increases in blood erythrocyte count and serum uric acid concentration and a significant linear decline in the serum lipase activity. Dietary inclusion of contaminated grains resulted in a significant quadratic effect on serum albumin and y-glutamyltransferase activity. Blood hemoglobin and biliary IgA concentrations, however, responded in significant linear and quadratic fashions. Supplementation of E-GM counteracted most of the blood parameter alterations caused by the Fusarium mycotoxin-contaminated grains and reduced breast muscle redness. It was concluded that broiler chickens may be susceptible to Fusarium mycotoxicoses when naturally contaminated grains are fed containing a combination of mycotoxins.

Dietary interaction of 1,4-diaminobutane (putrescine) and calcium on eggshell quality and performance in laying hens.

An experiment was conducted to evaluate the potential dietary interaction between 1,4-diaminobutane (putrescine) and calcium on eggshell quality and overall laying performance. One hundred ninety-two 30-wk-old White Leghorn hens were fed a corn-and soybean-meal-based diet supplemented with 0.00, 0.05, 0.10, or 0.15% putrescine and 2.5, 3.0, 3.5, or 4.0% calcium in a factorial design (12 birds per diet) for 4 wk. The percentage of egg production increased linearly (P < 0.05) with increasing levels of dietary calcium. Significant interactions (P < 0.05) were observed between dietary putrescine and calcium for eggshell thickness, eggshell deformation, percentage of eggshell, calcium intake, total calcium retention, total eggshell calcium, and percentage of eggshell calcium. Interactions were due to quadratic effects of putrescine or calcium on these parameters. Eggshell thickness and percent eggshell increased when hens were fed 3.5% calcium in combination with 0.1% putrescine; however, calcium intake and calcium retention were significantly lower (P < 0.05). Eggshell quality improved with increasing dietary levels of calcium due to increased calcium retention and calcium balance. Increasing levels of dietary putrescine did not have a negative effect on eggshell quality; however, calcium intake was lower at higher-supplemented levels of putrescine. It was observed that dietary calcium in excess of requirements resulted in increased egg production and eggshell quality. Eggshell quality improved when hens were fed 3.5% calcium diet in combination with 0.10% putrescine. It was concluded that small supplements of dietary putrescine may improve eggshell quality, depending on dietary calcium concentration.

Effects of dietary garlic on cholesterol metabolism in laying hens.

Experiments were conducted to evaluate the potential for dietary garlic to influence egg yolk cholesterol concentrations and overall performance in different layer strains. Thirty-six, 28-wk-old, Hisex Brown,Isa Brown, Lohmann, Starcross, Babcock, and Starcross-579 strains (six hens per strain) were fed diets supplemented with 0 (control), 2, 4, 6, 8, or 10% sun-dried garlic paste for 6 wk. There were no differences (P > 0.05) among diets or strains in egg weight, egg mass, feed consumption, feed efficiency, and BW gain as averaged over 6 wk. Yolk weight, however, responded quadratically with increasing levels of dietary garlic and differed among strains (P < 0.05). Egg production and yolk weights were significantly higher in the Babcock strain in comparison with other strains. Serum and egg yolk cholesterol concentrations decreased linearly (P < 0.05) with increasing levels of dietary garlic. Serum and egg yolk cholesterol concentrations also differed among different strains (P < 0.05). It was concluded that garlic paste in the diets of laying hens reduced serum and yolk cholesterol concentrations. It was also concluded that dietary garlic paste had no adverse effects on layer performance.

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on swine performance, brain regional neurochemistry, and serum chemistry and the efficacy of a polymeric glucomannan mycotoxin adsorbent.

