Physical, hematologic, biochemical, and immunologic effects of supranutritional supplementation with dietary selenium in Holstein cows.

OBJECTIVE: To measure responses of cows to supplemental Se intake in excess of nutritional requirements, but lower than recognized toxic dosages. ANIMALS: 24 healthy adult Holstein cows. PROCEDURE: Cows were allotted to 4 groups and fed sodium selenite to provide 0, 3, 20, or 50 mg of Se/cow/d for 90 days. Subsequently, the dosage for the group receiving 50 mg/cow/d was increased to 100 mg/cow/d for 28 d. Blood, liver specimens, feces, and urine were obtained at points during the trial. RESULTS: Serum and blood Se concentrations in groups receiving 20 or 50 mg/cow/d increased over time, compared with controls (P < 0.01). Increasing supplemental Se intake to 100 mg/cow/d further increased serum and blood Se concentrations (P < 0.05). Urine, fecal, and liver Se concentrations increased more markedly in response to treatment than did those of serum or blood. No effect of Se treatment was seen on blood cell counts or serum activities of hepatocellular enzymes. Likewise, neither titer response to rabies vaccination nor lymphocyte blastogenic response to nonspecific mitogens was affected by Se treatment. Objective or subjective physical signs of Se toxicosis were not observed at any Se dosage. CONCLUSIONS: Inorganic Se intakes of up to 50 mg/d for 90 days or 100 mg/d for 28 days by adult Holstein cows do not affect the variables measured. CLINICAL RELEVANCE: Intakes of Se as sodium selenite in amounts 10 to 30 times the nutritional requirements are unlikely to cause health problems in adult cows. Urine and feces are good test samples for detection of Se supplementation greater than requirements.

Effects of vitamin E and selenium on immune responses of peripheral blood, colostrum, and milk leukocytes of sows.

This study was designed to assess how dietary vitamin E (E) and (or) selenium (Se) concentrations affect immune responses of gestating and peripartum sows. Multiparous sows (24), assigned to one of four groups at breeding, were fed ensiled, shelled corn-soybean meal-based diets without supplemental E or Se (-E-Se), with .3 mg of Se/kg (-E+Se), with 60 IU of E/kg (+E-Se), or with both supplemental E and Se (+E+Se) during gestation and to d 4 of lactation. Blood was obtained on 0, 30, 60, and 90 d of gestation and at parturition for serum E and Se assays. Lymphocytes and polymorphonuclear cells (PMN) were isolated from the blood, colostrum, and 4-d milk samples for immune studies. Compared with the control (+E+Se) diet, the -E-Se diet reduced (P < .05) the serum tocopherol and Se concentrations, the mitogenic responses of lymphocytes of peripheral blood (PBL) and colostrum (CL), the phagocytic activity of blood and colostral PMN, and the microbicidal activity of blood, colostral, and milk PMN. The -E+Se diet reduced (P < .05) the serum tocopherol concentrations, the mitogenic responses of PBL and CL, and the phagocytic activity of PBL. The +E-Se diet reduced (P < .05) serum Se concentrations and the phagocytic activity of PMN. The data indicated that E restriction depressed PBL and PMN immune functions, whereas Se restriction depressed mainly PMN function.

Clinical assessment of selenium status of livestock.

Assessment of the selenium status of livestock is an important aspect of production medicine, but variations in reported values between laboratories and between methods may be > 30%. Reliable interpretations require considerable experience with an assay and an extensive database from field and research case samples of a variety of species. The Michigan State University Animal Health Diagnostic Laboratory (MSU-ADHL) has offered Se analyses by acid-digestion and fluorometric detection since 1982. This laboratory expects serum Se values (nanograms per milliliter) of livestock to increase gradually with age from starting ranges for neonates of 50 to 80 for calves and sheep and 70 to 90 for foals and pigs. Expected or "normal" values for the adults are in the ranges of 70 to 100 for cattle, 120 to 150 for sheep, 130 to 160 for horses, and 180 to 220 for swine. Normal liver Se concentrations are considered to range between 1.2 and 2.0 micrograms/g on a dry weight basis, regardless of the species or age. Based on samples submitted to MSU-AHDL between September 1990 and August 1991, contemporary feeding practices in the Michigan area resulted in mean serum Se values (nanograms per milliliter) of 75 +/- 19 for adult Holsteins, 170 +/- 27 for adult swine (mixed breeds), and 137 +/- 30 for adult race horses. Within that period of time, two field cases of Se toxicity were diagnosed. One involved feeder pigs with a recorded high serum Se value of 1,525 ng/mL due to a commercial premix manufacturing error.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.

