Effects of high but nontoxic dietary manganese and iron on their metabolism by calves

Sixteen male Holstein calves were fed one of four diets for 18 days in an experiment consisting of 0 and 1000 ppm supplemental manganese and 0 and 1000 ppm added iron as manganese carbonate and ferrous carbonate. The control diet contained 55 ppm manganese and 220 ppm iron. All calves were dosed orally 48 h prior to sacrifice with 500 muCi of manganese-54. Small intestinal iron was less in calves fed a high manganese diet, a possible interaction of these two elements at the absorption site. Feeding a high manganese diet tended to decrease iron (total) concentrations in liver and pancreas. When the high manganese diet was supplemented with additional iron, antagonistic effects of manganese on iron were eliminated. Neither iron nor manganese concentrations in tissues were affected by an increase of dietary iron. Manganese-54 content of tissue was reduced by the high manganese diet but was not affected by dietary iron. Total manganese and iron in feces fairly closely reflected dietary intake of each element with no evidence of interaction. Calves fed the high iron diet excreted less manganese-54 in their feces over 2 days. Total iron in blood serum was not affected significantly by the dietary treatments.     

Effect of excess iron in milk replacer on calf performance

Milk replacers containing 100, 500, 1000, 2000, or 5000 ppm iron were fed to 3-d-old calves for 6 wk to estimate the lowest amount of dietary iron (added as ferrous sulfate) that would reduce calf performance. Calves tolerated all iron treatments except 5000 ppm. At this intake calves showed reduced weight gains, DM intake, feed efficiency, and digestibility of DM and protein. There were no other signs of iron toxicity and no gross abnormalities were found on postmortem examination. Percent of dietary iron in feces increased with higher dietary iron and ranged from 65 to 84%. Elevated iron intakes caused relatively small increases in iron concentration of blood plasma, bile, kidney, heart, and muscle but marked increased in spleen and liver iron, particularly in liver for the 2000 and 5000 ppm treatments. At 100 ppm iron intake, nonheme iron in liver, spleen, and kidney was composed of similar proportions of ferritin and hemosiderin, but at 5000 ppm iron intake, hemosiderin predominated in these tissues. Thus, the preruminant calf tolerated between 2000 and 5000 ppm iron in milk replacer. At toxic iron intake, calf performance and feed efficiency were reduced; there was a characteristic change to higher liver than spleen iron; and hemosiderin became the predominant iron storage compound in both tissues.     

Biological availability of zinc from inorganic sources with excess dietary calcium

The effects of chemical form of supplemental zinc and elevated dietary calcium on intestinal absorption of zinc were measured. Calves and rats were fed diets low in zinc, and zinc availability was the percentage increase of zinc in plasma with dietary supplementation of zinc. Availabilities of zinc supplied as zinc chloride, zinc sulfate, zinc oxide, and zinc carbonate were comparable in both calves and rats. Elevated amounts of dietary calcium as ground limestone reduced absorption of zinc in rats fed soy-protein but had no effect on absorption of zinc in the lactating cow. Thus, for cows consuming large amounts of calcium, an increase in the concentration of zinc beyond 40 ppm of the diet appears unnecessary.     

Supplementation of Copper as Copper Sulfate or Copper Proteinate for Growing Calves Fed Forages Containing Molybdenum

Holstein calves (age > 12 wk old) were assigned to dietary treatments of 1) no supplemental copper, 2) copper proteinate, or 3) copper sulfate. The copper supplements were incorporated into premixes and added to a pelleted concentrate. The concentrates were fed at 1.8 kg per head per d and contained 5, 19, or 19 ppm copper and .6 ppm molybdenum by analysis. All calves were fed a grass hay free-choice, which contained 1 ppm copper and 5 ppm molybdenum. Ratios of copper to molybdenum were .9, 2.8, and 2.8 for diets 1, 2, and 3, respectively. Copper concentrations in plasma were significantly greater at wk 12 in calves fed copper proteinate than control or calves supplemented with copper sulfate. Liver copper also was higher at wk 12 in calves fed copper proteinate. Final body weights, plasma zinc, plasma iron, hemoglobin, and hematocrit were not affected by treatment. Bioavailability of dietary copper from copper proteinate was greater than from copper sulfate for calves fed diets containing molybdenum.     

