The effect of dietary mercury on vanadate toxicity in the chick

Three experiments were conducted investigating the interaction of dietary vanadate and mercury on the growth of chicks. The growth-retarding effect of 30 mg vanadium/kg diet was completely overcome by the inclusion of 500 mg mercury/kg diet. Restricting the feed intake of the mercury-supplemented animals to approximately those receiving vanadate alone still resulted in an amelioration of the growth retarding effect of vanadate. Analyses of femurs and kidneys revealed that mercury added to a vanadium-containing diet increased the vanadate concentration of the femur and had no effect on the vanadium concentration in the kidney. As little as 25 mg mercury/kg diet significantly reduced the growth retarding effect of vanadium. The inclusion of 100 mg mercury/kg in the diet resulted in a significant increase in renal glutathione concentration.     

Interaction of dietary calcium,manganese, and manganese source (Mn oxide or Mn methionine complex) on chick performance and manganese utilization

Two trials were conducted to determine the utilization of manganese (Mn) as influenced by the level and source of Mn and the level of dietary calcium (Ca) in broiler chickens. Trial One was a 2 x 2 x 3 factorial arrangement of two Mn sources (Mn methionine or manganous oxide), two levels of dietary Ca (1.8 or 1.0), and three levels of supplemental Mn (30, 60, or 200 mg/kg) fed until 4 wk of age. Total phosphorus (available phosphorus) levels were 0.70% (0.48%) during all ages. High levels of dietary Ca caused a slower early rate of growth (0.53 vs. 0.64 kg) for chicks fed 1.8 vs 1.0% Ca, respectively. Chick weight was equivalent for all diets within the Ca-treatment group, except the dietary combination of high Ca and 200 mg/kg Mn as Mn methionine. Bone and liver Mn were significantly increased as the Mn level increased, but were not affected by the Mn source. Chicks fed 1.8% Ca had higher levels of bone Mn (9.28 ppm) than chicks fed 1.0% Ca (7.23 ppm). High levels of dietary Ca and 200 ppm Mn methionine dramatically depressed early growth, feed intake, and bone ash in this trial, raising the question of a diet x environment (heat-stress) effect. Trial Two was a 2 x 2 factorial arrangement of two levels of dietary Ca (1.8 or 1.0%) and two Mn sources (200 mg/kg Mn as Mn methionine or MnO) up to 3 wk of age in a controlled heat-stress environment. No growth depression in the chicks fed high levels of Ca and Mn methionine was observed. In the presence of high levels of dietary Ca, bone Mn was significantly higher when chicks were fed the MnO source. In summary, dietary Ca did not decrease Mn utilization in these trials, and availability of Mn in Mn methionine as a source compared to MnO depended on dietary Ca levels.     

Amelioration in Growth and Phosphorus Assimilation of Poultry Birds Using Cell-Bound Phytase of Pichia Anomala

Summary Cell-bound phytase of Pichia anomala was produced in glucose–beef extract medium in shake flasks and in a laboratory fermenter at 25 °C for 24 h at 250 rev/min. In the fermenter the biomass production increased and the fermentation time was reduced from 24 to 16 h. Two-week-old broiler chicks were fed with the biomass-supplemented feed [at 100 g/7.5 kg; 50-phytase units/bird/day]. The overall weight gain in the biomass-fed chicks was higher (90.2%) than that of the control group (77.7%). The biomass incorporation in the feed of broiler chicks also resulted in a better phosphorus retention (29% in the control, and 73.68% in the biomass-fed) in the body, consequently an improved growth. There was a decrease in the excretion of phosphorus in the faeces of the chicks fed with phytase-supplemented diet (188.9 mg/g dry matter) as compared to the chicks fed on unsupplemented broiler finisher ration (509.4 mg/g dry matter). This eliminated the need to supplement phosphorus in their diet and also reduced phosphorus pollution. The feed conversion ratio was also lowered for chicks, which were biomass-fed as compared to the control.     

