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Zinc metabolism was studied in Zn-deficient and control Holstein calves over a 2-mo period following a single oral or i.v. 65Zn dose. In both orally and i.v. dosed animals, all gastrointestinal tissue sections from Zn-deficient animals contained more 65Zn than comparable tissues of controls. Contents of proximal small intestinal sections of Zn-deficient calves contained more 65Zn 8 to 10 wk after dosing than did those from controls; however, the reverse occurred in the distal small intestine, cecum, and large intestine. With both dosing methods, Zn-deficient calves retained more 65Zn throughout the study. Daily 65Zn excretion rate as a percentage of that retained declined for 6 wk after dosing, indicating a constantly increasing biological half-life. For deficient calves, the biological half-life was about 500 d in the later weeks of the experiments. In orally dosed, Zn-deficient animals, specific activity of fecal 65Zn exceeded that of serum Zn throughout the study. This shows a shortcoming in the basic assumption of measuring endogenous Zn loss from fecal and serum specific activities and total fecal stable Zn. Thus, endogenously excreted Zn is not representative of that remaining.

Eighty female Holstein calves were used to examine the effects of high amounts of added dietary Fe as ferrous carbonate on performance of young dairy animals. Experimental starters containing either 0, 500, 1000, 2000, or 4000 ppm supplemental Fe as ferrous carbonate were fed for 8 wk beginning at 1 wk of age. The control starter contained 170 ppm Fe, all of which came from the major feed ingredients. The calves were fed limited amounts of whole milk for the first 5 wk. Weight gains and feed consumption were not consistently reduced at the higher amounts of supplemental Fe, but the lowest average values were at 2000 ppm added Fe. However, during wk 7 and 8, when no milk was fed, calves fed 2000 or 4000 ppm had reduced feed intakes and weight gains. Feed efficiency and health of the calves were not affected by supplemental Fe. The results of this study indicate that the performance of calves was not affected appreciably by 4000 ppm supplemental Fe as ferrous carbonate from a pure lenses of siderite ore. This is a higher tolerance than shown previously for ferrous sulfate Fe.

Zinc-65 was injected directly into various sites throughout the small intestine of Holstein calves fed a low zinc diet. Zinc absorption was determined by comparing zinc-65 content of blood, liver, kidney, lung, heart, pancreas, rib, muscle, and other tissues. Tissue zinc-65 was plotted against site of injection expressed as percentage of intestinal length from proximal to distal ends. Zinc absorption occurred throughout the small intestine with the amount absorbed per centimeter of length about equal throughout the small intestine. This is in contrast to conclusions from studies of rats indicating more absorption in the proximal part of the small intestine. The difference appears to have been due to artifacts in the procedures with rats. However, species and dietary differences may have affected relative findings between this and earlier work.

Young dairy calves were fed diets containing 40 or 640ppm zinc with 0 or 5ppm aflatoxin for 3 wk. The aflatoxin mixture contained 80.5% B 1 , 19.5% G 1 , and less than .1% B 2 and G 2 . The aflatoxin fed calves exhibited characteristics signs of aflatoxicosis which included reduced feed intake, weight gains, nitrogen balance, pulse rate, and respiration rate, Feed intake and weight gains recovered some during the 3rd wk. No gross abnormalities were observed in the liver or other organs at autopsy. Addition of 600ppm zinc to diets containing aflatoxin did not alleviate the toxic conditions. Effects of aflatoxin or zinc metabolism were investigated during the 3rd week of treatment through oral dosing of zinc-65. Absorption of zinc-65 was slightly lower in aflatoxin-fed calve. However, the aflatoxin effect on absorption of zinc-65 was less than that of high dietary zinc. Retention of zinc-65 in small intestinal tissue was increased in aflatoxin-fed calves, but concentrations in other tissues were not affected. Stable zinc was reduced in liver and increased in kidney and three sections of the small intestine. Further research is needed to define more clearly the relationship of zinc to aflatoxin in dairy calves.