Selenium toxicosis in feeder pigs.

Selenium toxicosis was diagnosed in feeder pigs on a central Michigan farm. Use of a commercial supplement, found to contain approximately 20 times the intended Se concentration, resulted in a Se concentration of 8.1 mg/kg of the complete feed. This was fed for 34 days during which daily feed consumption decreased approximately 35%, several pigs developed weakness and forelimb paresis, and 1 pig died. The highest serum Se concentration measured was 1,550 ng/ml (normal range, 140 to 190 ng/ml). Normal feed consumption returned when an alternative feed was provided. Mean serum Se concentrations of representative pigs, monitored over the subsequent 26 days, decreased from 905 to 258 ng/ml. Histologic examination of a recovering pig revealed skeletal and cardiac myopathy and bilaterally symmetric malacia of the gray matter of the ventral horns of the spinal cord. During the developing toxicosis, the pigs consumed an estimated 11.4 mg of Se/pig/d.

Fat-soluble vitamin nutrition for dairy cattle.

The need for supplementation of dairy cow diets with fat-soluble vitamins depends on the amount of vitamins naturally present in the diet, the availability of dietary vitamins, and the vitamin utilization rate of the animal. Fresh forage contains ample amounts of the vitamin A precursor beta-carotene as well as vitamin E. Irrespective of the dietary amount, however, the availability of vitamins A, D, and E, as well as beta-carotene, can be adversely influenced by poor fat digestion, as commonly occurs due to enteric disease in young calves. In addition, high-grain diets appear to increase the amount of ruminal vitamin destruction and may thus increase vitamin requirements. The vitamin utilization rate may be increased by inflammation as well as dietary and environmental factors. The factors influencing vitamin availability and utilization rate should be considered when formulating rations. Because the vitamin requirement is variable, blood concentrations of vitamins should be monitored when conditions such as poor fertility, weak calves, and poor immune response are present.

The influence of gestational dietary calcium on serum 1, 25-dihydroxycholecalciferol in sows and their pigs.

Fifteen multiparous sows (three groups of five) were studied during one gestation-lactation cycle to measure the influence of dietary Ca (.5, .8[control], and 1.1%) on 1,25-dihydroxycholecalciferol (1, 25-(OH)2D3) in serum and colostrum of the sows and serum of their pigs. Concentrations of 1,25-(OH)2D3 and Ca, Mg, P, Cu, and Zn were determined on d 15 and 45 of gestation, at parturition, and at 3 wk postpartum in sow serum and at birth and d 10 and 21 in pig serum. Colostrum was assayed for 1,25-(OH)2D3. Serum 1,25-(OH)2D3 in sows was affected inversely (P less than .05) by dietary Ca within d 15 of gestation and was correlated (r = -.88) with serum Ca during gestation and lactation. Serum Ca was correlated (r = .52) with dietary Ca at d 15 and 45 of gestation and at farrowing. Sow serum Mg was inversely related (r = -.49) to serum Ca during gestation and early lactation. Serum 1,25-(OH)2D3 of the pigs at birth ranged from 38.7 to 44.2 pg/ml was decreased (P less than .05) by 1.1% maternal Ca intake. Sow colostrum 1,25-(OH)2D3 was related (P less than .05) inversely (r = -.40) to sow dietary Ca and directly (r = .90) to sow serum 1,25-(OH)2D3. Serum 1,25-(OH)2D3 of 10- and 21-d-old pigs was inversely related (P less than .05) to their dams' dietary Ca. These results indicate that 1,25-(OH)2D3 production in sows is quickly affected by modest changes in dietary Ca.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal and fetal selenium concentrations and their interrelationships in dairy cattle.

Paired dam-fetus serum, whole blood and liver samples were collected from 101 pregnant dairy cattle at slaughter to establish mean values for fetal tissue selenium concentration and to determine relationships between maternal and fetal selenium status. Samples were assayed for selenium concentration in serum, whole blood and liver and for whole blood glutathione peroxidase (GSH-Px) activity. Fetal age was estimated from fetal crown-to-rump length. Mean fetal liver (2.14 micrograms/g dry wt) and serum (21.4 ng/ml) selenium concentrations and whole blood GSH-Px activity (21.6 mu/ml) differed (P less than 0.0001, 0.0001 and 0.01, respectively) from corresponding maternal values (0.95 micrograms/g liver dry wt; 44.0 ng/ml; 16.7 mu/ml, respectively), while no differences were found between whole blood or erythrocyte selenium concentrations. Fetal liver selenium concentration was greater than corresponding maternal liver selenium in 99% (96/97) of the dam-fetal pairs, suggesting efficient placental transfer and fetal concentrating ability. Maternal liver selenium concentration was most highly correlated to all fetal tissue selenium concentrations and used to develop prediction models. These data suggest that selenium efficiently passes the placenta, and based on published values of adequate adult liver selenium concentrations and maternal-fetal relationships, we suggest an adequate liver selenium concentration in the bovine fetus to be greater than 2.2 micrograms/g liver dry wt, and in whole blood, greater than 120 ng/ml.