Effects of feeding deoxynivalenol (DON)-contaminated wheat to laying hens and roosters of different genetic background on the reproductive performance and health of the newly hatched chicks

A total of 216 23-week-old laying hens from two different genetic backgrounds (half of the birds were Lohmann brown [LB] and [LSL] hens, respectively) and 24 adult roosters were assigned to a feeding trial to study the effect of increasing concentrations of deoxynivalenol (DON) in the diet (0, 5, 10 mg/kg) on the reproductive performance of hens and roosters, and the health of the newly hatched chicks. Hatchability was adversely affected by the presence of DON in LB hens’ diet, while the hatchability of the LSL chicks was significantly higher than LB chicks. An interaction effect between DON in the hens’ diet and the breed was noticed on fertility, as the fertility was decreased in the eggs of LB hens receiving 10 mg/kg DON in their diet and increased in the eggs of LSL hens fed 10 mg/kg DON. Moreover, spleen relative weight was significantly decreased in the chicks hatched from eggs of hens fed contaminated diets, while gizzard relative weight was significantly decreased in LB chicks with 10 mg/kg DON in their diet compared with the control group. On the other hand, the chicks’ haematology and organ histopathology were not affected by the dietary treatment. Additionally, the presence of DON in the roosters’ diet had no effect on fertility (the percentage of fertile eggs of all laid eggs). Consequently, the current results indicate a negative impact of DON in LB hens’ diet on fertility and hatchability, indicating that the breed of the hens seems to be an additional factor influencing the effect of DON on reproductive performance of the laying hens.     

Silicon facilitation of copper utilization in the rat

An eight-week, 2 x 4 factorial rat experiment using two levels of dietary copper and four levels of dietary silicon was conducted to further delineate a previously observed silicon-copper interaction in which silicon appears to mimic copper in its effect on the composition of the aorta. Dietary copper concentrations were 1.4 (deficient) and 5.4 (adequate) mg/kg diet, and silicon concentrations were 5, 135, 270, and 540 mg/kg diet. Compared with the lowest level of silicon and copper, weight gains were 15.5% higher for rats fed 540 mg silicon/kg diet and 14.3% higher for those fed 5.4 mg copper/kg diet. The growth-promoting effects of silicon and copper were additive. Evidence that silicon elevated the copper status of copper-deficient rats includes an increase in packed-cell volume by 540 mg silicon/kg diet in the otherwise packed-cell volume-depressed, copper-deficient rats, accompanied by a trend toward higher hemoglobin values and lower relative heart weights. In the copper-adequate rats, evidence that 540 mg silicon/kg diet elevated their copper status includes a two-fold increase in the blood-plasma copper concentration, a three-fold increase in ceruloplasmin activity, and an increase in cardiac, renal, and hepatic copper concentrations. In addition, 540 mg silicon/kg diet resulted in higher aortic dry mass and aortic elastin content in both copper-deficient and copper-adequate rats. While dietary silicon concentrations of 135, 270, and 540 mg/kg diet were all effective in increasing aortic elastin in the copper-adequate rats, only 540 mg silicon/kg diet increased aortic elastin in the copper-deficient rats. These data indicate that some of the metabolic effects attributed to silicon may be manifested through a silicon-facilitated increase in copper utilization.     

Studies on the role of iron in the reversal of vanadium toxicity in chicks

The interaction of dietary iron levels on vanadium toxicity was studied in chicks. Dietary iron levels ranged from a deficiency, ca. 10 ppm, to an adequacy, 100 ppm supplemental iron. to an excess, 1000 ppm supplemental iron. Vanadium was fed at 10, 20, and 40 ppm. Vanadium toxicity as measured by chick growth was more severe in the iron-deficient animals than in those receiving supplemental iron. The increase in degree of toxicity in the iron-deficient animals was accompanied by an increase in the liver vanadium, both total and concentration. The addition, of vanadium to the diet did not influence the iron concentration of the liver or kidney. Radioisotope, studies with⁴⁸V revealed that the absorption of vanadium was not influenced by the iron concentration of the diet, but that the iron-deficient animals retained more vanadium in the blood and liver and less in the bone than did the iron supplemented animals. It is proposed that the degree of iron saturation of transferrin and ferritin to which vanadium can bind is a possible explanation for the results obtained. Paper No. 10687 of the Journal Series of the NC Agricultural Research Service, Raleigh, NC 27695-7601. The use of trade names implies neither endorsement of the products named nor criticism of similar products not mentioned by the NCARS.     