Chloride deficiency signs were produced in young Holstein calves by a low chloride diet (.063% chlorine) and daily removal of chloride in abomasal contents. General clinical signs included anorexia, weights loss, lethargy, mild polydipsia, and mild polyuria. In latter stages of the deficiency, severe eye defects (scleral injection, sunken eyes, scaliness around eyes) and reduced respiration rate became evident. Feces contained varying amounts of blood and mucus. The chloride imbalance resulted in severe alkalosis and hypochloremia leading to secondary hypokalemia, hyponatremia, and azotemia. All deficient calves died after 24, 28, 38, and 46 days of treatment. Chloride concentrations of plasma in each of the calves just prior to death were similar at 31 to 35 meq/liter, which compares with normal 96 meq/liter. One additional calf made chloride deficient was recovered to normal health in 9 days following a single treatment with salt water and feeding of control diet containing .48% chlorine. Control calves fed a diet with .48% chlorine and which also had their abomasal contents removed daily grew normally and exhibited no deficiency signs. When dietary chloride was adequate, removal of abomasal contents (and chlorine) had no adverse effects on the animals.

Ten male Holstein calves were fed diets with or without 5% added animal fat in combination with low and high dietary calcium (.15 or .98%) for 4 wk. After 3 wk, the animals were orally dosed with calcium-45. One week later they were killed and tissue samples taken. Except for lower calcium-45 in bile, added dietary fat had no marked influence on calcium metabolism. Net absorption of calcium-45 (not excreted in feces) ranged from 82% for calves fed low calcium to 53% for those given high calcium. Calcium-45 in bone was substantially higher in calves fed .15% calcium. Tailbone biopsies revealed rapid uptake of calcium-45 with approximately as much incorporated during the 1st d as in the following 6 d. Calcium-45 in blood peaked 24 h following dosing. Calves fed .15% calcium had higher calcium-45 in blood and bile than those receiving .98% calcium. Calcium-45 values in soft tissue were low and did not differ materially among treatments. The decreases in radioactive calcium absorption and bone deposition with higher dietary calcium indicated that variable absorption was a major factor in calcium homeostasis. Added fat did not materially effect calcium metabolism with either low or high dietary calcium.

Fifteen intact male Holstein calves averaging 101 d of age were utilized to determine the effects of dietary Mn concentration and routes of administration on its metabolism. They were fed a practical grain diet containing 23ppm Mn with 0, 100, or 1000ppm supplemental Mn (MnSO 4 ·H 2 O) for 7 d prior to intravenous or duodenal dosing with 54 Mn. Animals were killed 4h later. With added Mn there was a significant decrease in 54 Mn content of some small intestine parts. However, in most tissue, including organs, bones, intestinal tract tissues, and blood, added Mn did not have a significant effect on 54 Mn concentrations. Concentrations of 54 Mn in tissues, except in small intestine, were far higher following intravenous dosing than with duodenal dosing. This further confirms that absorption of Mn is very low. Dosing method had a sizable effect on the relative amounts of 54 Mn in different tissues. This suggests that intravenously administered Mn, at least initially, is not metabolized in the same way as that absorbed. In most tissues, unlabeled Mn was not affected greatly by supplemental Mn. This is in contrast to earlier results with very young calves and indicates that Mn metabolism changes sharply before 3 to 4 mo of calf age.

Retention of 75 Se following a single oral dose and stable Co, Cu, Zn, and Mg were determined in tissues of calves fed a diet containing 0, 10, or 40ppm supplemental Co for 21 d. Concentrations of 75 Se in tissue were numerically higher with 10ppm Co than with the other two diets, but the effect was significant only in small intestine tissues of calves fed 40ppm Co. Dietary Co did not affect fecal 75 Se. Average total fecal 75 Se excretion was 53, 48, and 51% of the dose over 6 d in calves fed 0, 10, and 40ppm added Co. Concentrations of Co in tissues increased with increased supplementation. Dietary Co did not significantly affect growth, feed intake, tissue Zn, tissue Cu, blood hemoglobin, packed cell volume, plasma alkaline phosphatase, or plasma glutamic oxaloacetic transaminase. Magnesium in heart and skeletal muscle was increased in calves fed 40ppm Co. Although high amounts of added dietary Co had some influence on metabolism of Se, the magnitude and extent of the effects appeared to be too small to be of practical concern.