Dietary fibers and supplementary iron in a milk replacer for veal calves

Thirty 1-wk-old male Holstein calves were allotted randomly to six groups into a 3 X 2 factorial design. The control diet was skim milk, whey, tallow, vitamins, and minerals. Either Alpha-Floc or pectin was added at 5% dry matter. Supplementary iron was added at 30 and 50 ppm (dry basis). The six diets were fed for 14 wk. Calves without supplementary iron were mildly anemic at 6 wk and severely at 14 wk (7 and 5 g/dl hemoglobin). At 14 wk, both fibers had decreased blood hemoglobin in calves given supplementary iron. Feed refusal began at 8 wk with the appearance of anemia for calves unsupplemented with iron, but both Alpha-Floc and pectin decreased feed refusal. Supplementary iron practically eliminated feed refusal. Supplementary iron improved average daily gain and feed conversion, but dietary fibers had no effect. Adding Alpha-Floc and pectin to the diets reduced frequency of diarrheic feces. Mean carcass weight of calves fed supplementary iron was 11.6% higher than that of unsupplemented calves. Supplementary iron decreased liver lipids and increased glutamic oxaloacetic transaminase activity in blood plasma.     

蛋氨酸螯合铁对大鼠肝脏物质代谢相关基因表达的影响

研究缺铁日粮中补充蛋氨酸螯合铁与硫酸亚铁对大鼠铁利用及肝基因表达的影响。20只SD断奶大鼠,建立缺铁大鼠模型,然后均分成两组,分别饲喂加入等量铁(35mg/kg)的蛋氨酸螯合铁和硫酸亚铁日粮,补铁后4、7d后测定体重、血红蛋白,组织器官铁含量及血清总铁结合力;并提取大鼠肝组织总RNA,用Afymetrix基因芯片进行基因表达分析,研究硫酸亚铁与蛋氨酸螯合铁对缺铁大鼠物质代谢基因表达的差异。结果表明,蛋氨酸螯合铁组大鼠增重明显高于硫酸亚铁组,血红蛋白、总铁结合力含量有升高趋势。与硫酸亚铁组比较,蛋氨酸螯合铁组肝组织珠蛋白与转铁蛋白合成相关基因,以及胆固醇合成,脂肪代谢、ATP合成相关基因明显上调。补充蛋氨酸螯合铁动物铁代谢和物质代谢存在显著差异。     

Availability of Soybean Hull Iron Fed to Humans in a Mixed, Western Meal

Century soybeans were grown in a greenhouse and labeled by stem injection of iron-59. The intrinsically labled soybean hulls were incorporated into bread rolls and fed in mixed meals containing beef to six free-living female volunteers. Iron-59 retention, measured by whole body counting of these volunteers, was compared with retention from similar meals containing extrinsically labeled soybean hulls or bakery grade ferrous sulfate. Iron-59 retention averaged 23% from meals containing the intrinsically labeled soybean hulls, 18% from meals containing extrinsically labeled soybean hulls, and 22% from meals containing bakery grade ferrous sulfate. There were no statistically significant differences in retention among the various iron sources, indicating that soybean hulls were an excellent source of iron for bread enrichment.     

The effects of different levels of dietary lead on zinc metabolism in dairy calves

The effects of feeding diets containing 500 or 1500 ppm added lead as lead sulfate on zinc and zinc-65 metabolism in Holstein bull calves were investigated. Zinc absorption was slightly (not significantly) reduced in the calves fed lead. Fecal zinc excretion was increased by the lead diets by day 24 of the experiment. Dietary lead had no significant effect on zinc in blood. Except for the tibia, muscle, and brain, stable zinc decreased in all tissues of calves fed the 1500 ppm lead diets, and differences were significant in pancreas, heart, and testicle. A significant decrease was noted in pancreatic zinc in pancreas of calves fed 500 ppm lead. Tissue zinc-65 concentrations were decreased significantly by lead in the tibia and muscle. Intestinal tissue zinc was not affected materially by lead. Dietary lead had very little effect on cellular distribution of zinc in the liver and kidney. In the mucosal cells of the small intestine, lead increased zinc-65 in the cytosol while decreasing it in the crude nuclear fraction. This effect occurred in a linear fashion in all three sections of the small intestine as dietary lead increased.     

Effects of dietary zinc upon tissue zinc and percent unsaturated plasma-zinc binding capacity.