Improved performance and immunological responses as the result of dietary genistein supplementation of broiler chicks

The present study aimed to investigate the effect of supplemental genistein (an isoflavonoid) on performance, lymphoid organs’ development, and cellular and humoral immune responses in broiler chicks. A total of 675-day-old male broiler chicks (Ross 308) were randomly assigned to the five replicate pens (15 chicks each) of nine experimental diets. Dietary treatments included a negative (not-supplemented) control diet, two positive control groups (virginiamycin or zinc-bacitracin, 20 mg/kg), and diets containing 10, 20, 40, 80, 160 and 320 mg/kg of genistein. The cutaneous basophil hypersensivity (CBH) test was measured at day 10 of age after toe web injection with phytohemagglutinin-P. In addition, sera samples were collected after different antigen inoculations to investigate antibody responses. At day 28 of age, three randomly selected birds from each pen were euthanized to evaluate the relative weights of lymphoid organs. Results showed that dietary supplementation of both antibiotics increased (P<0.01) feed intake during 1 to 42 days of age. Furthermore, daily weight gain was influenced (P<0.01) by dietary treatments throughout the trial, so that the birds fed on antibiotics and 20 to 80 mg/kg genistein diets revealed the greater weight gains compared with other experimental groups. The best (P<0.05) feed conversion ratio assigned to the birds fed on diets containing antibiotics and moderate levels (40 to 80 mg/kg) of genistein. Although the relative weights of thymus (P<0.05) and bursa of Fabricius (P<0.01) were greater in birds fed on genistein-supplemented diets compared with antibiotics-supplemented birds, the spleen weight was not affected by experimental diets. Similarly, CBH response and antibody titers against Newcastle and infectious bronchitis disease viruses were markedly (P<0.05) greater in chicks fed on diets supplemented with 20 to 80 mg/kg of genistein. Interestingly, the higher dosages of genistein suppressed CBH and antibody responses to the levels seen by control and antibiotics chicks. Dietary inclusion of genistein increased (P<0.05) lymphocytes and subsequently reduced (P<0.01) heterophil to lymphocyte ratio. The present findings indicate that dietary genistein supplementation at the levels of 20 to 80 mg/kg not only improves growth performance, but also could beneficially affect immunological responses in broiler chicks.     

Effects of dietary pyrroloquinoline quinone disodium on growth performance,carcass yield and antioxidant status of broiler chicks

Pyrroloquinoline quinone (PQQ), a putative essential nutrient and redox modulator in microorganisms, cell and animal models, has been recognized as a growth promoter in rodents. Growth performance, carcass yield and antioxidant status were evaluated on broiler chickens fed different levels of PQQ disodium (PQQ.Na₂). A total of 784 day-old male Arbor Acres (AA) broilers were randomly allotted into seven dietary groups: negative control group (NC) fed a basal diet without virginiamycin (VIR) or PQQ.Na₂; a positive control group (PC) fed a diet with 15 mg of VIR/kg diet; and PQQ.Na₂ groups fed with 0.05, 0.10, 0.20, 0.40 or 0.80 mg PQQ.Na₂/kg diet. Each treatment contained eight replicates with 14 birds each. The feeding trial lasted for 6 weeks. The results showed that chicks fed 0.2 mg PQQ.Na₂/kg diet significantly improved growth performance comparable to those in PC group, and the feed efficiency enhancement effects of dietary PQQ.Na₂ was more apparent in grower phase. Dietary addition of PQQ.Na₂ had the potential to stimulate immune organs development, and low level dietary addition (<0.1 mg/kg) increased plasma lysozyme level. Broilers fed 0.2 mg PQQ.Na₂/kg diet gained more carcasses at day 42, and had lower lipid peroxide malondialdehyde content and higher total antioxidant power in plasma. The results indicated that dietary PQQ.Na₂ (0.2 mg/kg diet) had the potential to act as a growth promoter comparable to antibiotic in broiler chicks.     