Calves fed a high-zinc diet were used to study zinc absorption from various sections of the small intestine. Absorption was determined by measuring zinc-65 in various tissues and plotting the tissue concentrations against dosing site, expressed as percentage of intestinal length. Zinc absorption, per unit of intestinal length, was similar throughout the small intestine and was as great in the distal as in the proximal end. Apparently, early researchers using isolated loops and everted sac techniques failed to recognize rate of digesta passage and tissue homeostasis as major factors associated with zinc uptake when they concluded that the duodenum was the primary site of zinc absorption. The data show that the duodenum is not the major site of zinc absorption in calves regardless of dietary zinc. In a separate experiment, zinc-65 was injected directly into the large intestine of calves fed a low zinc diet. Only about 2% of total zinc absorption was from the large intestine.

Young male Holstein calves were fed diets containing 40 or 640ppm zinc with 0 or 5ppm aflatoxin for 3 wk. The aflatoxin mixture contained 80.5% B 1 and the calves consumed 143mg of B 1 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 1wk. 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 alfatoxin in calves. The protection of zinc against aflatoxicosis appears to be no more than a partial effect.

Sixteen male Holstein calves in a 2 X 2 factorial design with four animals per treatment were fed 0 and 100 ppm supplemental copper from copper carbonate and 0 and 1 ppm added selenium from sodium selenite for 15 days in a practical diet containing .1 ppm selenium and 15 ppm copper. On day 13, calves received an oral dose of selenium-75 and were sacrificed 48 h later. Feed consumption, serum glutamic oxaloacetic transaminase, creatine phosphokinase, and stable copper in blood and urine were unaffected by diets. Stable copper in pancreas, spleen, kidney, muscle, and spinal cord along with selenium-75 in lung, pancreas, liver, heart, and muscle also were unaffected. In calves fed high selenium, selenium-75 was lower in blood, kidney, and spinal cord, and more was excreted in the urine, indicating less retention. Urine was the major excretory pathway of excess selenium-75. Liverstable copper was greater for high copper diets. Stable copper in the lung was higher in calves fed high selenium-high copper than in either control or calves fed high copper. Stable copper was greater in heart tissue in both groups fed high selenium than in controls and slightly higher than the group fed high copper.

Calves were fed a corn-skim milk or a purified diet to determine if the large differences in manganese metabolism in rats fed such diets also occurred in ruminating calves. The calf purified diet was similar to the rat purified diet but with potassium bicarbonate and sodium bicarbonate added as buffers to be suitable for ruminating calves. In contrast to the huge differences in rats, retention of manganese-54 was the same in calves fed the corn-skim milk diet as in calves fed the purified diet. It is unlikely that the minor differences in the diets caused such large differences in effects between calves and rats. A likely reason for the difference is the functional rumen in the calf. The active rumen may metabolize ingredient(s) that affect manganese absorption in the rat and, therefore, would not be in the small intestine to affect absorption by the calf.

Bioavailability of P from defluorinated phosphate and dicalcium phosphate and the P requirement were studied with 63 male Holstein calves. A P depletion diet containing .08% total P on a dry matter basis was fed to all animals for 4 wk beginning at 6 wk of age and 61kg weight. Calves developed typical signs of P deficiency. The depletion period was followed by a 6-wk experimental period in which the same depletion diet was used as a control. Phosphorus from each of the two sources was added to make diets containing .14, .20, and .32% total P. Source of supplemental P did not affect weight gains, feed consumption, feed efficiency, serum inorganic P, serum alkaline phosphatase, or bone ash. Weight gains, feed intake, feed efficiency, and serum inorganic P were more sensitive measures of dietary P content than were serum alkaline phosphatase or bone ash. Tibia joint ash was a more sensitive measure than tibia shaft ash or rib ash. Growth rate, feed intake, serum inorganic P, and tibia joint ash each increased linearly with increasing dietary P. The data suggest that the P requirement of 2 to 4 mo calves may need to be revised upward.