The co-occurrence of Fusarium mycotoxins in contaminated swine diets has been shown to result in synergistic toxicity beyond that observed for individual toxins. An experiment was conducted, therefore, to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth, brain regional neurochemistry, serum immunoglobulin (Ig) concentrations, serum chemistry, hematology, and organ weights of starter pigs. Three levels of glucomannan polymer (GM polymer, extract of yeast cell wall, Alltech Inc.) were also tested for its efficacy to overcome Fusarium mycotoxicoses. A total of 175 starter pigs (initial weight of 10 +/- 1.1 kg) were fed five diets (seven pens of five pigs per diet) for 21 d. Diets included (1) control, (2) blend of contaminated grains, (3) contaminated grains + 0.05% GM polymer (4) contaminated grains + 0.10% GM polymer and (5) contaminated grains + 0.20% GM polymer. Diets containing contaminated grains averaged 5.5 ppm deoxynivalenol, 0.5 ppm 15-acetyldeoxynivalenol, 26.8 ppm fuuric acid, and 0.4 ppm zearalenone. Feed intake and weight gain of all pigs fed contaminated grains was significantly reduced compared to controls throughout the experiment. The weights of liver and kidney, expressed as a percentage of body weight, were lower in pigs fed the contaminated diet than in those fed the control diet. The feeding of contaminated grains significantly reduced concentrations of dopamine in the hypothalamus and pons and concentrations of dihydroxyphenylacetic acid and norepinephrine in the pons. The ratios of 5-hydroxyindoleacetic acid to serotonin, however, were elevated in the hypothalamus and pons. The feeding of contaminated grains increased serum IgM and IgA concentrations, while serum IgG concentrations were not altered. The supplementation of GM polymer prevented some of the mycotoxin-induced alterations in brain neurotransmitter and serum Ig concentrations. In summary, the feeding of grains naturally contaminated with Fusarium mycotoxins reduced growth, altered brain neurochemistry, increased serum Ig concentrations, and decreased organ weights in starter pigs. Some of the Fusarium mycotoxin-induced changes in neurochemistry and serum Ig concentrations can be prevented by the feeding of yeast cell wall polymer at appropriate concentrations, although this was not reflected in increased growth rate under these experimental conditions.

Effects of dietary 1,4-diaminobutane (putrescine) on eggshell quality and laying performance of hens laying thin-shelled eggs.

Experiments were conducted to evaluate the potential for dietary 1,4-diaminobutane (putrescine) to influence eggshell quality and overall laying performance in hens. Forty-eight, 60-wk-old White Leghorn hens laying thin-shelled eggs were fed a corn and soybean meal-based diet supplemented with 0.00 (control), 0.05, 0.10, or 0.15% putrescine for 4 wk. Twelve hens that laid thick-shelled eggs were also fed the control diet. The feeding of supplemental putrescine decreased feed consumption; however, egg weight decreased only at higher levels of supplementation. Increasing dietary levels of putrescine responded quadratically in eggshell deformation, eggshell weight, and eggshell weight as a percentage of egg weight (P < 0.05). There were no significant differences in shell deformation, shell thickness, or shell weight when comparing hens laying thick-shelled eggs and those laying thin-shelled eggs that were fed 0.05% supplemental putrescine. Calcium intake, calcium retention, and calcium balance decreased linearly (P < 0.05) with increasing levels of dietary putrescine. Pancreatic putrescine concentrations were significantly higher (P < 0.05) in hens laying thick-shelled eggs compared with hens laying thin-shelled eggs. It appeared that pancreatic cells synthesized more polyamines in hens laying thick-shelled eggs. This increase in polyamines might have caused improved eggshell quality by increasing calcium transport. It was concluded that 0.05% supplemental putrescine improved eggshell quality; however, higher levels proved to be toxic.

Effect of feeding raw soybeans on polyamine metabolism in chicks and the therapeutic effect of exogenous putrescine.

The inclusion of isolated soy protein in milk replacer diets for calves and neonatal pigs inhibits development of intestinal mucosal cells. Simultaneous administration of putrescine partially overcomes this effect. We therefore conducted experiments to determine the potential for dietary putrescine to overcome the toxicity of raw soybeans in chicks. In the first experiment, week-old chicks were fed either an isolated soy protein-based control diet or an isoenergetic and isonitrogenous diet containing 52% raw, ground soybeans for 14 d. The feeding of raw soybeans depressed (P < .001) growth and feed consumption, caused enlargement (P < .001) of the duodenum and pancreas, depressed (P < .001) activities of polyamine synthetic enzymes in the duodenum, and reduced (P < .01) duodenal tissue concentrations of putrescine. In the second experiment, the diet containing raw soybeans was fed with and without .2, .3, and .4% supplemental putrescine. The feeding of supplemental putrescine largely overcame the inhibition of growth due to the feeding of raw soybeans and increased intestinal putrescine concentrations. Putrescine supplementation had no effect, however, on pancreatic and intestinal enlargement in birds fed raw soybeans and tended to depress the activity of polyamine synthetic enzymes. The beneficial effects of putrescine supplementation were confirmed in the third experiment when up to 1.0% supplemental putrescine was fed. We conclude that the toxicity of raw soybeans to chicks can be overcome by feeding putrescine. These effects are likely due to improved nutrient uptake by overcoming the adverse effects of lectins in the intestinal tract and are not likely due to alleviation of the pancreatic enlargement caused by protease inhibitors.