Effect of Dietary Vanadium on Intestinal Microbiota in Broiler

The purpose of this 42-day study was to examine the effect of dietary vanadium on intestinal microorganism diversity in the duodenum, ileum, cecum, and rectum segments of broilers by the plate count and polymerase chain reaction?Cdenaturing gradient gel electrophoresis (DGGE). A total of 420 1-day-old avian broilers were divided into six groups and fed on a control diet or the same diet supplemented with vanadium at the doses of 5, 15, 30, 45, and 60?mg/kg in the form of ammonium metavanadate. In comparison with control group, the dietary vanadium at the doses of 45 and 60?mg/kg could decrease the counts of Bifidobacterium spp. in the intestinal tract at 21 and 42?days of age. With increasing level in dietary vanadium, the counts of Escherichia coli were significantly increased in the ileum, cecum, and rectum and were decreased in the duodenum at 21 and 42?days of age. However, the counts of Lactobacilli were decreased in the cecum and rectum and increased in the ileum of 45 and 60?mg/kg groups. The colonization of these three bacteria could be affected by dietary vanadium. DGGE analysis showed that the number of bands in duodenum, ileum, cecum, and rectum were obviously decreased in the 30, 45, and 60?mg/kg groups at 21 and 42?days of age. In conclusion, the dietary vanadium in excess of 30?mg/kg could alter the amount and diversity of intestinal bacteria in broilers, implying that the structure and initial balance in the intestinal microbiota were disrupted.     

Dietary boron modified the effects of magnesium and molybdenum on mineral metabolism in the cholecalciferol-deficient chick

The metabolic effects of dietary boron, magnesium, and molybdenum on mineral metabolism in the cholecalciferol-deficient chick, with emphasis on growth cartilage histology, were studied. One-day-old cockerel chicks were assigned to groups in a fully-crossed, three factor, 2 x 2 x 2 design. The basal diet was based on ground corn, high-protein casein, and corn oil and contained 125 IU cholecalciferol (inadequate), 0.465 mg B, 2.500 mg Mg, and 0.420 mg Mo/kg. The treatments were the supplementation of the basal diet with B at O or 3; Mg at 300 (inadequate) or 500 (adequate); and Mo at 0 or 20 mg/kg. At d 25, B depressed mortality, alleviated the cholecalciferol-deficiency induced distortion of the marrow sprouts (MS) of the proximal tibial epiphysial plate, and elevated the numbers of osteoclasts within the MS. Adequate Mg exacerbated the cholecalciferol-deficiency induced bone lesions. Mo widened the MS markedly. In Mg-deficient chicks, B elevated plasma Ca and Mg concentrations and growth, but inhibited initiation of cartilage calcification; B had the opposite effect in Mg-adequate chicks. An interaction among B, Mg, and Mo affected plasma uric acid and glucose concentrations. B may function to modify mineral metabolism in cholecalciferol deficiency, suppressing bone anabolism in concurrent Mg deficiency and bone catabolism in concurrent Mg adequacy.     

The effects of betamethasone, low calcium and low phosphorus diets on growth in chicks

The effects of oral betamethasone (25 micrograms/kg/d), low calcium (1 g/kg), and low phosphorus (2,5 g/kg) diets on weight gain were investigated in 513 growing chicks. The chicks were divided according to initial weight into a lower weight group (less than 100 g each) and a higher group (more than 100 g each). The increases in weight were recorded after periods of 7, 14 and 21 days. The increases in weight in the older chicks (high weight group) were less than in the younger chicks. There was a greater reduction in rate of growth in chicks fed the low phosphorus diet than in those fed the low calcium diet, particularly in the older birds. Betamethasone administration also reduced the rate of growth but this was not additive to the effect of a low calcium diet. In contrast, the greatest reduction in growth rate was observed in the chicks fed the low phosphorus diet and given betamethasone.     