Calves were fed 520 ppm zinc for 21 days, then placed on a low zinc diet (20 ppm zinc) for 35 days to determine the biological availability of zinc reserves of tissue. Concentrations of zinc in liver and kidney were elevated greatly by feeding high dietary zinc for 21 days and continued to increase with time. On the low zinc diet, the tissue burden of zinc decreased within 35 days to those comparable to calves initially fed low zinc. Likewise, both zinc in plasma and percent capacity of unsaturated plasma for binding zinc were near negative controls 21 days after removal of calves from high zinc diets. Tissue stores of zinc will not maintain adequate zinc in blood for extended periods, and hence, they probably will not sustain optimal feed intakes and growth rates of calves on low-intakes of zinc.     

Effects of amount of colostrum replacer,amount of milk replacer,and housing cleanliness on health,growth, and intake of Holstein calves to 8 weeks of age

Newborn Holstein bull calves (n = 96) were assigned randomly at birth to receive 150 g (C150) or 450 g (C450) of IgG in the first 24 h of life from a lacteal-based colostrum replacer in 2 trials. Mass of product fed was 500 and 1,500 g, respectively. Replacer was reconstituted with warm water and administered by esophageal feeder at approximately 1, 6, and 12 h of age. Thereafter, calves were fed 2 L of whole milk twice daily at approximately 0700 and 1700 h until transported to the experimental facility at 2 to 3 d of age. Calves fed C450 had greater serum total protein and IgG concentrations at 2 to 3 d of age. Failure of passive transfer of immunity (serum IgG <10 g/L) was detected in 100 and 11% of calves fed C150 and C450, respectively. Calves (n = 48) in trial 1 were assigned randomly within colostrum group to receive 0.68 kg/d of milk replacer (MR) for 42 d, and then 0.34 kg/d for 7 d (moderate MR, MMR) or 1 kg/d of MR for 5 d, 1.36 kg/d for 37 d, and 0.68 kg/d for 7 d (high MR, HMR). Starter and water were available for ad libitum consumption. Calves fed HMR had greater average daily gain, higher average fecal scores, more days with abnormal fecal scores, and more medical days than calves fed MMR. Calves fed HMR also had lower starter intake and tended to have lower gain-to-feed ratio than calves fed MMR. Calves fed C450 and MMR began eating calf starter earlier and ate more starter than other groups from 3 wk. In trial 2, calves (n = 48) were assigned randomly within colostrum group to housing in nursery pens bedded with clean, dry straw (clean bedding) or soiled straw used in previous studies (dirty bedding). Milk replacer was fed at 0.68 kg/d for 39 d, and then 0.34 kg/d for 3 d along with free-choice texturized starter and water. Calves fed C450 had fewer days with abnormal fecal scores and days with medical treatments compared with calves fed C150. Calves housed in dirty bedding tended to grow more slowly and have lower gain-to-feed ratio than calves housed with clean bedding. Temporal changes in serum IgG and total protein varied by treatment. Serum IgG in calves fed C150 varied little from 0 to 4 wk and increased thereafter, whereas IgG in calves fed C450 declined to 4 wk (estimated half-life = 23.9 d) and increased thereafter. Differences in serum IgG concentrations caused by feeding different amounts of colostrum replacer did not markedly affect growth or intake when calves were fed different amounts of milk replacer or when they were housed with clean or dirty bedding.     

Tolerance of the calf for excess copper in milk replacer

Calves were fed milk replacer containing 10, 50, 200, 500, or 1000 ppm Cu, from 3 d to 45 d of age, to estimate the Cu concentration that would adversely affect calf performance. Weight gains and feed efficiency were similar for 10 and 50 ppm Cu but were reduced at 200 and 500 ppm Cu. All calves survived 500 ppm Cu and lower intakes, but only 4 of 7 calves survived the 1000 ppm concentration. Typical clinical symptoms of chronic Cu toxicity and hemolytic crisis were evident for the 1000 ppm calves before death. Additional 1000 ppm Zn prevented deaths for 1000 ppm Cu, but calf performance was poor. Increased Cu intakes elevated plasma ceruloplasmin and glutamic oxalacetic transaminase activity, reduced packed cell volume (hematocrit), markedly increased fecal excretion of Mo and Zn, increased Cu concentration of liver, muscle, heart, blood, and bile, and decreased Mo and Zn in liver. We found 50 ppm Cu a safe intake where milk replacer contained 48 ppm Zn and 1.1 ppm Mo. However, at lower intakes of these elements, and for longer feeding periods than 6 wk, the calf may be much more susceptible to Cu toxicity.     