Toxicity and growth-promoting potential of spermine when fed to chicks.

Previous studies have shown that the feeding of putrescine, a biogenic amine and the precursor of the mammalian polyamines, can promote whole-body growth of chicks. The current study was undertaken to determine the effect of spermine, also a biogenic amine and the most cationic of the polyamines, under similar conditions. In Exp. 1, 120 week-old chicks were fed purified crystalline amino acid-based diets containing 0, .2, .4, .6, .8, or 1.0% spermine for 14 d. Spermine proved highly toxic and growth rates were reduced compared with controls when even .2% was fed. In Exp. 2, chicks were fed 0, .0375, .0750, or .1000% spermine. These concentrations proved less toxic than those used in Exp. 1. Supplemental dietary cysteine was then provided at 0, .3, .6, and .9% together with 0, .025, .050, or .400% spermine (Exp. 3) because depletion of cellular glutathione has been suggested as contributing to spermine's toxicity. Even high levels of cysteine supplementation did not overcome spermine's toxicity. Subsequent dietary provision of L-2-oxothiazolidine-4-carboxylic acid (OTC, Exp. 4), a cysteine prodrug, showed that depletion of cellular glutathione was not likely a cause of spermine toxicosis. A trend toward increased weight gain and feed efficiency was observed when low concentrations of spermine were fed. It was concluded, however, that dietary spermine was more toxic to chicks than was previously seen for putrescine, that any growth-promoting effects of dietary spermine are small, and that supplements of dietary cysteine or OTC are unlikely to increase these effects by overcoming spermine toxicosis.

Methionine toxicity in the rat in relation to hepatic accumulation of S-adenosylmethionine: prevention by dietary stimulation of the hepatic transsulfuration pathway.

Rats were fed toxic levels of methionine with or without simultaneous dietary supplements of glycine and serine. Feed intake, growth rate, and metabolite concentrations in intestine, plasma, liver, skeletal muscle, and kidneys were monitored. Both toxic amounts of methionine and supplemental glycine and serine affected the tissue distribution of several amino acids resulting in similar, opposite, and diet-specific effects on the parameters studied. These changes were considered to be normal responses of amino acid metabolism to diet and to reflect metabolite flows between tissues. The feeding of toxic levels of methionine resulted in the accumulation of methionine, taurine, and glutathione in all tissues measured, but caused marked accumulation of S-adenosylmethionine and its catabolites only in liver. Hepatic accumulation of S-adenosylmethionine was accompanied by 40% stimulation of methionine adenosyltransferase and 40% repression of spermine synthase over a 2-week period. Simultaneous dietary supplements of glycine and serine combined with toxic levels of methionine markedly stimulated hepatic methionine catabolism. As a result, tissue distribution of methionine and glutathione returned close to normal in all tissues measured and accumulation of hepatic S-adenosylmethionine and its catabolites was prevented. Concentrations of taurine in liver, blood, and kidneys were further elevated, suggesting increased conversion of methionine to taurine followed by urinary excretion. These changes were accompanied by normalization of the above enzyme activities and the absence of symptoms of methionine toxicity. It was concluded that methionine toxicity is likely to be linked to hepatic accumulation of S-adenosylmethionine, resulting in liver dysfunction probably due to nonenzymatic methylation of liver macromolecules. Accumulation of tissue glutathione may also contribute to toxicity.

Effect of dietary cysteine supplements on canola meal toxicity and altered hepatic glutathione metabolism in the rat.

Experiments were conducted to determine the effects of feeding canola meal (Brassica campestris and Brassica napus) on the rat hepatic glutathione detoxification system and whether dietary cysteine supplements might modify such effects. Rats were fed test diets for 14 d. Body weight change, feed consumption, hepatic glutathione concentration, and hepatic glutathione-S-transferase (GSH-S-T) activities were determined. Weight gain was decreased when canola meal was fed, whereas hepatic glutathione concentrations increased, as did hepatic GSH-S-T activity. All effects correlated with total glucosinolate concentration in the canola meal. Dietary cysteine supplements, however, did not influence the growth reduction and increased hepatic glutathione concentrations caused by feeding canola meal. Supplemental cysteine prevented the elevation in hepatic GSH-S-T activity. The elevation in hepatic glutathione concentration caused by canola meals was not an overcompensation caused by an initial depletion and therefore reflected a general hepatotoxicity. Feeding supplemental cysteine increased hepatic glutathione levels at early time intervals and delayed the induction of GSH-S-T caused by canola meal toxicity. There was no beneficial effect of supplemental dietary cysteine in overcoming the toxicity of high levels of canola meal, but supplemental cysteine did modify the canola meal-induced changes in hepatic glutathione metabolism.