The Effect of Dietary Vanadium on Cell Cycle and Apoptosis of Liver in Broilers

The objective of this study was to clarify the effects of dietary vanadium on cell cycle and apoptosis of liver in broilers. Four hundred and twenty one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60?mg/kg vanadium supplied as ammonium metavanadate for 42?days. As tested by flow cytometry, hepatocytes in G (0)/G (1) phase were significantly increased in number in 45 and 60?mg/kg groups, and hepatocytes in S, G (2)?+?M phases in 45 and 60?mg/kg groups and the proliferation index of hepatocytes in 30, 45, and 60?mg/kg were markedly decreased when compared with those of control group. At the same time, the percentage of hepatocyte apoptosis was markedly increased in both 45 and 60?mg/kg groups. The results showed that dietary vanadium in the range of 45?～?60?mg/kg caused cell cycle arrest and apoptosis of hepatocytes in broilers.     

Effect of dietary copper on vanadate toxicity in chicks

The addition of copper to a corn-soybean diet at levels of 200 mg/kg and above lessened the growth-retarding effect of vanadate for chicks. This interaction between vanadate and copper was evident in bothad libitum-fed chicks and chicks in which feed consumption was restricted to approximately equal amounts. The ameliorating effect of copper was not accompanied by changes in the femur levels of vanadium nor by changes in the hepatic or renal glutathione concentrations. Zinc added at 515 mg/kg of diet had no effect on the toxicity of vanadium. Sodium sulfate added at a level to supply the same amount of sulfate, as supplied by 500 mg/kg copper sulfate, was without effect on the vanadate-induced growth depression. The underlying mechanism of the interaction of copper and vanadium is not known, but it does not lie in changes in feed consumption or organ burdens of vanadium, as represented by the femur vanadium concentrations.     

The role of vitamin E or clay in growing Japanese quail fed diets polluted by cadmium at various levels

This study was conducted to verify whether vitamin (Vit) E or natural clay as feed additives has the potential to modulate the deleterious effects resulting from exposure to cadmium (Cd) in growing Japanese quail. 648 Japanese quail chicks (1 week old) were used to evaluate the effects of dietary Cd (0, 40, 80 and 120 mg/kg diet) and two levels of Vit E (0, 250 mg/kg diet) or two levels of natural clay (0 and 100 mg/kg diet) to study the influences of Cd, Vit E, clay or their different combinations on growth performance, carcass traits, some blood biochemical components and Cd residues in muscles and liver. Live BW and weight gain of quails were linearly decreased with increasing dietary Cd levels. Moreover, feed conversion was significantly worsened with increasing Cd level. Mortality percentage was linearly increased as dietary Cd level increased up to 120 mg/kg diet. Carcass percentage was linearly decreased as dietary Cd level increased. While, giblets percentage were linearly and quadratically differed as dietary Cd level increased. Cd caused significant changes in total plasma protein, albumin, globulin, A/G ratio, creatinine, urea-N and uric acid concentrations as well as ALT, AST and ALP activities. Increasing dietary Cd level was associated with its increase in the muscles and liver. Dietary supplementation with 250 mg of Vit E/kg diet or 100 mg clay/kg improved live BW, BW gain and feed conversion when compared with the un-supplemented diet. Quails fed diet contained 250 mg Vit E/kg and those fed 100 mg clay/kg had the highest percentages of carcass and dressing than those fed the un-supplemented diet. Blood plasma biochemical components studied were better when birds received 250 mg of Vit E/kg diet and those received 100 mg clay/kg. Cd residues in the muscles and liver were significantly less in the birds had 250 mg of Vit E/kg or those received 100 mg clay/kg diet than those un-supplemented with Vit E. Growth performance traits and blood plasma biochemical components studied were significantly affected linearly by the interactions among Cd and each of Vit E and clay levels. In conclusion, the present results indicate that the deleterious effects induced by Cd plays a role in decreasing the performance of Japanese quail and that dietary supplementation with natural clay or Vit E may be useful in partly alleviating the adverse effects of Cd.     

