Supplementation Of Drinking Water Research Articles

2-Hydroxy-4 (Methylthio) Butanoic Acid as a Drinking Water Supplement for Broiler Chicks

Two experiments were conducted to study the effects on chick performance of a commercially available liquid methionine analog [2-hydroxy-4 (methylthio) butanoic acid; HMB] supplied through drinking water. Methionine activities of .025 and .05% were added to drinking water and compared with levels of .03, .06, or .09% included in a low-methionine basal diet from 0 to 21 days of age.Mortality was not significantly altered by any dietary treatment. Neither feed nor water intake was affected adversely by HMB inclusion in drinking water. Only male body weight in Experiment 1 did not respond to HMB feed supplementation. Equivalent levels of total sulfur amino acid intake among water treatments were associated with significantly heavier body weights than the control. In both experiments, body weight and feed efficiency of birds receiving .05% methionine activity as HMB in water were equal or superior to those of groups that received supplemented feed. The results indicate that, under the study conditions, HMB provided in drinking water can be effectively assimilated by broiler chicks, at least through 21 days of age.

Responses in egg shell quality from dietary ascorbic acid supplementation of hens receiving saline drinking water

Three experiments were conducted to determine whether the poor shell quality of eggs from hens receiving saline drinking water could be improved by the simultaneous addition of ascorbic acid to the diet. In one experiment, the responses were compared with those of hens receiving ascorbic acid in the drinking water. In this experiment, providing the ascorbic acid in the drinking water on a daily basis was compared with dosing the water on alternate days. The results showed that saline water increased the incidence of egg shell defects without affecting food and water intakes, egg production or egg weight. Changes in a range of shell quality measures mirrored the changes in the incidence of egg shell defects. Supplementation of the diet or drinking water with ascorbic acid prevented the increase in shell defects and the decrease in shell quality. The degree of response to dietary ascorbic acid was dependent on the concentration used, a response similar to that observed previously when the ascorbic acid was added to the drinking water.

Research Note: Sodium and Potassium Chloride Drinking Water Supplementation Effects on Acid-Base Balance and Plasma Corticosterone in Broilers Reared in Thermoneutral and Heat-Distressed Environments

One experiment utilizing 188 Vantress × Arbor Acres broilers was conducted to evaluate the effects of isomolar KCl (.5%) and NaCl (.39%) drinking water supplementation on venous pH, PO2, PCO2, HCO–3, hematocrit, and plasma corticosterone as well as rectal temperature and water consumption of broilers reared in heat-distressed and thermoneutral environments. Birds were allotted at 5 wk posthatch into either a thermoneutral (TN; 24 C) or cycling temperature (24 to 35 C) environmental chamber. Heat-distressed (HD) controls had elevated (P<.05) body temperature (42.9 versus 41.7 C) and PO2 (144.5 versus 108.4 mm Hg). Blood pH, PCO2, and HCO–3 (P>.1) were not affected by high ambient temperature, but hematocrit (31 versus 32%) for HD controls was reduced (P = .07) compared with TN control birds. At 35 C, drinking water NaCl supplementation decreased (P<.05) venous PCO2 and HCO–3, increased (P<.05) PO2, and had no effect on venous pH and water consumption relative to HD controls. Potassium chloride lowered (P = .07) venous pH, decreased (P<.05) HCO–3, and increased water consumption at 35 C, but PO2 and PCO2 were unaffected relative to HD controls. Heat distress increased (P<.05) plasma corticosterone by 53%. Sodium chloride failed to impact (P>.1) plasma corticosterone but KCl reduced (P<.05) its concentration during heat distress and increased (P<.05) bird survivability as compared with heat-distressed controls. The data reported herein suggests that KCl and to a lesser extent NaCl reduces HD consequences by a mechanism as yet undefined.

Effects of Sodium Bicarbonate and Potassium Chloride Drinking Water Supplementation.: 2. Meat and Carcass Characteristics of Broilers Grown Under Thermoneutral and Cyclic Heat-Stress Conditions