Long-term feeding of high zinc sulfate diets to lactating and gestating dairy cows

Thirty dairy cows, fed a control diet consisting of silage and concentrates, were given either 0, 1000, or 2000 ppm of supplemental Zn (DM basis), from zinc sulfate monohydrate (ZnSO4.H2O) for most of a lactation. Feeding 2000 ppm Zn decreased milk yield and feed intake after several weeks. Some cows were affected more severely than others. Generally, primiparous animals were more tolerant of the high Zn diet than multiparous cows. Milk Zn was materially higher for cows fed 1000 ppm added Zn than controls. With 2000 ppm Zn, milk Zn was elevated further but returned to control values when the high Zn diet was discontinued. Plasma Zn was higher in cows fed supplemental Zn with the increase from 1000 to 2000 greater than that for the first addition. Plasma Cu was lower in cows feed 2000 ppm Zn but milk Cu was not reduced. Milk fat content was not affected, but protein and SNF were reduced by the 12th wk with the 2000 ppm Zn diet. There was no apparent effect on long-term health or performance after the cows were removed from the 2000 ppm Zn diet. Except for lower calf weights with 2000 ppm Zn, reproductive performance was not measurably affected by the dietary treatments. The 1000 ppm added Zn diet had no adverse effect on the cows in any parameter measured.     

Effects of diet on rumen proliferation and fecal shedding of Escherichia coil O157:H7 in calves

Calves inoculated with Escherichia coli O157:H7 and fed either a high-roughage or high-concentrate diet were evaluated for rumen proliferation and fecal shedding of E. coli O157:H7. Calves fed the high-roughage diet had lower mean rumen volatile fatty acid concentrations and higher rumen pH values than did calves fed the high-concentrate diet. Despite these differences in rumen conditions, the calves fed the high-roughage diet did not have greater rumen populations of E. coli O157: H7 and did not exhibit increased or longer fecal shedding compared with the calves fed the high-concentrate diet. Two calves shedding the highest mean concentrations of E. coli O157:H7 were both fed the high-concentrate diet. There was a significant (P < 0.05) positive correlation between fecal shedding and rumen volatile fatty acid concentration in calves fed a high-concentrate diet. The effects of diet on E. coli O157:H7 proliferation and acid resistance were investigated using an in vitro rumen fermentation system. Rumen fluid collected from steers fed a high-roughage diet, but not from steers fed a high-concentrate diet, supported the proliferation of E. coli O157:H7. Rumen fluid from steers fed a high-concentrate diet rapidly induced acid resistance in E. coli O157:H7. The impact of diet on fecal shedding of E. coli O157:H7 is still unclear and may depend on dietary effects on fermentation in the colon and on diet-induced changes in the resident microflora. However, rapid development of acid tolerance by E. coli O157:H7 in the rumens of calves fed high-concentrate diets, allowing larger populations to survive passage through the acidic abomasum to proliferate in the colon, may be one factor that influences fecal shedding in cattle on feed.     

Bioavailability of iron in goat milk compared with cow milk fed to anemic rats

Bioavailabilities of iron from dehydrated whole and skim goat milk were investigated using iron-deficient rats. Hemoglobin regeneration efficiencies were determined as the percent conversion of dietary iron into hemoglobin. The respective hemoglobin regeneration efficiencies for groups fed whole goat milk, whole cow milk, skim goat milk, and skim cow milk were 50.6, 13.1, 26.0, and 13.0%, indicating that iron bioavailability of goat milk was greater than cow milk. However, rats fed each milk had negative net increases in hemoglobin concentrations, implying that the iron contents of each milk were not adequate. For animals consuming whole goat milk supplemented with ferrous sulfate, the slope relating hemoglobin iron gained versus iron intake was .95. Respective bioavailabilities relative to ferrous sulfate were 54, 14, 28, and 14% for the four sources of milk. Iron bioavailability of goat milk is superior to cow milk when fed to anemic rats.     

Effects of varying the amounts of dietary calcium on selenium metabolism in dairy calves

Influence of dietary Ca on Se metabolism was studied with 16 intact male Holstein calves averaging 86 kg. Calves were assigned randomly and fed one of four diets containing, .17, .67, 1.31, and 2.35% Ca at 3% of their body weight for 4 wk. The diets contained .062 ppm Se and .34% P. Four days prior to the end of the experiment, calves were dosed orally with radioactive 75Se. Dietary Ca had no significant effect on 75Se absorption. There was a slight curvilinear relationship between apparent 75Se absorption and dietary Ca intakes. Urinary excretion of 75Se and stable Se tended to decrease with increasing dietary Ca, but differences were not significant. No significant differences were found in concentration of 75Se in several tissues. Kidney and liver had the highest concentration with that in kidney being about four times that of liver. Apparent 75Se absorption was decreased 10 to 6%, respectively, in calves fed extremely low and high amounts of Ca, compared with those receiving the requirement (.67% Ca). These small reductions along with a small R2 suggest that dietary Ca probably is of little practical importance relative to Se metabolism in calves.     