The zinc homeostatic control breakdown in cattle fed a high but nontoxic among 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.

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.

SummaryThe absorption and tissue distribution of organic and inorganic forms of 65Zn were studied in the rat following single tracer oral doses. Rats dosed with 65Zn grown into young corn and rye plants (organic form) absorbed and retained more 65Zn in tissues than those given 65Zn mixed with tissue paper (inorganic forms). A part of the beneficial effect was evident when 65Zn was mixed with forage. The relatively high absorption values indicate that both forms were readily available, and thus incorporating zinc into young forage protein is not of major practical importance.

The effect of iron, lactose and copper on manganese retention was studied in rats fed two diets. Thirty-six male albino rats (75 to 100 g) were allotted to six groups of six rats each. Three groups received a purified manganese-free dextrose-casein diet, and three groups received the same purified diet with 17% lactose added at the expense of dextrose. One group fed each of the above diets received either a manganese-free mineral mixture, the mineral mixture with 5 ppm supplemental Cu or the same mineral mixture with Fe removed. After 7 days on the diets, each rat was given, by gavage, 10 muCi of 54Mn activity as 54MnCl2 in a sodium acetate buffer. On the third day after dosing, the rats were sacrificed and samples of liver, kidneys, semitendinosus muscle, spleen and tibia were taken for stable and radioactive manganese analysis. Lactose added to the purified diet depressed 54Mn retention in all tissues studied. Lactose addition also decreased specific activities of the livers and kidneys but tended to increase stable manganese values. Copper apparently had little direct effect on 54Mn retention but tended to reduce the effect of lactose on 54Mn retention. Omission of Fe greatly increased 54Mn retention values in all tissues studied with or without added lactose. Fe omission also significantly increased the specific activities and stable Mn values of livers and the specific activity of kidneys. The results indicate that low dietary Fe may be a contributing factor to the increased manganese retention observed in this study and a previous study.

In successive years two conventional tower silos were filled with unwilted Coastal Bermudagrass forage plus 5% feed grain additive, and two with comparable forage wilted to a low moisture level prior to filling. When fed, the unwilted silages ranged from 32.7 to 40.2% dry matter and the low moisture silages varied from 58.4 to 76.4% dry matter. Each year the four silages were fed to 24 lactating cows. In the first years, cows fed the wilted silage consumed 1.2kg per day more forage dry matter (P = 0.05), but produced 1.2kg per day less fat-corrected-milk (FCM) (P = 0.05) than those fed unwilted material plus 5% ground barley. Also, those fed the unwilted silage produced milk containing 0.12% more solids-not-fat (P = 0.01). There were no significant differences in milk, solids-corrected-milk (SCM) production, weight gains, or level of fat or protein in milk the first year. In the second year none of the treatment differences was significant and the two-year combined averages were quite close for all measures of cow performance. The only carry-over effect in the period immediately after the experimental silages were fed was in the SNP content of the milk for the first year. Invisible or gaseous dry matter losses were somewhat lower for the low moisture silage, but there was also considerably more moldy material in this silage. The low moisture silage had a higher pH, but less ammoniacal N. Although these studies indicate that it is possible to make low-moisture silage successfully from Coastal Bermudagrass in conventional tower silos by wilting without additives, this procedure does not offer obviously important advantages over ensiling the forage unwilted under many conditions. Hazards in ensiling Coastal Bermudagrass as low-moisture silage include increased mold and difficulty in controlling the moisture level with changing weather conditions.

