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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.

The metabolism of a single oral zinc-65 dose was studied in young dairy calves fed two concentrations of added A1 (0 and .20% A1) and two concentrations of added P (0 and .22% P) for 7 wk. The four treatments were 1) normal P-low A1, 2) low P-low A1, 3) normal P-high A1 and 4) low P-high A1. The basal diet (low P-low AL) contained, by analysis, .132% P, .74% Ca, .021% A1 and 59 ppm Zn. Zinc-65 absorption was greater (66.5 vs 63.2% of dose, P less than .10) with the low-P diet; added A1 reduced (P less than .05) 65Zn absorption. Calves fed low-P diets had higher (P less than .10) concentrations of 65Zn in liver, kidney, spleen, heart, small intestine and testicle than those fed normal-P diets. Zinc-65 was reduced (P less than .10) in pancreas, heart, testicle and muscle of calves fed high A1. Iron was increased in liver and kidney (P less than .10), Zn (P less than .10) and Mn (P less than .01) were increased in liver, but Fe in small intestine and Cu in muscle and tibia shaft were decreased (P less than .10) in calves fed the low-P diets compared to those fed adequate-P diets. High A1 reduced (P less than .10) Cu in small intestine and tibia shaft. The results suggest that zinc metabolism may be moderately affected in calves fed either low-P or high-A1 diets.

The metabolism of Mg was studied in young dairy calves fed two levels of added Al (0 and .20% Al) and two levels of added P (0 and .22% P) for 7 wk. The four treatments were 1) normal P - low Al, 2) low P - low Al, 3) normal P - high AI and 4) low P - high AI. The basal diet (low P - low Al) contained, by analysis, .132% P, .021% Al and .17% Mg. Added AI did not affect (P > .lo) serum Mg. An AI x P interaction on bone Mg was detected (P c .01). Magnesium was reduced in tibia shaft (.34 vs .44%) and in tibia joint (.43 vs .53%) in calves fed high Al in the presence of normal dietary P, but Mg was not reduced in the calves fed low-P diets. Apparent absorption of Mg was reduced by approximately five-fold (.I8 g/d vs -.84 gld, P c .Ol): urinary Mg excretion was reduced 31% (1.12 g/d vs .77 g/d, P < .Ol); and Mg retention declined 41% (-95 g/d vs -1.61 g/d, P e .01) in calves fed added Al. Compared with calves fed low-P diets, calves fed normal levels of P had a higher Mg concentration in tibia shaft (P < .01) and tibia joint (P < .05). The data indicate that supplemental AI may adversely affect Mg metabolism in calves. (Key Words: Dairy Cattle, Calves, Aluminum, Phosphorus, Magnesium, Metabolism.)

The metabolism of Zn and tissue mineral concentrations were studied after a single oral 65Zn dose in 10 6-wk-old Holstein calves injected subcutaneously daily with 0 (control) or 10 mg of sometribove (recombinant methionyl bST) for 6 wk. Zinc-65 absorption was not significantly affected by bST; its concentration in the semitendinosus muscle was reduced by 32% in the bST calves, but concentrations in liver, pancreas, spleen, kidney, heart, small intestine, testicle, and rib were not different from controls. Manganese content was reduced by 27% in liver, 60% in kidney, 99% in spleen, 92% in testicles, and 33% in rib. Iron content of pancreas, spleen, and testicle and Zn content of rib were increased in the bST calves. The data indicate that Zn metabolism was not affected adversely by bST. Manganese content of several tissues was significantly reduced in the bST calves; however, no clinical signs of an Mn deficiency were evident.

Ten intact male Holstein calves averaging 75kg of BW and 59 d of age were used to study the effects of daily injections of 0 (control) or 10mg of sometribove (recombinant methionyl bST) for 6 wk on performance, health, carcass composition, N metabolism, chemical blood characteristics, and hormone profiles. Average daily gain, feed intake, feed:gain ratio, and height at withers, hip, and hock were not influenced by bST. Carcasses from bST-treated calves contained 5% more protein and 36% less lipid than controls. Circulating concentrations of Ca, P, glucose, urea N, alkaline phosphatase, creatine phosphokinase, insulin-like growth factor-I and insulin were not affected by bST. Packed cell volume was decreased about 7% (29.9 vs. 32.4%) in the bST calves. Hormone injection did not adversely affect health of the calves as measured by body temperature and by pulse and respiration rates. The most profound effects of sometribove were a reduction in carcass lipid and an increase in body proteins. These effects may be of some practical importance when leanness of carcass is desirable.