Two broiler trials were conducted to investigate the effect on post-mortem carcass and meat quality of NaHCO3 and KCl drinking water supplementation under thermoneutral and cyclic heat-stress climatic conditions. Water chill carcass weight change, water- and oven-cooked breast fillet yields, and breast meat tenderness were measured. In Trial 1, neither environmental regimen, nor water treatments, nor their interaction was a significant (P<.05) source of variation for the parameters measured. In Trial 2, environmental regimen was a highly significant (P<.01) source of variability for chilled carcass weight change; the cyclic heat-stressed broiler carcasses gained more weight than the thermoneutral (control) broiler carcasses during ice-water chilling. Oven-cooked fillet yield was significantly (P<.05) affected by environmental regimen; fillets from cyclic heat-stressed broilers had lower yields than thermoneutral (control) broiler fillets. Drinking water treatments were a significant (P<.05) source of variation for breast meat tenderness in Trial 2. Broilers given .5% NaHCO3 from 5 to 8 wk of age had higher shear resistance values than broilers given a combination of .5% NaHCO3 and .5% KCl or tap water-fed controls. Breast meat shear values were negatively correlated (P<.05) with 8-wk broiler body weight and 5- to 8-wk gain.

Effect of Dietary Fluoride on Performances and Bone Characteristics of Broilers and the Influence of Drying and Defatting on Bone-Breaking Strength

A trial with broiler males, housed in cages, was conducted to determine the effect of (added) dietary fluoride at 0, 200, and 400 mg/kg on performance and bone characteristics and the influence of preconditioning (drying, defatting) on bone-breaking strength. The F administration resulted in a significantly (P<.05) lower weight gain. Feed conversion, however, was not affected. Tibial ash deposition and ash-percentage increased significantly (P<.05) at both dietary levels of added F. Broiler males fed supplemented F had a significantly (P<.05) higher incidence of tibial dyschondroplastic plugs and epiphyseal bone with looser structure, as judged macroscopically. Tibial bone strength was significantly (P<.05) affected not only by dietary F level, but also by preconditioning, resulting in a significant interaction. Administration of F had a significantly negative or positive effect on breaking strength, depending on whether the measurements were carried out on fresh bones or dried (defatted) bones, respectively. This diverging response of F on breaking strength offers a valid explanation for the contradictory results in the literature, demonstrating at the same time that F supplementation of feed or drinking water should be discontinued as a method to improve bone-breaking strength.

Liquid Methionine as a Drinking Water Supplement for Broiler Chicks

Three experiments were conducted to study the effect of a liquid methionine source supplied through the water on chick performance. Methionine at .025, .05, and .075% (Experiment 3, only) from the liquid source were added to the drinking water and compared with .05 and .075% (Experiment 2 and 3) dry methionine supplementation in a methionine-deficient basal. A dry DL-methionine was used for diet supplementation in Experiments 1 and 2, and both liquid and dry sources were used in Experiment 3. Day-old (Cobb) feather-sexed broiler chicks received these treatments for 3-week periods. Mortality was not significantly altered by any of the treatments. In two of the three experiments neither feed nor water intake was significantly affected by treatment. In Experiment 2, control birds consumed significantly less feed than other groups, and daily water intake of birds that received .05% supplemental feed methionine was elevated above that of other regimens. Fecal moisture and fecal sodium levels were not elevated above those measured from the unsupplemented basal.In all three studies comparable levels of methionine from feed or water supported equivalent body weights. Within the limits of these tests, liquid DL-methionine provided in the drinking water was effectively assimilated by broiler chicks and increased total methionine intake, which increased growth.

Trace element inhibition of carcinogenesis and angiogenesis

In separate experimental models the effects of selenium, zinc, potassium, and copper on angiogenesis and carcinogenesis are compared. Inhibitory effects of Se as Na2SeO3 and of chloride salts of K and Zn, but not of Cu, on vascularization induced by amelanotic tumor implants (A Mel-4B32) in the Syrian hamster cheek pouch membrane are reported. In an earlier study the induction of new vasculature, angiogenesis, in control chambers implanted with A Mel-4B32 was initially observed on day 4 after implant. Addition of 5, 10, and 50 μg Se at the time of tumor implant delayed the initial capillary proliferation to days 7, 9, 10, respectively (Cancer Lett. 9, 353, 1980). Similarly, in this report addition of 50 μg Zn or 50 μg K delayed angiogenesis to days 7.and 6, respectively. By contrast, addition of 50 μg Cu caused severe inflammation and necrosis of the membrane before capillary proliferation could be observed and the animals had to be sacrificed.In an earlier study we reported the colon tumor incidence in 1,2-dimethylhydrazine (20 mg DMG/kg body weight for 20 weeks) -treated Sprague Dawley rats was reduced from 87 to 40% by a 4 ppm Se (as Na2SeO3) supplement in the drinking water (Cancer Lett. 2, 133, 1977). In this study rats were treated with the same dose of carcinogen, but were sacrificed 14 weeks following the last DMH injection. Drinking water supplements with 0.02% Zn (as ZnCl2), 0.5% K (as KCl), or 0.01% Cu (as CuCl2) were provided concurrently with the carcinogen and were continued until death or sacrifice. The colon tumor incidence was 18/20 in the DMH control and was reduced to 16/20 by supplemental Zn, reduced to 12/20 by supplemental K, and was unchanged (18/20) by Cu. The tumor incidences in the small intestine and Zymbal gland were all reduced by Zn, K, and Cu supplements compared with the DMH control. The hamster cheek pouch technique may provide a prescreen for potential inhibitors of chemical carcinogenesis in other experimental models.