Effect of dietary putrescine on whole body growth and polyamine metabolism.

Putrescine (1,4-diaminobutane) is the simplest of the mammalian polyamines. These are small, positively charged molecules which are essential for cell growth and are thought to play a role in regulation of anabolic events such as synthesis of DNA, RNA, and protein. Recent reports have indicated the potential for dietary precursor amino acids of putrescine to alter tissue putrescine concentrations. The current study was conducted to determine the physiologic significance of these effects by feeding up to flooding doses of putrescine to determine any influence on whole body growth and polyamine metabolism. A total of 96 chicks were fed purified crystalline amino acid diets containing 0.0, 0.2, 0.4, 0.6, 0.8, or 1.0% purified putrescine (four birds per pen, four pens per diet) for 14 days. The feeding of 0.2% putrescine increased growth rate beyond that of controls while further supplements reduced growth and were toxic when 0.8 and 1.0% putrescine were fed. Hepatic and muscle concentrations of ornithine increased with dietary putrescine while the effect in kidney was much less. Putrescine concentrations in liver, kidney, and muscle rose when 0.4% putrescine or more was fed. This effect was particularly obvious in muscle in which there were also increases in the concentrations of spermidine and spermine. In a subsequent similar experiment, putrescine was fed at 0.0, 0.1, 0.2, 0.3, 0.4, or 0.5% to determine the effect on the activities of the key enzymes regulating polyamine synthesis. The feeding of putrescine at even 0.1% caused a rapid reduction in hepatic ornithine decarboxylase activity while S-adenosylmethionine decarboxylase and arginase activities were not influenced by diet. It was concluded that excess tissue putrescine can be toxic to whole organisms but small, orally administered doses of this metabolite can promote growth.

Adaptation of adenosylmethionine metabolism and methionine recycling to variations in dietary methionine in the rat.

Weanling rats were fed a casein-based diet supplemented to give dietary methionine (Met) concentrations of 0.41, 0.61, and 1.50%. After 2 weeks of feeding, the rats received intraperitoneally 800 nCi of 2-14C-labeled and/or methyl-3H-labeled L-Met. The animals were killed 20 min, 1 hr, or 2 hr after the isotope injection and the specific radioactivity of adenosylmethionine (AdoMet) as well as the total acid-soluble radioactivity was analyzed in the liver and skeletal muscle. Met concentrations of the liver and skeletal muscle were increased 20-fold by the diet containing 1.50% of Met. In the liver, but not in skeletal muscle, accumulation of AdoMet closely followed changes in Met concentration. Within 2 hr after intraperitoneal injection, the rate of disappearance of 3H label from the acid-soluble fraction was slow in both tissues; increasing in the liver and decreasing in skeletal muscle with increasing dietary Met concentration. At the same time, disappearance of 14C label was slow in both tissues in the rats fed the toxic Met diet, and also in the liver of the rats fed the Met-deficient diet. Decline of the specific radioactivity of the AdoMet pool with respect to 3H label was similar to that of 14C label in the skeletal muscle at all dietary Met concentrations. In the liver, the rate of disappearance of 14C label from the AdoMet pool was markedly increased and that of the 3H label slightly decreased with increasing dietary Met supply. Met deprivation resulted in rapid disappearance of 3H label from the hepatic AdoMet pool, whereas the disappearance of the 14C label was very slow. The results indicate that hepatic Met recycling is very effective with deficient or adequate dietary Met concentrations. In skeletal muscle, the capacity to catabolize extra Met is very limited and continuous flow of Met to liver takes place. Unlike in the liver, in skeletal muscle the transsulfuration route is not adaptable to changes in Met supply and plays a minor role in Met catabolism. The approach used to determine the efficacy and adaptation of methionine salvage pathways by following simultaneously the decline of the specific radioactivities of the methyl group and the methionyl carbon chain of AdoMet following intraperitoneal injection of double-labeled Met has several advantages over that used in literature reports. It offers a reliable means of observing these metabolic pathways in whole animals without disruption of metabolite fluxes.

Effects of dietary polyamine precursors on the metabolism and tissue concentrations of amino acids in the rat.