Sixteen male intact Holstein calves averaging 72kg and 64 d of age were used to study the effects of high dietary Al on calf performance and P bioavailability. The main effects were two concentrations of added aluminum (0 and .20% Al) and two of added P (0 and .22% P). The basal diet contained, by analysis, .132% P, .74% Ca, and .021% Al. The calves were assigned to four treatment groups balanced according to body weight. The four treatments were 1) normal P, low Al; 2) low P, low Al; 3) low P, high Al; and 4) normal P, high Al. Calves had ad libitum access to their respective diets for 7 wk. Metabolism of a single oral 32 P dose was determined during wk 6. The adverse effects of high dietary Al include a 17% reduction in feed intake and a 47% reduction in body weight gains. Alkaline phosphatase and plasma glutamic oxaloacetate transaminase activities increased in calves receiving the high Al diets. A negative balance of P and Ca was noted in the calves fed high concentrations of Al. Apparent absorption of 32 P was reduced (37%) in calves fed diets high in Al (44% of dose vs. 69%). Urinary excretion of 32 P was not affected by dietary Al concentrations. Calves fed the low P (deficient) diet showed significant reductions in feed intake, weight gain, serum inorganic P, bone ash, and P content of bone. Dietary P did not significantly affect 32 P absorption. Adding .20% dietary Al severely affects P metabolism and performance of young growing calves.

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.

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.

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.

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.

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 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.

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.

Routine vaccination of dairy heifers for brucellosis, with Strain 19 Brucella abortus, and with triple bacterin for blackleg, malignant edema, and pasteurellosis (shipping fever) is followed by a very large depression in serum alkaline phosphatase activity (SAP). This was serendipitously observed in another experiment and subsequently verified in controlled experiments. The reduction in phosphatase activity was not accompanied by important reductions in feed intake. Phosphatase activity levels were depressed from two to eight days after vaccination and probably to a lesser degree after 11 days. Additional experiments indicated that Strain 19 brucella vaccine from different manufacturers had a comparable effect on depressing phosphatase, but that the diluent for the brucella vaccine and the triple bacterin did not have an important influence. Phosphatase activity in bull calves was affected comparably to that in heifers. Endotoxins in amounts comparable to those in the Strain 19 brucella caused a significant reduction in SAP in one experiment, but not in another. There were considerably different levels of phosphatase activity in calves of comparable age, size, and condition in different herds, and also of individual animals within herds. Within treatments, there were large positive correlations between SAP levels for the same animals in samples obtained prior to vaccination and several days later.

Three Holstein cows were each given 3.0 g of cadmium daily (two equal doses) for two weeks by gelatin capsules. There was a sharp drop in concentrate consumption for the first few days of cadmium administration but, by the second week, consumption returned to normal. Milk production declined sharply for several days and then increased appreciably, but to a level still substantially lower than that of controls during the last five days cadmium was given. When cadmium treatments ceased, milk production increased by 50%. Fat content of milk was elevated considerably during the week when production was most reduced. Cows given cadmium lost considerable weight. There were no other clinical manifestations of toxicity. As determined by the chromic oxide indicator method and twice-daily grab samples, fecal excretion of cadmium for the second week averaged 82% of that given. The cadmium level in the urine was below the limits of detectability of the method (0.5 ppm of urine). The cadmium content of the milk was less than 0.1 ppm of the milk, which was the lower reliability limit of the procedure used. On this basis less than 0.022% of the amount administered appeared in the milk. In vitro studies demonstrated that cadmium combines with the casein and whey protein fractions of the milk readily, with the amount combined being linear when levels from 1.0 to 25.0 ppm are added to milk. Smaller amounts were present in the lactose and mineral fractions.

Twenty-three male dairy calves were fed (a) 0, (b) 62.5, (c) 250, or (d) 1000 ppm elemental nickel as NiCO/sub 3/ in the total diet from 13 to 21 weeks of age. Three animals on each treatment were subjected to digestion and balance trials and killed for tissue histological comparisons, and a like number (two for 62.5 ppm) were fed the basal ration in a 6-week posttreatment recovery period. Feed intake and growth rate were slightly retarded by 250 ppm Ni. Even though the calves fed 1000 ppm Ni had greatly reduced feed intake and lost weight during the 8-week treatment period, they were not emaciated and appeared to be younger than the others. During the posttreatment recovery period, growth rate of those which had been given 1000 ppm Ni was at least equal to that of the others. Digestibility coefficients were not affected by the Ni treatments but nitrogen retention was significantly lowered by 1000 ppm Ni and was associated with reduced feed intake. On a molar percentage basis, propionate was increased and butyrate decreased in rumen fluid from animals on the higher levels of nickel supplementation. Relative to body weight, the fresh weight of lung, heart, spleen, liver,more » gall bladder, kidney, brain, and testis was unaffected by treatments. Nickel did not affect ruminal, abomasal, duodenal, liver and testicular tissues histologically. Kidneys were nephritic, and the degree of severity increased with the nickel level. 26 references, 1 figure, 5 tables.« less

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.