Attempts to induce cytogenetic effects with sulphite in sulphite oxidase-deficient Chinese hamsters and mice

Chinese hamsters and mice were made sulphite-oxidase deficient by the feeding of a low-molybdenum diet with sodium tungstate as a drinking-water supplement. Hepatic sulphite-oxidase activity was checked spectrophotometrically. Under normal conditions, sulphite-oxidase activity is high in the mouse and low in the Chinese hamster. Sulphite (SO 3 - -) was given in a single or double oral dose in aqueous solution or dissolved in fruit juice or by repeated subcutaneous injections up to the maximum tolerated doses. Possible cytogenetic effects were studied in bone-marrow cells using three test systems—the sister chromatid exchange, chromosome aberration and micronucleus tests. No induction of cytogenetic effects was observed with any of the three tests in either species, indicating that no damage at the chromosomal level was induced by sulphite in these animals, even when sulphite-oxidase activity was reduced to a very low level.

Toxicological effects of sodium selenite in swiss mice

Se as sodium selenite was administered by gavage (three consecutive times) and as drinking water supplements for 46 d to male and female Swiss mice. With respect to survival in 7-wk-old mice, Se was less toxic in males than in females when gavaged. Drinking water supplements of 1-64 ppm Se resulted in 1 male and 1 female death in mice first given Se at 7 wk of age. Se supplements to the drinking water of adult (18-wk-old) mice was less toxic in females. All young (7-wk-old) and adult (18-wk-old) mice provided 1-16 ppm Se in the drinking water survived the 46-d treatment, but in adult mice 64 ppm Se significantly reduced survival. Only 64 ppm Se supplements caused a sharp reduction in body weight in young and adult mice of both sexes. Supplements of 1-8 ppm Se in all mice elicited growth responses similar to those of untreated controls. Occasional liver and kidney congestion, liver necrosis, parenchymal cell degeneration, and bile duct proliferation were observed in control and treatment groups. Serum alkaline phosphatase and glutamic-oxaloacetic transaminase (SGOT) increased with 32 ppm Se and higher supplements. Survival, growth, serum enzymes, and pathology were normal in untreated controls and in mice of growth ages and sexes give 1, 4, and 8 ppm Se supplements. A chronic toxicity study was conducted in female Swiss mice given 1, 4, and 8 ppm Se supplements for 50 wk. The survival of Se-treated groups was more than 90% and that of controls was only 72% after 50 wk. All mice gained weight, but the group treated with 8 ppm Se gained half as much as other groups. Both liver Se and glutathione peroxidase activity increased in Se-treated mice compared to controls at 25 and 50 wk. A reduced white blood cell count and increased alkaline phosphatase and SGOT suggested a mild toxic effect of the 8 ppm Se supplement in the chronic study.

Influence of selenium on vascularization in the hamster cheek pouch

The inhibitory effect of selenium (Na 2SeO 3) on the vascularization induced by amelanotic tumor implants (A Mel-4B32) in the Syrian hamster cheek pouch membrane is reported. Among control animals receiving A Mel-4B32 implants, 19 developed tumors out of 19 chambers with capillary proliferation being observed on day 4 after implant. Addition of 50 μg Se to the chamber at the time of tumor implant delayed the initial observation of capillary proliferation until day 10 after implant. In the 50 μg Se treated group, tumor-induced vascularization developed in 11 of 15 chamber implants and not in the remaining 4. Intermediate doses of 5 and 10 μg Se added to the chamber at the time of tumor implant delayed the initial observation of capillary proliferation to days 7 and 9, respectively, with tumors developing in all chambers. Neither sodium nor sulfite altered the vascular pattern. Capillary proliferation was observed on day 4 after tumor implant when either 50 μg NaCl or 50 μg S as Na 2SO 3 were added to the chamber at the time of implant. Provision of Se as a drinking water supplement also delayed the onset of capillary proliferation.