Evidence that sodium deprivation influences vitamin D dependent rat renal calcium binding protein

In order to provide some insight concerning the role of renal calcium binding protein (CaBP) in the functioning of the mammalian kidney, the response of renal CaBP to dietary alterations was examined. Three week old rats were fed diets deficient in calcium, phosphorous or sodium supplemented with vitamin D for a four week period. The specific activity of renal CaBP (as measured by the chelex resin assay; Ca²⁺ bound protein/Ca²⁺ bound resin per mg protein) in the 28,000 M_r region was found to increase four fold in rats fed the low phosphorus diet and two fold rats fed the low calcium diet when compared to rats fed the control diet. Renal CaBP/mg protein from rats fed the low sodium diet decreased 50% from the control values. Changes in renal CaBP were confirmed by polyacrylamide gel analysis of the 28,000 M_r fraction by densitometric tracing using a purified CaBP marker. The greater response to dietary phosphorus restriction suggests that renal CaBP may be regulated by a mechanism different from that of intestinal CaBP. The decrease in renal CaBP in rats fed the low sodium diet suggests for the first time that sodium is required for vitamin D dependent distal tubular calcium transport processes.     

Manganese alters mitochodrial integrity in the hearts of swine marginally deficient in magnesium

It was previously reported that pigs marginally deficient in magnesium (Mg) and fed diets high in manganese (Mn) died suddenly with signs of sudden cardiac death. Manganese, which has properties similar to Mg, may exacerbate Mg-deficiency and be accumulated by mitochondria resulting in ultrastructural damage. The objective of this study was to determine whether deaths of the type previously observed were mediated by adverse interactions of Mn and Mg resulting in ultrastructural damage to the myocardium, alterations in electrocardiographic recordings and tissue retention of Mn, Mg and calcium (Ca). Forty-eight pigs were fed one of six diets in a 2 X 3 factorial arrangement of Mg (100 or 1000 mg Mg/kg) and Mn (5, 50 or 500 mg Mn/kg) for 8 weeks. Left ventricle muscle samples were collected for examination by transmission electron microscopy. No differences in heart muscle ultrastructure were observed between pigs fed low and adequate dietary Mg. However, marked myocardial necrosis and mitochondrial swelling were observed in pigs fed high dietary Mn when combined with low Mg. Feeding low dietary Mg elevated minimum (P < 0.01), maximum (P < 0.05) and average (P < 0.001) heart rates. Low dietary Mg resulted in a 55% probability of a ventricular beat being recorded (P = 0.05) and lower Mg (P < 0.02) and Ca (P < 0.04) contents in heart atria and ventricles. These results suggest that high Mn, when fed in combination with low Mg, disrupts mitochondrial ultrastructure and is associated with the sudden deaths previously reported.     

The effect of an acute phase response on tissue carotenoid levels of growing chickens (Gallus gallus domesticus)

Plasma, liver and skin carotenoids decrease following infectious disease challenges. Since these challenges often involve substantial host pathology and chronic immune responses, the mechanism underlying altered carotenoid deposition is unclear. Therefore, changes in tissue carotenoid levels were examined during an acute phase response induced by lipopolysaccharide (LPS) or interleukin-1 (IL-1). In two experiments, chicks were hatched from carotenoid-deplete eggs (n=28, n=64, respectively) and fed 0, 8 or 38 mg carotenoids (lutein+canthaxanthin)/kg diet. For chicks fed 38 mg carotenoids, but not those fed 0 or 8 mg, LPS generally reduced plasma lutein, canthaxanthin and total carotenoids (P<0.05), and liver lutein, zeaxanthin, canthaxanthin and total carotenoids (P<0.05). Additionally, LPS reduced thymic total carotenoids (P=0.05) and increased thymocyte lutein (P=0.07), zeaxanthin (P=0.07) and total carotenoids (P=0.07). Finally, LPS increased bursal canthaxanthin (P<0.01), but had no effect on shank carotenoids (P>0.5). In chicks hatched from carotenoid-replete eggs (n=36) and fed dietary lutein (38 mg/kg diet), LPS reduced plasma and liver zeaxanthin and liver total carotenoids (P<0.05); IL-1 reduced plasma and liver lutein, zeaxanthin and total carotenoids (P<0.05). Therefore, an acute phase response plays a role in reduced tissue carotenoids during infectious disease.     