Using chromic oxide as a nonabsorbed marker, endogenous secretion and reabsorption of 65 Zn in various segments of the gastrointestinal tract were studied in seven zinc-deficient and six normal calves and in eight deficient and eight normal goats. All were fed a highly digestible low zinc purified diet. The animals were euthanatized 14 days following a single oral dose of 65 Zn, at which time all the gastrointestinal 65 Zn was assumed to be of endogenous origin, though the amount present would be reduced by reabsorption. Dry matter digestibility, 65 Zn, and chromic oxide were determined in each section. Dry matter was absorbed in the rumen of both species with large amounts of secretion into the upper small intestine and reabsorption in the lower small intestine. Zinc-65 was secreted into the rumen and reticulum followed by variable amounts of reabsorption in the abomasum. Large amounts of 65 Zn were secreted into the anterior section of the small intestine with nearly all of it reabsorbed farther down the small intestine. The feeding of EDTA and cadmium did not have a clear-cut effect on 65 Zn or dry matter secretion or reabsorption in most sections. Likewise, a zinc-deficiency did not have a marked and consistent influence in most sections. There were appreciable differences in apparent dry matter and 65 Zn secretion into the upper small intestine between calves which fasted overnight and goats fed three hours prior to sacrifice. It is believed that this effect was due primarily to difference in the length of time since feeding the low residue diet.

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.

Cadmium metabolism was studied in six 2.5-month-old goats following a single oral or intravenous tracer dose of 109 Cd. Whereas, more than 90% of the oral dose was excreted in the feces within five days after dosing, only 5.6% of the intravenous dose was excreted via feces during this time. Feces was the predominant route of excretion regardless of method of dosing. Following a peak level of endogenous excretion on the second day after intravenous dosing, there was a very sharp reduction ia rate of endogenous excretion so that 12 days after dosing endogenous excretion was only 7% of the peak. Fourteen days after intravenous dosing, highest concentrations were observed in the liver, kidney, and spleen, in descending order. In contrast, following oral dosing highest concentrations were found in the small intestine wall, kidney, and liver. A much higher level of 109 Cd was found in the liver, heart, and spleen of intravenously dosed animals relative to other tissues than in orally dosed ones. It is theorized that intravenously administered cadmium is transported in a different form from that absorbed from the gastrointestinal tract and that this materially affects cadmium metabolism.

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.

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.

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

Twelve intact male Holstein calves averaging 90 kg and 12 wk of age were fed one of three dietary treatments for 28 d. The diets were A) control, B) control plus 1000 ppm iron as ferrous carbonate, and C) control plus 1000 ppm iron as ferrous sulfate monohydrate. Calves were dosed orally on d 15 of the treatment period with 1 mCi of iron-59. Neither source of added iron had a significant effect on weight gains, feed consumption, hemoglobin, packed cell volume, serum total iron, serum total iron-binding capacity, unbound iron-binding capacity, serum copper, tissue copper, fecal dry matter, or a consistent effect on fecal pH. The ferrous carbonate had no significant effect on stable zinc or stable iron in any tissue studied. Calves fed ferrous sulfate had higher average stable iron in most tissues and significantly more in the small intestine. Tissue zinc was lower in spleen and pancreas of ferrous sulfate-fed calves. Both sources of added iron sharply reduced iron-59 in serum, whole blood, and body tissues. The reduction was substantially greater in calves fed the ferrous sulfate iron. Iron in ferrous sulfate had a higher biological availability than that in the ferrous carbonate; however, bioavailability of the ferrous carbonate iron appeared to be substantial and considerably more than that noted in previous studies in which a different source of ferrous carbonate was used. The maximum safe level of dietary iron is materially influenced by the source of iron with a higher tolerance indicated for ferrous carbonate than ferrous sulfate monohydrate.

Sixteen Holstein intact male calves averaging 85 kg and 74 days of age were assigned randomly to four dietary lead treatments according to body weight. They were fed for ad libitum consumption a control diet containing no added lead or the control diet supplemented with 500, 1500, or 4500 ppm lead as lead sulfate. One calf fed 1500 ppm lead and all four calves fed 4500 ppm lead died within 6 to 10 days after initiation of treatments. Death was sudden with few or no clinical signs prior to death. Those clinical signs that did appear included muscular tremors, gnashing of teeth, bellowing, and convulsions. Four control, four 500 ppm lead, and two 1500 ppm lead-fed calves survived the 7-wk experimental period. Feed consumption, body weight changes, glutamic oxaloacetic transaminase and alkaline phosphatase activity in blood plasma, and hemoglobin were not affected significantly by lead treatments. Packed cell volume in calves fed 500 and 1500 ppm added lead was reduced. Lead concentrations in blood, kidney, liver, bone, brain, and muscle were elevated in lead supplemented calves above those of controls. The highest concentrations of lead were in kidney and liver.