SummaryFollowing duodenal dosing, 65Zn was rapidly accumulated by several calf tissues, with a considerable amount in the liver and other tissues within 1 hr. With adequate dietary zinc, liver contained a substantial quantity of labile zinc which was greatly depleted in calves fed a zinc-deficient diet for 2 weeks. Other soft tissues had a very limited amount of labile zinc. Zinc turnover rate was much slower in muscle than in the softer tissues, and was not greatly affected by dietary zinc level. Transfer of zinc from the intestinal mucosa to the blood appeared to be the rate-limiting step in zinc absorption. This step was accelerated by feeding a zinc-deficient diet for 2 weeks. However, 65Zn uptake by the mucosa from the intestinal contents was vastly increased by the zinc-deficient diet.

Cadmium metabolism was investigated following a single oral dose of 109 Cd in four- to six-month-old male goats fed a practical diet with and without 100ppm of supplemental cadmium as CdCl 2 . Tissue distribution of 109 Cd and total body retention were determined 14 days after dosing. Highest concentrations were found in the kidneys, liver, duodenum, and abomasum, respectively. Total body retention was 0.3 to 0.4% of the dose with about one-half of this in the liver, one-fourth in the kidneys, and a large part of the remainder in the gastrointestinal tissue and contents. Bone, muscle, blood, hair, skin, and connective tissues contained very small amounts. Feeding the high metabolic load of 100ppm of dietary cadmium significantly decreased 109 Cd concentrations in the gastrointestinal tract tissues, but the effect was not sufficient to produce a detectable change in over-all body retention. 109 Cadmium levels in other tissues were not materially influenced by cadmium feeding. Daily rate of 109 Cd fecal excretion declined linearly and rapidly during the second week, with about 20% of the body burden eliminated on Day 8 and less than 5% on Day 14. After 21 days of cadmium feeding, kidney, duodenum, and liver concentrations of stable cadmium were 62, 28, and 18ppm of dry matter, compared to 2.7, 2.5, and 1.6ppm in comparable tissues of control animals. Ruminants do not have a homeostatic control mechanism for controlling cadmium absorption or excretion which is affected by level of dietary or tissue cadmium content. However, very low levels are absorbed.

SummaryAbsorption and metabolism of 65Zn in the natural chemical form of forage and as 65ZnCl2 were studied in Holstein calves following single tracer oral doses. Chemical form did not affect 65Zn excretion or total retention but 65Zn was higher in calves given 65Zn as forage in metabolically more active tissues (liver, spleen, heart, lungs, duodenum, and small intestines, p < .05). Thus, chemical form of 65Zn dose affected tissue distribution but not absorption. It is theorized that 65Zn in the two chemical forms was metabolized differently after absorption due to different 65Zn-ligand combinations being transported from the intestine to the tissues.

Following oral dosing, zinc-65 metabolism was studied in 10 first-lactation Holstein cows during the 5th and 6th wk of an experiment in which a high beet pulp, low-zinc diet (16.6ppm) was fed without and with (39.5ppm total zinc) supplemental zinc. For the 14 days after dosing, cows fed low zinc had a much higher net zinc-65 absorption (53.4 versus 34.8%) and consistently secreted far more zinc-65 into milk (14.4 versus 6.3%). The zinc secreted into milk of cows fed low zinc during the 14 days had been in the body a shorter time than in controls, indicating greater dependences on recently consumed zinc for secretion into milk. The biological halflife (in lactating ruminants defined as the time required for one-half of the zinc-65 dose to leave the body via feces and milk) was shorter for the cows fed low zinc. Lactating cows are able to absorb a high percentage of dietary zinc, and lactation is a major factor in zinc metabolism and homeostasis. Major changes in zinc metabolism occur before performance is affected.