Effect of copper loading of preruminant calves on intracellular distribution of hepatic copper, zinc, iron, and molybdenum

The subcellular distribution of Cu, Zn, Fe, and Mo was investigated in liver homogenates from preruminant calves fed control Cu (10 ppm), high Cu (1000 ppm), or high Cu plus high Zn (1000 ppm) milk replacer. For controls, Cu was located primarily in the nuclei and large granule fractions, Zn mainly in the cytosol, and Fe in the cytosol and nuclei fraction; Mo was present in all compartments but least in microsomes. Calves fed high Cu had markedly increased hepatic Cu concentration in the nuclei and cytosol fractions, reduced cytosol Zn, increased nuclei Fe, and decreased Mo concentration in all cell compartments. Feeding high Zn with high Cu (which prevented deaths from high Cu) reversed some changes in hepatic trace element patterns caused by high Cu while initiating new alterations. The marked increase in hepatic Cu and reduced Mo in nuclei and cytosol after Cu loading indicate that these compartments may have a predominant role in the development of Cu toxicity in the preruminant calf.     

Relative Bioavailability of Dietary Iron from Three Processed Soy Products

The relative bioavailability of iron from soy flour (SF), freeze-dried soy beverage (SB) and soy concentrate (SC) was determined utilizing a hemoglobin repletion bioassay. Weanling male rats were fed a low iron depletion diet (3.5 ppm Fe) for 4 wk. For the next 2 wk groups of rats were fed repletion diets containing 0, 6, 12, or 18 ppm added iron from ferrous sulfate, SF, SB, or SC. Slope ratio analysis revealed that the relative iron bioavailabilities from SC (92%) and SF (81%) were not different from the reference standard, ferrous sulfate added to a casein-based diet, whereas that from SB (66%) was significantly less (P<0.01) than the inorganic source of iron. Analysis of results at individual iron levels suggested an iron bioavailability of SC>SF>SB.     

Intracellular distribution of zinc and zinc-65 in calves receiving high but nontoxic amounts of zinc.

The zinc homeostatic control breakdown in cattle fed a high but nontoxic amount of zinc was investigated. Liver copper was decreased by the 600 ppm added dietary zinc indicating altered copper metabolism. However, duodenal copper, liver and duodenal iron and manganese were not affected. Zinc-65 in blood was reduced 90% by the high dietary zinc 48 h following oral zinc-65 dosing. The 600 ppm supplemental zinc increased zinc by 500% in liver, 20 times in pancreas and kidney, and 100% in the duodenum. The increased liver and duodenal zinc was confined largely to the soluble cell fraction. This concentrating of excess tissue zinc in the soluble fraction may be an adaptive mechanism which detoxifies large quantities of zinc and prevents disruption of normal cellular activity.     

Effects of dietary aflatoxin and zinc on enzymes and other blood constituents in dairy calves

Young male Holstein calves were fed diets containing 40 or 640 ppm zinc with 0 or 5 ppm aflatoxin for 3 wk. The aflatoxin mixture contained 80.5% B1 and the calves consumed 143 mg of B1 over 3 wk. Plasma glutamic-oxaloacetic transaminase and alkaline phosphatase concentrations were increased substantially, and lactic dehydrogenase was reduced in aflatoxin-fed calves. Supplemental zinc partially counteracted the effect of aflatoxin on these enzymes. Hemoglobin, packed cell volume, and total solids in blood plasma were increased in aflatoxin-fed calves, but high dietary zinc had no effect on these blood constituents. Glucose in plasma was reduced in calves receiving aflatoxin. High dietary zinc was only partially effective in protecting against the reduced glucose effect for about 1 wk. Total protein, albumin, globulin, ratio of albumin/globulin in blood plasma, and liver lipid were not affected by aflatoxin. Several enzymes and blood constituents are affected by aflatoxin in calves. The protection of zinc against aflatoxicosis appears to be no more than a partial effect.