Maternal and fetal vitamin E concentrations and selenium-vitamin E interrelationships in dairy cattle.

Paired dam-fetus liver and serum samples were collected from 101 pregnant dairy cattle at slaughter to determine mean fetal and maternal liver and serum vitamin E concentrations, relationships between maternal and fetal vitamin E status and interrelationships between selenium and vitamin E status. Fetal age was estimated from fetal crown-to-rump length. Fetal alpha-tocopherol concentration ranged from 0 to 31.4 micrograms/g dry wt with a mean of 7.1 micrograms/g dry wt and from 0 to 0.92 micrograms/ml with a mean of 0.29 micrograms/ml for liver and serum, respectively. Mean maternal liver (12.5 micrograms/g dry wt) and serum (2.16 micrograms/ml) alpha-tocopherol concentrations and vitamin E to cholesterol ratio (1.45) were 1.8, 7.4 and 3.5 times greater (P less than 0.0001) than fetal means, indicating limited placental transfer of vitamin E to the fetus. Gestational age had no effect on maternal vitamin E concentration, however, fetal tissue alpha-tocopherol concentration declined (P less than 0.05) with fetal age. Maternal serum alpha-tocopherol concentration and fetal age were found to best predict fetal alpha-tocopherol concentration in serum. Interrelationships between selenium and vitamin E status were minimal. These data suggest inefficient placental transfer of vitamin E, resulting in minimal protection of the neonate from vitamin E-deficiency disease as a result of prepartal maternal supplementation.

Responses of dairy cattle to long-term and short-term supplementation with oral selenium and vitamin E1.

In a two-lactation-gestation cycle experiment, 152 Holstein cows with low serum Se and vitamin E were fed total mixed rations and assigned at parturition to four groups (1, control; 2, 500 IU vitamin E/d; 3, 2 mg Se/d; 4, 500 IU vitamin E plus 2 mg Se/d). Supplements were not fed during dry periods. Serum Se and vitamin E were increased within 1 mo by oral supplements. Maximal mean serum Se in cycles 1 (67 ng/ml at 7 mo) and 2 (74 ng/ml at 4 mo) occurred in groups 3 and 4, respectively. Maximal mean serum vitamin E in cycle 1 (3.3 micrograms/ml at mo 8) and 2 (3.03 micrograms/ml at mo 2) occurred in groups 4 and 2, respectively. Selenium treatment of the dams increased Se in colostrum and in serum of presuckle calves. Vitamin E supplementation of dams did not affect vitamin E in serum of presuckled calves. Reproductive performance was not affected by supplement. In an 8-wk study, 24 lactating cows with low serum Se were assigned (6/group) to 0, 2.5, 5, and 10 mg supplemental Se/d. Maximal mean serum Se concentrations of 23, 56, 71, and 79 ng/ml were attained by wk 4 in the above respective groups. These data indicate that 2 to 2.5 mg supplemental Se/cow per d were inadequate for desirable serum Se concentrations and support recent changes in allowed Se supplementation for dairy cattle.

Comparison of cupric and sulfate ion effects on chronic selenosis in rats.

The ameliorating effects of Cu++ and SO4--ions on concurrent selenite toxicity were compared in two factorial experiments using 60 weanling rats each. In the first experiment, 0, 500 and 1,000 mg Cu (as CuCl2)/kg diet were fed in conjunction with 0, 5, 10 and 20 mg Se (as Na2SeO3)/kg diet. In the second experiment, the treatments were 0, 500 and 1,000 mg SO4 (as Na2SO4)/kg fed in conjunction with 0, 5, 10 and 20 mg Se/kg diet. A paired-feeding experiment using 10, 15 and 20 mg Se/kg diet was also conducted with 28 rats to compare the influence of inanition in control and selenite-fed rats. Cupric++ ion, but not SO4--ion, prevented mortality among selenite-intoxicated rats. There were significant Cu X Se interaction effects on feed intake, daily gain, packed cell volume (PCV), serum Cu and Fe, sperm counts, and weights of liver, kidney and testis. There were main effects of Cu and Se on serum Se and liver Cu. In Exp. 2 there were significant SO4 X Se interaction effects on feed intake, daily gain, serum Cu and testis weight. There were main effects of Se on PCV, sperm count, serum testosterone, liver Se, liver Cu and the absolute weights of liver and kidney. The only main effect of SO4 was that of increased liver Cu concentrations. Among the pair-fed rats, the selenite-fed rats, with one exception, died before their paired rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial.

Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum vitamin E concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following vitamin E supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a vitamin E-responsive disorder of Equidae with a possible familial predisposition.

Importance of diet of dam and colostrum to the biological antioxidant status and parenteral iron tolerance of the pig.

Fifteen second-parity sows were used to determine the importance of vitamin E (E) and selenium (Se) supplementation of the sow's diet and colostrum consumption by the neonatal pig on tolerance to parenteral iron. Selenium (.1 ppm) and E (50 IU/kg) supplementation of the diet of the sow increased plasma tocopherol and Se concentrations, but did not increase plasma glutathione peroxidase (GSH-Px) activity. Colostrum had greater concentrations of E (primarily alpha-tocopherol) and Se than milk. Plasma biological antioxidant status (tocopherol level and GSH-Px activity) of pigs at birth was very low, but by 2 d of age had increased, especially in alpha-tocopherol (nearly a 20-fold increase). Liveability and body weight gain of pigs were not affected by the pre-colostrum iron injection (200 mg Fe as gleptoferron); however, plasma tocopherol concentrations of Fe-injected pigs were lower and plasma Se concentration and GSH-Px activities were higher at 2 d of age than values of pigs not receiving parenteral Fe. Supplementation of the dam's diet with E and Se maintained high tocopherol and Se levels in her colostrum and milk and a high biological antioxidant status in her pigs throughout the nursing period.

Multielement assays of canine serum, liver, and kidney by inductively coupled argon plasma emission spectroscopy.

Inductively coupled argon plasma emission spectroscopy was used to measure Al, As, Ca, Cd, Cr, Cu, Fe, Pb, Mg, Mn, Hg, Mo, P, K, Se, Na, Tl, and Zn in canine specimens (70 serum, 270 liver, and 200 kidney). Mean concentrations of each of these elements in detectable amounts in these samples were established, and histograms of the concentration distributions of elements in the samples were developed.

Multielement assays of bovine tissue specimens by inductively coupled argon plasma emission spectroscopy.

Inductively coupled argon plasma spectroscopy was used to generate multielement profiles of bovine serum (n = 607), liver (n = 229), and kidney (n = 90) samples submitted to the Animal Health Diagnostic Laboratory at Michigan State University, East Lansing. The presented frequency distribution histograms of element concentrations in the different samples provided a data base for diagnostic interpretations and illustrated some of the advantages, as well as limitations, of inductively coupled argon plasma for this purpose.

Effects of riboflavin supplementation and selenium source on selenium metabolism in the young pig.

The effect of dietary riboflavin (B2) supplementation and selenium (Se) source on the performance and Se metabolism of weanling pigs was studied. Pigs fed a B2-supplemented (10 mg/kg) casein-glucose diet for 18 d gained faster than pigs fed the B2-unsupplemented diet. Percentage active erythrocyte glutathione reductase (GR) declined rapidly when pigs were placed on the B2-unsupplemented diet and was lower (P less than .01) than that of B2-supplemented pigs after 12 d on test. Percentage active erythrocyte GR values fell below 50% before other B2 deficiency signs became evident. Supplementation of diets with 10 mg B2/kg resulted in increased kidney and muscle glutathione peroxidase (GSH-Px) activity. The Se concentration of liver and heart increased and plasma Se levels decreased with dietary B2 supplementation. Riboflavin supplementation and Se source did not alter apparent Se absorption, but B2 supplementation decreased urinary Se and thus increased Se retention. Also, there was less urinary Se excretion when selenomethionine was the dietary Se source and consequently more Se was retained than when sodium selenite was the dietary Se source. In a final trial, B2 supplementation increased kidney, muscle, heart and brain GSH-Px activity when sodium selenite was the dietary Se source, but not when selenomethionine was the dietary Se source.

Genetic predisposition of pigs to hypo- and hyperselenemia.