Ten young, sexually mature goats were fed a zinc-deficient purified diet (4 ppm Zn) ad libitum and five a control diet (deficient diet + 36 ppm Zn) in amounts restricted to maintain comparable weights for 20 weeks. Less feed was required in the control group to maintain the weight in the deficient group. Inasmuch as there was no difference in digestibility of diets, the difference in feed efficiency was due to endogenous metabolism. Feed intake of deficient goats increased sharply from the 10th to 18th week without affecting body weight. Goats given the deficient diet developed zinc deficiency symptoms, which increased in severity with time. In comparison with controls, plasma zinc was much lower; growth rate and zinc content of hair were considerably less, testicles were smaller; and libido was lower in zinc-deficient goats. After an extended period on the severely restricted feed intake, testicle size in controls also decreased. As evidenced by testicle biopsies, spermatogenesis was not severely affected by zinc deficiency until 4 weeks post-treatment. At this stage, only spermatagonia were present and tubular size was reduced. The severely restricted feed intake of controls produced similar effects. Eighty percent of zinc-deficient and 60% of control goats died during the experiment. In a post-treatment period two goats from each group were fed the control diet ad libitum for four weeks. Feed intake of controls increased, but that of the goats which had been deficient did not increase markedly, suggesting that adaptation which appeared to have taken place was not readily reversible.

SummaryThe effects of feeding a high but nontoxic zinc level to young rats for varied time periods on zinc metabolism and adaptations were investigated. Adding 600 ppm supplemental zinc to a “corn-soy” diet for periods from 7 to 42 days did not materially affect stable zinc level in any tissue studied. However, in every tissue, 65Zn retention from a single oral dose declined sharply with duration of added zinc feeding to 21 days, indicating a continuing adaptation in zinc metabolism for at least this period of time. Likewise, fecal 65Zn excretion increased with length of feeding time on high zinc, indicating a continuing reduction in net absorption for most of the 42-day period. When the data are compared with similar previous cattle studies, it is evident that there are major qualitative differences in zinc metabolism and homeostatic control between rats and cattle.

SummaryDecreasing energy and protein intake in young ruminants resulted in lower weight gain and nitrogen balance. This was accompanied by reduced stable zinc absorption and retention both as milligrams/day and as a percentage of intake. Similarly, 65Zn absorption and retention were reduced. Nitrogen balance was well correlated with stable zinc and 65Zn retention (r = 0.67 and 0.49, respectively). These data support the concept that regulation of zinc homeostasis is controlled at the tissue level and is closely related to protein deposition changes.The authors thank Mr. Y. G. Martin for technical assistance and Mrs. Dan E. Fowler for editorial assistance.

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.

Zinc metabolism and homeostasis were studied in young growing rats fed a 38 ppM zinc diet with added zinc levels ranging from 0 to 8400 ppM for 21 days. High dietary zinc did not cause toxicity symptoms. Stable zinc in feces increased linearly with dietary zinc intake but fecal /sup 65/Zn, from a single oral dose, did not increase above the 1200 ppM dietary level. Stable zinc in liver, kidney, and tibia increased two to three times with 2400 ppM added zinc, but was not further elevated until 8400 ppM was fed. Stable zinc in muscle and heart was not affected appreciably by dietary zinc level. In all tissues, /sup 65/Zn retention was drastically reduced with 1200 ppM added dietary zinc. Additional dietary zinc reduced /sup 65/Zn in muscle and heart but had little effect on liver and kidney /sup 65/Zn. The data indicate that rats have fairly effective homeostatic control mechanisms for tissue zinc below about 7200 ppM dietary zinc. Whereas, with dietary zinc up to about 1200 ppM, decreasing absorption is the main route of homeostatic control, above this level, more rapid zinc turnover rates and increasing endogenous zinc excretion appear to have major importance.