Studies were conducted with 35 animals to determine whether addition of 350ppm of cadmium (as CdCl 2 ) or of 300ppm of EDTA (as disodium EDTA) affected dry matter digestibility or relative organ weights (as a percentage of body weight) of zinc-deficient calves or goats. In contrast with previous work, zinc-deficient animals had small but significantly lower dry matter digestibilities. Neither EDTA nor cadmium had a consistent or material effect on digestibility of a purified diet. Testicles of zinc-deficient goats were reduced in size. In general, tibiae were somewhat larger in zinc-deficient animals. Livers were larger in deficient goats but not in deficient calves. In some instances, lungs of zinc-deficient animals fed cadmium were larger relative to body size than those in animals given other treatments. Neither EDTA, cadmium, nor the zinc deficiency materially and consistently affected size of kidney, heart, or spleen. The predominant influence of EDTA and cadmium on health, performance, and metabolism of young ruminants does not appear to be through an effect on dry matter digestibility and probably not by gross effects on sizes of the organs studied.

Following a 1-week standardization period, a high beet pulp, low-zinc diet (16.6 parts per million) was fed with (39.5 parts per million total zinc) and without supplemental zinc as zinc oxide to 10 first-lactation Holstein cows (linearly declining phase of lactation) for 6 weeks. The low-zinc diet did not adversely affect milk production, fat-corrected milk, solids-corrected milk, milk fat, solids-not-fat, protein, feed intake, or body weight changes, indicating that zinc intake was adequate for these functions. However, with the low-zinc diet zinc content of milk was reduced 23% and percentage of ingested zinc in milk doubled. Thus, major adjustments to the diet were reduction in milk zinc and more efficient translocation of dietary zinc to milk zinc. Milk zinc content of a cow was highly repeatable (correlation coefficient = .92) from one measurement period to another, indicating that factors affecting milk zinc can be investigated more efficiently if standardization period data are used in covariance analyses. The correlation coefficient between milk zinc content and milk protein content was .65 and between milk zinc and milk production – .33.

In experiments involving 24 animals, zinc and dry matter contents of various tissues were studied in zinc-deficient and control goats and calves at various time intervals after control animals were fed the zinc-deficient diet. All samples were obtained before any symptoms of a deficiency occurred in the controls. Length of time, from 9 to 35 days, which controls were fed the deficient diet did not affect zinc content of tissues. Zinc content of hair, blood, liver, lung, kidney, femur, skin, and testicles was reduced in zinc-deficient animals. Zinc level was unaffected in brain and muscle tissues. In most tissues there was considerable overlapping between zinc content of controls and deficient animals, so that differences due to the deficiency are a statistical phenomenon rather than one of important value for diagnostic purposes with individual animals. Zinc content of hair may have some potential as a diagnostic aid. Dry matter content of tissues was affected relatively little by zinc deficiency or by species. Zinc excretion via feces was decidedly lower in zinc-deficient animals, but urinary excretion tended to be higher than for controls. Thus, fecal excretion is an important route of homeostatic conservation of zinc in deficient animals, but urinary excretion does not contribute to this conservation.

In experiments involving 18 male Holstein calves and 17 male goats, zinc and dry matter content of various tissues were studied in zinc-deficient and normal animals fed purified diets containing either: no additive, 300ppm EDTA (as disodium EDTA), or 350ppm cadmium (as CdCl 2 ). All of the animals were given the same low zinc (4ppm zinc) purified diet beginning seven days before fecal collections were initiated and 21 days before tissue samples were obtained. None of the normal animals exhibited any zinc deficiency symptoms. Addition of EDTA to the diet had little effect on fecal zinc excretions or zinc content of most tissues studied. Feeding cadmium increased fecal excretion of zinc in calves but not in the goats which were more mature. Livers of cadmium-fed zinc-deficient calves had an increased concentration of zinc, but this phenomenon was not observed in goat livers. The zinc content of heart, lung, kidney, spleen, testicles, muscle, and bone was not consistently or materially affected by cadmium feeding. Neither EDTA nor cadmium had much effect on dry matter content of most tissues. Differences in tissue zinc level between zinc-deficient and normal animals, in most instances, were nonsignificant. Samples from the epiphyseal-diaphyseal junction of tibia from zinc deficient calves contained less dry matter than those from normal calves.