A continuing, sporadic incidence of vitamin E-selenium (Se) responsive disease among confinement-reared pigs believed to be fed complete and adequately supplemented diets prompted these studies on the potential genetic influence over vitamin E and Se metabolism in pigs. The initial study revealed a wide range of serum Se and vitamin E concentrations among age-matched, commonly housed and commonly fed growing pigs. Pigs found relatively hyposelenemic (hypo-Se) or hyperselenemic (hyper-Se) early in life retained their relative Se status while commonly reared. The persistence of vitamin E status was poor. Selected matings between identified, relatively hypo-Se gilts and boars and between relatively hyper-Se gilts and boars produced similarly affected baby pigs. In Exp. 2, representative hypo-Se (20) and hyper-Se (20) pigs were identified from a total of 107 baby pigs by 30 d of age. These pigs were allotted to an experiment to compare the responses of these two populations to .1 and .3 ppm supplemental dietary Se through 150 d of age. The difference in mean serum Se of the selected hypo- and hyper-Se pigs fed .1 ppm Se was significant at each sampling time. This difference approximated that observed between pigs (either hypo- or hyperselenemic) fed .1 and .3 ppm Se. The increase in serum Se due to .3 ppm supplemental dietary Se was greater among the selected hypo-Se pigs than among the hyper-Se pigs. Plasma Se-dependent glutathione peroxidase (GSH-Px) was a better indicator of dietary or serum Se status than was erythrocyte GSH-Px. The selected hyper-Se pigs maintained a more rapid rate of growth than did the hypo-Se pigs and were approximately 10 kg heavier at 150 d than the hypo-Se pigs.

Vitamin A status, polybrominated biphenyl (PBB) toxicosis, and common bile duct hyperplasia in rats.

The interaction between dietary concentrations of vitamin A and PBB was evaluated in two experiments. In the first experiment, male weanling rats were used in a 2 X 3 factorial experiment. Concentrations of PBB were 0, 10, or 100 mg/kg of diet and diets were either vitamin A-deficient or were supplemented with 3000 IU vitamin A palmitate/kg of diet. In the second experiment the design was similar except that two vitamin A-supplemented diets were used, one containing 3,000 IU/vitamin A palmitate/kg of diet and the other 30,000 IU. Diets contained either 0 or 100 mg of PBB/kg. Clinical signs of vitamin A deficiency and mortality occurred early in rats fed vitamin A-deficient diets containing 100 mg of PBB/kg. Vitamin A supplementation provided partial protection against decreased weight gain associated with PBB. Decreases in thymic weight associated with PBB toxicosis were prevented by supplementation with vitamin A. Massive enlargement of the common bile duct occurred in rats fed a vitamin A-deficient diet containing 100 mg of PBB/kg. Histologically, this lesion consisted of extensive hyperplasia. A significant decrease in retinol concentrations in the sera was recorded in rats fed vitamin A-deficient diets containing 100 mg of PBB/kg. Interaction between vitamin A deficiency and PBB toxicosis affected vitamin A metabolism as manifested by the appearance of appreciable amounts of retinyl acetate in the liver vitamin A profile. These results suggest an interaction between PBB toxicity and vitamin A and emphasize the importance of nutritional factors such as vitamin A in assessment of PBB toxicosis.

Effect of dietary zinc levels on health and productivity of gilts and sows through two parities.

The influence of 0, 50, 500 or 5,000 ppm supplemental Zn on productive characteristics, weight change, and serum and organ mineral concentrations of 60 crossbred and purebred Yorkshire gilts was evaluated. Gilts were fed their respective treatment from 30 kg body weight until the completion of two parities. Sows fed 5,000 ppm supplemental Zn weighed significantly less than sows from the other treatments when killed. Serum alkaline phosphatase activity was higher for the sows fed the highest level of Zn in all replications at 10 and 14 mo of age than for sows from the other treatments. Sows fed 0, 50 or 500 ppm had lower serum Zn and higher serum Cu concentrations than sows fed 5,000 ppm Zn at 10 and 14 mo of age. The number of pigs farrowed (total and live) and birth weight were not affected by dam's dietary treatment. However, sows receiving no additional Zn had a higher number of abnormal pigs/litter than sows on the other treatments. Sows fed 5,000 ppm additional Zn weaned fewer pigs that weighed less at weaning than sows on the other treatments. The concentration of Zn in the sow's liver increased significantly and liver Cu decreased as dietary level of Zn increased. Sows receiving 5,000 ppm Zn had lower hepatic Fe stores compared with sows receiving 500 ppm Zn. Elevated renal Cu and Zn concentrations were found in sows fed the highest level of Zn supplementation. The Zn concentration was higher and the Cu concentration lower in the aorta of sows fed 5,000 ppm Zn compared with sows fed 0 or 50 ppm additional Zn. Incidence of osteochondrosis was higher in sows supplemented with 5,000 ppm Zn than for sows from the other treatments.