Metabolism of orally dosed 75 Se was studied in 10 intact male Holstein calves that were fed ad libitum a control diet containing no added Pb or supplemented with 1000ppm Pb as PbSO 4 for 4 wk. Lead-supplemented calves did not exhibit any clinical signs of Pb toxicity. Voluntary feed intake was reduced by 9.5% and average daily gain by 23%. Lead content of rib, liver, and kidney increased. Serum glutamic oxaloacetate transaminase activity was increased during the last 2 wk of the experiment in calves fed Pb. In calves receiving supplemental Pb, 75 Se absorption, blood concentration, and urine concentration were reduced by 26, 21, and 42%, respectively. Tissue 75 Se concentrations were significantly lower in kidney, liver, testicle, pancreas, small intestine, heart, spinal cord, and muscle in calves fed Pb. There was a significant negative correlation (r = −.78) between 75 Se and stable Pb concentrations in the liver. It is not clear whether the ingestion of subclinical amounts of Pb could affect the absorption and utilization of Se in dairy calves to the extent of Se deficiency when dairy calves are kept in areas known to be low in Se.

Sixteen intact male Holstein calves averaging 86 kg and 63 d of age were assigned randomly to four treatment groups. The four treatment diets contained .17, .67, 1.31, and 2.35% Ca on an as-fed basis. The resulting Ca:P ratios with P held constant at about .34% were .47:1, 1.92:1, 3.83:1, and 7.20:1. Calves were fed diets at 3% of their body weights for 4 wk. Magnesium in the bone ash and serum was lowered by the 2.35% Ca treatment. Serum inorganic P was also reduced by the highest Ca diet during the last 2 wk of the experiment. Liver had the highest concentration of Zn in calves fed .67% Ca, and the muscle from calves fed 1.31% Ca diet had the lowest amount of Zn. Copper was reduced in pancreas for 1.31% Ca diet, but Ca was highest in the muscle and heart at the .67% Ca treatment. Weight gains and feed efficiencies were not affected by Ca. Fecal pH was different among treatments and increased as Ca intake increased. Young growing dairy calves can adapt to a wide range of Ca intakes and Ca:P ratios and maintain a moderate growth rate for 4 wk. It appears that excessive dietary Ca may affect concentrations of Zn, Fe, Cu, and Mn in some body tissues, but the magnitude of the effect is relatively small.

Metabolism of cadmium-109 and methyl mercury-203 was studied in six lactating Jersey cows for 14 days following single tracer oral doses. Most of the cadmium-109 was excreted in feces with only .05% in urine. When the cows were killed 14 to 16 days after dosing, kidney and liver had highest cadmium-109. About .75% of the cadmium-109 was retained in the body with 34% of this in gastrointestinal tract and contents, 32% in liver, and 10% in kidney. In fetal tissues highest cadmium-109 was in kidney, tibia, and liver whereas fetal liver had highest methyl mercury-203. Apparent methyl mercury-203 absorption was 59% with 1.1% in urine. Highest concentration was in kidney, followed by liver, skeletal muscles, heart, smooth muscle, spleen, lung, brain, ovaries, and pancreas. Of total body mercury-203, muscle had about 72% and liver 7%. In 14 days, only .17% of mercury-203 dose was secreted into milk. Cadmium-109 in milk was below detectable limits of .00008% of the dose/day. Feed of cattle kept for meat should be protected from methyl mercury, at least near slaughter. Milk is protected from methyl mercury. In sharp contrast to zinc, little of the ingested cadmium appears in muscle or milk.

SUMMARY The role of bile in manganese metabolism and homeostasis was studied in Holstein bull calves fed diets containing 32 ppm manganese (normal) (control) or 1,000 ppm supplemental manganese (high-manganese) for 2 weeks before and 1 week after intravenous (IV) and duodenal S4Mn dosing. After dosing, all the bile was collected at 15 and 60 minutes, hourly to 12 hr and daily to 7 days. All calves were sacrificed 7 days after dosing to determine the tissue S4Mn distribution. High-Mn-fed calves secreted 48% of the IV S4Mn dose in bile over the 7-day period; which was 12 times that in bile of control calves. In contrast, after duodenal dosing, only a very small amount of S4Mn was secreted in bile by either control (.32%) or high-Mn-fed (.30%) calves over the 7-day period. With both methods of dosing, calves fed the high-Mn diets had a lower average S4Mn concentration in most tissues taken than calves fed the control diet. These data from IV dosing confirm earlier work that excretion and tissue distribution of injected S4Mn is very sensitive to dietary Mn. The data from duodenally-dosed calves showed that the amount of Mn absorbed is decreased by higher dietary Mn intake. In contrast to previously held theory, enterohepatic circulation of Mn apparently plays only a minor role in homeostasis of fed Mn. Manganese homeostasis in calves appears to be the result of changes both of absorption and

Holstein calves and cows in first lactation were fed a low-zinc (16.6 ppm) experimental diet. Zinc-65 absorption and tissue distribution were determined following a single oral tracer dose of zinc-65 given 14 days prior to sacrifice. Net zinc-65 absorptions for the cows and 2- and 6-mo-old calves were 53.4, 49.7 and 47.2% of the dose. Tissue zinc-65 content, adjusted for body weight and zinc-65 of milk of the cows was not significantly different from that of either age calves in 13 of 20 comparable tissues. Greatest differences in tissue zinc-65 were in tibia and rib with the 6-mo-old group highest and cows lowest. Lactation represents a major homoeostatic demand for zinc, and the intestinal absorptive ability of adult cattle remains responsive to physiological need.

Weight gains of young broiler chicks were not reduced by up to 2400 ppm added zinc fed to four weeks of age. Tissue zinc was not changed significantly by 600 or 1200 ppm supplement dietary zinc, but at 2400 ppm added zinc, blood, kidney, and liver zinc were significantly elevated (P < 0.05). In the heart, zinc was not affected by the added dietary zinc but increased over time with all diets. Unlike the calf weanling pig, the metabolism of zinc in the young chick does not appear to change appreciably with increasing maturity. Thus, the homeostatic control mechanisms of the young chick are effective for up to 1200 ppm dietary zinc, but are partially overcome by 2400 ppm added dietary zinc. 17 references, 1 figure, 2 tables.

Holstein bull calves were fed 1, 2, and 4% supplemental magnesium as magnesium oxide. The control diet contained .3% magnesium and consisted of ground corn, soybean meal, cottonseed hulls plus mineral, vitamin, and antibiotic supplements. Diarrhea was the most obvious effect of high intake of magnesium. The extent and intensity of the diarrhea was related closely to the dietary magnesium content. High (2 and 4%) magnesium reduced feed consumption and weight gains. Although there were traces of blood in feces, no abnormalities were observed at autopsy. Large tubular sections of mucus were voided in the feces with a greater prevalance among calves fed 2 and 4% supplemental magnesium. Magnesium in plasma rose sharply in response to the increased intake of magnesium. In calves receiving the 4% added magnesium, the plasma values were triple those of controls. When high magnesium was fed, magnesium increased much more in urine than in plasma. Within 1 wk after calves were returned to control diet, magnesium in urine and plasma declined to control.

Fifteen male Holstein calves were fed diets containing .25 (control), .7, or 1.15% magnesium (from supplemental magnesium oxide) for 28 days. Feed consumption and growth rate were not affected adversely by .7% magnesium but were depressed with 1.15% magnesium. Fecal dry matter percentage was reduced slightly with .7% magnesium and substantially decreased with 1.15% magnesium. However, feces from calves fed .7% magnesium were more fluid in consistency. Urinary and fecal magnesium content increased in calves fed .7 and 1.15% magnesium, with changes closely related to dietary magnesium. Magnesium in plasma increased slightly with .7% magnesium and materially with 1.15%. Magnesium in liver, kidney, and heart was not affected by diets. Apparently calves can tolerate safely .7% magnesium, but 1.15% is detrimental. On day 21 of treatment, all calves received zinc-65 orally and were killed 7 days later. Calves fed .7 and 1.15% magnesium excreted less zinc-65 and retained more, especially in liver and large intestine. Liver and kidney of calves receiving higher percents magnesium had elevated stable zinc. Calcium and copper in tissue were not elevated. The effect of high dietary magnesium on zinc metabolism appears to be systemic in tissues.