Experiments were conducted to determine the effects of dietary supplements of amino acid precursors of polyamines on amino acid metabolism in the rat in order to better understand comparative aspects of polyamine metabolism. Rats were fed isonitrogenous combinations of methionine, ornithine, arginine and 2-difluoromethylornithine in casein-based diets. It was observed that hepatic concentrations of methionine, 5'-deoxy-5'-methylthioadenosine and decarboxylated S-adenosylmethionine were more easily influenced by diet than were arginine and metabolites. It was concluded that rats may be more refractory to exogenous polyamine precursor amino acids than are chicks because of the presence of a functional urea cycle.

Regulation of polyamine synthesis by dietary alpha-aminoisobutyric acid and ornithine.

An experiment was conducted to determine the effect of feeding ornithine in combination with alpha-aminoisobutyric acid (AIB), an inhibitor of arginase, on the regulation of polyamine synthesis in chicks. A total of 48 chicks with genetically elevated renal arginase activity was fed diets containing crystalline amino acids and 1% AIB with or without 2% ornithine. Feeding AIB reduced renal arginase activity, while renal and hepatic ornithine decarboxylase (ODC) activity increased. Feeding AIB plus ornithine caused no further reduction in renal arginase activity compared with that in chicks fed the AIB-supplemented diet. Renal and hepatic ODC activities, however, fell to below control levels. Renal, hepatic, and breast muscle ornithine concentrations increased substantially when ornithine was fed. AIB plus ornithine increased renal putrescine and spermidine concentrations. It was concluded that AIB could partially overcome the ornithine-induced inhibition of ODC activity. These findings support the hypothesis that dietary manipulation of precursor amino acids of polyamines in the presence of metabolites that induce ODC activity can influence tissue polyamine concentrations.

Effect of dietary protein deficiency and L-2-oxothiazolidine-4-carboxylate on the diurnal rhythm of hepatic glutathione in the rat.

Maximizing hepatic glutathione (GSH) concentration may provide greater protection against toxic compounds. A dietary supplement of L-2-oxothiazolidine-4-carboxylate (OTC), a stable derivative of cysteine, increased hepatic GSH in rats fed for 2 wk a diet deficient in protein (7.5%) but not in rats fed a diet adequate in protein (15%). Experiment 2 determined whether a dietary supplement of OTC could maintain the maximum GSH concentration over 24 h. Rats acclimatized for 5 d to a 7.5% protein diet and then fed a 7.5% protein diet supplemented with either 2.5 mmol OTC or cysteine-HCl (CYS)/100 g diet had a more rapid increase in hepatic GSH (4 and 8 h after beginning of feeding, P less than 0.05) than did rats fed an unsupplemented 7.5% protein diet. This response was not due simply to the greater supply of cysteine for GSH synthesis because supplementing the 15% protein diet with OTC or CYS had no effect on the hepatic GSH of rats acclimatized to a 15% protein diet. In experiment 3, rats acclimatized to the 7.5% protein diet had a more rapid rate of increase in hepatic GSH concentration in response to feeding than did rats acclimatized to a 15% protein diet, regardless of which diet they were fed during the 24-h period. It was concluded that in addition to cysteine availability, previous dietary protein status plays a key role in the regulation of the feeding-induced diurnal rhythm of hepatic GSH concentration in rats.

Potential for dietary amino acid precursors of neurotransmitters to overcome neurochemical changes in acute T-2 toxicosis in rats.

Experiments were conducted to determine the potential for overcoming T-2 toxin-induced changes in brain neurotransmitter concentrations through dietary manipulation. Rats were fed either a tryptophan-deficient, gelatin-based diet or the same diet supplemented with a mixture of large neutral amino acids for 4 d. Rats were then dosed with 0 or 2.0 mg T-2 toxin/kg body weight and killed 4, 8 or 12 h after dosing. The large neutral amino acid supplements successfully reduced brain concentrations of tryptophan and serotonin in control rats, but this was not enough to overcome the acute effects seen in T-2 toxin-treated rats. A further experiment was then conducted to monitor the effect of T-2 toxin on the ratio of free to protein-bound tryptophan in plasma. Total plasma tryptophan increased in T-2 toxin-treated rats, although there were no significant differences in the ratio of free to protein-bound tryptophan. A final experiment was conducted to determine the specificity of the T-2 toxin effect on concentrations of plasma amino acids. Concentrations of amino acids that use the large neutral amino acid transport system into the brain were higher in T-2 toxin-treated animals. The only other amino acid that had a higher concentration was arginine. It was concluded that acute doses of T-2 toxin may selectively alter membrane transport of amino acids.