Influence of probiotic supplementation on blood parameters and growth performance in broiler chickens

Effects of commercial probiotic (Bactocell®) on growth performance and blood parameters were evaluated. A total of 800 one day-old Ross broiler chicks were raised over 42 days. Chicks were wing-banded, weighed individually and randomly allocated into four equally major groups each having two replicates. Chicks of group 1 (control group) were fed the starter and finisher diets that did not supplemented with probiotic. The chicks of groups 2, 3, and 4 were fed the control starter and finisher diets supplemented with 1.6 g, 1 g and 0.8 g of probiotic per kg feed, respectively. Weekly body weight, feed consumption and feed conversion were measured. Blood parameters at 1, 4 and 6 weeks of age including packed cell volume (PCV), haemoglobin (Hb), total protein, albumin, total lipid and cholesterol were determined. All birds were kept under similar environmental, managerial and hygienic conditions. The results of the current study revealed that there was no significant change for Hb and PCV concentrations among different groups at all studied times. Also, total protein, lipids and albumin concentrations were not affected by probiotic supplementation. Chicken fed a diet containing various levels of probiotic showed a significant decrease (p ⩽ 0.05) in cholesterol concentration compared to control group. Probiotic supplementation significantly increased the body weight and daily weight gain of broiler chicks at late ages (3–6 weeks). Also, the birds fed on probiotic levels 1 and 0.8 g/kg diet exhibited higher body weight among chicken groups at 6 weeks of age. Improved feed conversion was noticed in birds fed a diet supplemented with probiotic. There was no significant difference in mortality rate among groups. We concluded that use of selected commercial probiotic resulted in improved performance parameters and reduced serum cholesterol in broiler chickens. Moreover, supplementation of the probiotic to broilers in the levels of 1 and 0.8 g/kg diet was found to be better than control and 1.6 g/kg level indicating that increasing dietary probiotic level does not has the best performance.     

Effects of dietary vitamin B₁ (thiamine) and magnesium on the survival, growth and histological indicators in lake trout (Salvelinus namaycush) juveniles

An interaction of two essential nutrients, thiamine and magnesium (Mg) has been documented in in vitro and in vivo studies in mammalian metabolism. However, the role of this association in poikilothermic vertebrates, such as fish, remains elusive. The purpose of this study was first to investigate the effects of dietary thiamine and Mg, and their interaction in lake trout and second to better understand the mechanism leading to early mortality syndrome (EMS), which is caused by a low thiamine level in embryos of many species of salmonids in the wild. Semi-purified diets (SPD) were prepared to accomplish 2 × 2 factorial design that were either devoid of or supplemented with thiamine mononitrate (20 mg/kg diet), magnesium oxide (700 mg/kg diet), or both. Lake trout alevins at the swim-up stage were fed for 10 wk one of the SPD diets or a commercial diet at the same rate (2.0-1.5%) based on recorded biomass. Our results showed that the concentrations of thiamine in the trunk muscle and Mg of whole body were closely associated with the dietary level of two nutrients. The interaction of low dietary Mg and thiamine resulted in apparently worsened overt symptoms of thiamine deficiency in lake trout leading to a higher mortality of fish during the seven week long trial (P<0.05). The fish fed a thiamine-devoid and Mg-supplemented diet were presumed to survive longer (10 wk) than the fish fed diets devoid of both nutrients (discontinued after 7th wk due to high mortality). However, we did not observe histopathological changes in the brain and liver corresponding to thiamine concentrations in tissues. These data suggest that Mg enhanced utilization of the thiamine remaining in the fish body and its interdependence was consistent with observations in mammals. EMS severity might be worsened when Mg is deficient in parental diets (and consequently in yolk sac) and/or first feed.     

Dietary High Vanadium Causes Oxidative Damage-Induced Renal and Hepatic Toxicity in Broilers

The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; and 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30–60 mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers.