Use of 1 alpha-hydroxyvitamin D3 to prevent bovine parturient paresis. VI. Concentrations of vitamin D metabolites and vitamin D3 equivalence in milk

Concentration of vitamin D metabolites was determined in the milk of control and 1 alpha-hydroxyvitamin D3-injected (700 micrograms) cows that calved 36 to 43 h after treatment. Milk samples were taken 60 h after calving. Concentrations of vitamin D, 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D in milk of the control cows were 372 +/- 24, 264 +/- 68, 68 +/- 26, and 21 +/- 3 ng/L, respectively. Concentrations of vitamin D metabolites in the milk of the treated cows did not differ significantly from those of controls. Concentration of 1 alpha-hydroxyvitamin D3 in milk of treated cows was less than 20 ng/L. In a second experiment, cows were injected twice, at 72-h intervals, with 350 micrograms 1 alpha-hydroxyvitamin D3. Milk was taken 60 h after parturition from cows that calved 37 to 60 h after the second injection. The vitamin D3 equivalence of the milk was 40 +/- 3 IU/L. Results indicate that injection of 700 micrograms 1 alpha-hydroxyvitamin D3 did not affect the concentration of vitamin D metabolites or the vitamin D3 equivalence of milk taken 60 h after calving.     

Effect of large oral and intravenous doses of vitamins D2 and D3 on vitamin D in milk

Vitamins D2 and D3 were measured in milk after high performance liquid chromatography of unsaponifiable lipids first on a silica column and then on a reverse-phase column. Milk from cows kept indoors contained barely detectable vitamin (less than 2 IU/100 ml) predominantly in the form of vitamin D3. When cows were given 5 or 10 million IU vitamin D3, maximums were in milk 3 to 7 days after oral doses and up to 10 days after intravenous injections. Maximums ranged from 7 to 90 IU/100 ml. Two cows were given given a mixture of 1 million IU vitamin D2 and 1 million IU vitamin D3 orally, and of the vitamins were maximum 2 to 3 days after the dose in blood plasma and a day later in milk. Equal amounts of the two forms of the vitamins were in milk, but vitamin D3 in plasma was double vitamin D2. Different mechanisms control concentrations of vitamins D2 and D3 in blood and milk after large doses.     

Effect of vitamin D source and amount on vitamin D status and response to endotoxin challenge

The objectives were to test the effects of dietary vitamin D₃ [cholecalciferol (CHOL)] compared with 25-hydroxyvitamin D₃ [calcidiol (CAL)] on vitamin D status and response to an endotoxin challenge. Forty-five Holstein bull calves (5 ± 2 d of age) were blocked into weekly cohorts, fed a basal diet that provided 0.25 µg/kg body weight (BW) CHOL, and assigned randomly to 1 of 5 treatments: control [(CON) no additional vitamin D], 1.5 µg/kg BW CHOL (CHOL1.5), 3 µg/kg BW CHOL (CHOL3), 1.5 µg/kg BW CAL (CAL1.5), or 3 µg/kg BW CAL (CAL3). Calves were fed milk replacer until weaning at 56 d of age and had ad libitum access to water and starter grain throughout the experiment. Treatments were added daily to the diet of milk replacer until weaning and starter grain after weaning. Measures of growth, dry matter intake, and serum concentrations of vitamin D, Ca, Mg, and P were collected from 0 to 91 d of the experiment. At 91 d of the experiment, calves received an intravenous injection of 0.1 µg/kg BW lipopolysaccharide (LPS). Clinical and physiological responses were measured from 0 to 72 h relative to LPS injection. Data were analyzed with mixed models that included fixed effects of treatment and time, and random effect of block. Orthogonal contrasts evaluated the effects of (1) source (CAL vs. CHOL), (2) dose (1.5 vs. 3.0 µg/kg BW), (3) interaction between source and dose, and (4) supplementation (CON vs. all other treatments) of vitamin D. From 21 to 91 d of the experiment, mean BW of supplemented calves was less compared with CON calves, but the effect was predominantly a result of the CHOL calves, which tended to weigh less than the CAL calves. Supplementing vitamin D increased concentrations of 25-hydroxyvitamin D in serum compared with CON, but the increment from increasing the dose from 1.5 to 3.0 µg/kg BW was greater for CAL compared with CHOL (CON = 18.9, CHOL = 24.7 and 29.6, CAL = 35.6 and 65.7 ± 3.2 ng/mL, respectively). Feeding CAL also increased serum Ca and P compared with CHOL. An interaction between source and dose of treatment was observed for rectal temperature and derivatives of reactive metabolites after LPS challenge because calves receiving CHOL3 and CAL1.5 had lower rectal temperatures and plasma derivatives of reactive metabolites compared with calves receiving CHOL1.5 and CAL3. Supplementing vitamin D increased plasma P concentrations post-LPS challenge compared with CON, but plasma concentrations of Ca, Mg, fatty acids, glucose, β-hydroxybutyrate, haptoglobin, tumor necrosis factor-α, and antioxidant potential did not differ among treatments post-LPS challenge. Last, supplementing vitamin D increased granulocytes as a percentage of blood leukocytes post-LPS challenge compared with CON. Supplementing CAL as a source of vitamin D to dairy calves was more effective at increasing serum 25-hydroxyvitamin D, Ca, and P concentrations compared with feeding CHOL. Supplemental source and dose of vitamin D also influenced responses to the LPS challenge.     

Effect of lipopolysaccharide infusion on serum macromineral and vitamin D concentrations in dairy cows

Four multiparous lactating cows (175 to 220 d in milk) were used in a 4 x 4 Latin square design to assess the effects of four doses (0.0, 0.5, 1.0, 1.5 microg/kg of body weight) of lipopolysaccharide (LPS; Escherichia coli 0111:B4) on circulating concentrations of macrominerals and vitamin D metabolites. Treatments were dissolved in 100 ml of sterile saline and infused intravenously over a period of 100 min. Blood was sampled immediately before infusion (0 h), at 60-min intervals for 8 h, and at 24 and 48 h postinfusion. Vitamin D metabolites were analyzed in samples collected at 0, 2, 6, 24, and 48 h only. Serum Ca and P concentrations decreased after LPS infusion, but there was no effect on serum magnesium concentration. Plasma 25-OH vitamin D3 and 1,25-(OH)2 vitamin D3 were not affected by LPS infusion; however, when analyzed as 0 vs. all other doses of LPS combined, there was a tendency for plasma 1,25-(OH)2 vitamin D3 concentration to decrease when cows were infused with LPS. The inflammatory response elicited by LPS altered plasma macromineral concentrations, a result that may have important implications for calcium homeostasis and metabolic health of lactating dairy cows.     

Effects of dietary vitamin D3 on concentrations of vitamin D and its metabolites in blood plasma and milk of dairy cows

To determine the effect of supplemental dietary vitamin D3 on concentration of vitamin D and its metabolites in milk, 20 Holstein cows were assigned to four groups and fed either 0, 10,000, 50,000, or 250,000 IU of vitamin D3/d beginning approximately 2 wk prepartum and continuing through wk 12 of lactation. Samples of blood plasma and milk were assayed for concentrations of vitamin D, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D. Only the daily dosage of 250,000 IU caused significant increases of concentrations of vitamin D or 25-hydroxyvitamin D in plasma. Concentrations of vitamin D and 25-hydroxyvitamin D in milk were approximately equal and averaged .2 ng/ml. Little 1,25-dihydroxyvitamin D and no 24,25-dihydroxyvitamin D could be detected in milk from any of the four treatment groups. Cows fed 250,000 IU of vitamin D3/d produced milk containing 54 IU of vitamin D activity per liter, whereas unsupplemented cows produced milk containing 17 IU/L. Oral supplementation with up to 250,000 IU of vitamin D3/d does not increase effectively vitamin D activity of milk.     

Vitamin D3 toxicity in dairy cows

Large parenteral doses of vitamin D3 (15 to 17.5 x 10(6) IU vitamin D3) were associated with prolonged hypercalcemia, hyperphosphatemia, and large increases of vitamin D3 and its metabolites in the blood plasma of nonlactating nonpregnant and pregnant Jersey cows. Calcium concentrations 1 day postpartum were higher in cows treated with vitamin D3 about 32 days prepartum (8.8 mg/100 ml) than in control cows (5.5 mg/100 ml). None of the cows treated with vitamin D3 showed signs of milk fever during the peripartal period; however, 22% of the control cows developed clinical signs of milk fever during this period. Signs of vitamin D3 toxicity were not observed in nonlactating nonpregnant cows; however, pregnant cows commonly developed severe signs of vitamin D3 toxicity and 10 of 17 cows died. There was widespread metastatic calcification in the cows that died. Because of the extreme toxicity of vitamin D3 in pregnant Jersey cows and the low margin of safety between doses of vitamin D3 that prevent milk fever and doses that induce milk fever, we concluded that vitamin D3 cannot be used practically to prevent milk fever when injected several weeks prepartum.     

Vitamin D3 and D3 metabolites in young goats fed varying amounts of calcium and vitamin D3

Twenty-four male goats, 2 to 4 wk of age, were allotted to four dietary treatments in a 2 X 2 factorial design and, for 20 wk, were fed a milk diet at 12.5% body weight. Treatments varied in amounts of supplemental calcium and vitamin D3. Daily allowances per kilogram body weight were: 9.4 IU vitamin D3 (basal), 9.4 IU vitamin D3 plus 406 mg calcium carbonate (basal plus Ca), 940 IU vitamin D3 (basal plus D3), and 940 IU vitamin D3 plus 406 mg calcium carbonate (basal plus Ca plus D3). At the end of wk 7, a corn supplement was added to all diets at 1% body weight daily. Addition of vitamin D3 to the diet resulted in a dramatic increase in plasma concentrations of vitamin D3. Goats in the basal plus D3 and basal plus Ca plus D3 groups had nearly 100 X greater concentrations of vitamin D3 than goats in the basal and basal plus Ca groups. When greater amounts of vitamin D3 were fed, dietary calcium interacted to decrease plasma vitamin D3 concentrations. Plasma concentrations of 25-hydroxyvitamin D3 were unaffected by additional dietary calcium but were increased by dietary vitamin D3, increasing sixfold to seven-fold in the basal plus D3 and basal plus Ca plus D3 groups. Supplemental calcium resulted in decreased plasma 1,25-dihydroxyvitamin D3. No signs of vitamin D toxicity were noted. The physiological responses reported implicate the goat as a potential animal model for vitamin D research in dairy cattle.     

Estimation and fortification of vitamin D3 in pasteurized process cheese

The objective of this study was to develop methods for the estimation and fortification of vitamin D3 in pasteurized Process cheese. Vitamin D3 was estimated using alkaline saponification at 70 degrees C for 30 min, followed by extraction with petroleum ether:diethyl ether (90:10 vol/vol) and HPLC. The retention time for vitamin D3 was approximately 9 min. A standard curve with a correlation coefficient of 0.972 was prepared for quantification of vitamin D3 in unknown samples. In the second phase of the study, pasteurized Process cheeses fortified with commercial water- or fat-dispersible forms of vitamin D3 at a level of 100 IU per serving (28 g) were manufactured. There was no loss of vitamin D3 during Process cheese manufacture, and the vitamin was uniformly distributed. No losses of the vitamin occurred during storage of the fortified cheeses over a 9-mo period at 21 to 29 degrees C and 4 to 6 degrees C. There was an approximately 25 to 30% loss of the vitamin when cheeses were heated for 5 min in an oven maintained at 232 degrees C. Added vitamin D3 did not impart any off flavors to the Process cheeses as determined by sensory analysis. There were no differences between the water- and fat-dispersible forms of the vitamin in the parameters measured in fortified cheeses.     

Mammary transfer of vitamin A alcohol and ester in lactating dairy cows.

The effect of intravenous injection of vitamin A alcohol and vitamin A ester on the vitamin A concentration of bovine milk was studied. Holstein cows received either an intravenous injection of 1 million international units (IU) of vitamin A alcohol, 1 million international units of vitamin A palmitate, or served as controls. Blood serum and milk were sampled at intervals prior to and following injection. Mean concentrations of vitamin A in milk at time 0 were 59.0, 52.0, and 58.4 mug/100 ml for the control, alcohol, and palmitate treatments. Mean contrations of vitamin A in milk, expressed as mug/100 ml or mug/g fat of cows receiving vitamin A alcohol at +195, +451, and +678 min postinjection, were greater than concentrations for either control cows or cows receiving palmitate. Partition of milk Vitamin A at +195 min postinjection for cows injected with vitamin A alcohol showed 4.1% of the recovered vitamin A in the alcohol and 95.9% in the ester form. Injection of vitamin A palmitate had little effect on milk vitamin A concentration. Vitamin A in serum (mug/100 ml) at 195 min after vitamin A alcohol injection was higher (100.4) than for either control (84.0) or cows injected with vitamin A palmitate (89.0).     

Effect of vitamin D on lead assimilation

It was established in experiments on rickety chickens given and not given an additive of 0.5% lead acetate to the diet and vitamin D3 (10 IU/day intramuscularly) for a week that vitamin D induced an appreciable increase of lead deposition in the tissues. The degree of lead poisoning assessed according to the content of delta-aminolevulinic acid in red cells was 8 times as increased as compared with the same indicator in chickens not injected with vitamin D. The balance studies demonstrated that retention of the diet lead under the effect of vitamin D rose 2 times. Vitamin D noticeably stimulated 210Pb absorption from chicken duodenum in experiments in situ.     

Short communication: serum and tissue concentrations of vitamin D metabolites in beef heifers after buccal dosing of 25-hydroxyvitamin D3

Sixteen crossbred (British x Continental; average un-shrunk body weight = 507.9 kg; SD = 45.6 kg) beef heifers fed a steam-flaked corn-based finishing diet with melengestrol acetate (0.4 mg/heifer daily) included to suppress estrus were used in a completely random design to evaluate the efficacy of buccal administration of 0, 10, 100, or 1000 mg of 25-hydroxyvitamin D3, (25-OH D3). Serum Ca, P, Mg, 25-OH D3, 1,25-dihydroxyvitamin D [1,25-(OH)2 D3], albumin, and protein were measured 24 h before dosing (-24 h), at dosing (0 h), and 6 and 24 h after dosing, after which the cattle were slaughtered at a commercial facility. Samples of kidneys, liver, longissimus lumborum, and triceps brachii were collected and evaluated for concentrations of 1,25-(OH)2 D3. With -24 and 0 h as baseline covariates, a significant time x treatment interaction was observed for serum 25-OH D3 and Ca concentrations, but not for serum 1,25-(OH)2 D3. Supplemental 25-OH D3 doses of 100 and 1000 mg significantly increased serum 25-OH D3 at 24 h after dosing, 1,25-(OH)2 D3 at 6 and 24 h after dosing, and serum Ca at 24 h after dosing. Similarly, buccal dosing of 1000 mg of supplemental 25-OH D3 significantly increased (approximately 2- to 3-fold) concentrations of 1,25-(OH)2 D3 in the kidney, liver, and longissimus lumborum relative to the other 3 treatments but not in triceps brachii. Serum albumin, protein, P, and Mg were not affected by treatment. Based on these results, buccal administration of 100 and 1000 mg 25-OH D3 increased vitamin D3 metabolites in serum and tissues, and it should be an effective method of delivering the vitamin.     

Efficacy and safety of 1alpha-hydroxyvitamin D3 for prevention of parturient paresis

Four trials involved intravenous or intramuscular injections of 1alpha-hydroxyvitavin D3 to test efficacy in preventing parturient paresis. Use of .1 mg intravenously afforded total protection compared with an incidence of 33% (2/6) in controls. Intramuscular injections of .1 mg in 2 ml propylene glycol and .3, .5, and 1.0 mg in 5 ml corn oil resulted in 0, 15.7, 20, and 0% incidence of parturient paresis compared with 33, 16.7, 37.5, and 37.5% incidence of parturient paresis in the controls. There was a rapid increase in serum calcium (12 to 24 h) in response to intravenous treatment, whereas the response to intramuscular injections was gradual but was maintained longer. To evaluate the safety of 1alpha-hydroxyvitamin D3, eight cows, two per treatment, were given intramuscular doses of .5, 1.0, 1.5, or 3.0 mg (three 1.0 mg injections) in 5 ml corn oil. No clinical or pathological evidence of hypervitaminosis C or soft tissue calcification was found. Tissue taken from the injection site 15 days after last injection contained 3 to 38 IU vitamin D activity per 100 g wet tissue compared with control of 8 to 15 IU per 100 g. Total vitamin D activity of milk taken the 11th milking postpartum from cows receiving .5 or 1.0 mg had a mean of 13.4 and 22.6 IU vitamin D activity per liter compared to 19 IU per liter for control milk. Milk from the 5th milking postpartum in the cows receiving .5 mg had a mean activity of 14.5 IU per liter. Milk from animals slaughtered for retention studies had a mean activity of 22 IU per liter.     

1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 reduces parturient paresis in dairy cows fed high dietary calcium.

The effectiveness of a combination of 1 alpha-hydroxyvitamin D3 and 25-hydroxyvitamin D3 for reducing incidence of parturient paresis in aged Holstein cows was tested. Intramuscular injection of .5 mg of 1 alpha-hydroxyvitamin D3 plus 4 mg of 25-hydroxyvitamin D3 increased plasma 1,25-dihydroxyvitamin D concentrations through parturition. Treatment with 1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 raised prepartum serum Ca approximately 2 mg/dl and prepartum serum P approximately 4 to 5 mg/dl higher than untreated controls. Both treated and control cows had approximately a 2-mg/dl decrease in serum Ca following parturition. The prepartum diet of alfalfa silage and hay was supplemented with a grain mixture supplying 100 g of Ca/d from ground limestone. Under these dietary conditions, incidence of parturient paresis was reduced from 33 to 8%. In a separate experiment, treatment with 1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 did not reduce incidence of parturient paresis when cows consumed mixed diets of different feed-stuff composition. Further experiments are required to determine specifically the factor or factors responsible for the difference in response to active vitamin D compound administration between the two experiments. Prepartum dietary Ca intake may be one such factor.     

The determination of vitamin D3 in bovine milk by liquid chromatography mass spectrometry

A renewed international interest in vitamin D status has revealed significant deficiencies in several populations, including Australia. Vitamin D exists in two forms, cholcalciferol (D₃) and ergocalciferol (D₂). The main source of vitamin D₃ is from exposure of 7-dehydrocholesterol present in the skin to UV irradiation. However, there is an absolute requirement for vitamin D through proper dietary intake if humans live in the absence of sunlight or exclusively indoors. Bovine milk is considered to be a good dietary source of vitamin D₃, even though the levels are quite low. This paper describes robust methods using liquid chromatography–linear ion trap mass spectrometry (LC–MSⁿ) and liquid chromatography–tandem mass spectrometry (LC–MS/MS) to measure the levels of vitamin D₃ in fresh bovine milk (0.05 μg/100 ml), commercial (natural and fortified) milk samples (0.01–2 μg/100 ml) and a dairy based infant formula (8 μg/100 g), without the need for extensive clean-up procedures. The limits of quantification (LOQ) are 0.01 μg/100 ml and 0.02 μg/100 ml for LC–MSⁿ and LC–MS/MS, respectively. Recoveries of vitamin D₃ added to the samples prior to saponification were satisfactory (range 60–90%). 25-Hydroxyvitamin D₃ was not present in any of the samples analysed (LOQ = 0.01 μg/100 ml, recovery range 30–40%).     

Fate of tritium-labeled vitamin D3 and 25-hydroxyvitamin D3 in rabbit does and their pups

Mammary transfer of label from intraperitoneally injected 50 microCi [1 alpha, 2 alpha(n)-hydrogen-3] cholecalciferol, and 50 microCi (26,27-methyl-hydrogen-3)cholecalciferol was studied in nursing rabbits. Does were injected at 3 days postpartum with one of the two labeled compounds. Pups were killed at either 1, 2, 3, 4, or 5 days after dosing of the does, and does were killed after 5 days. Concentrations of radioactivity were greater in tissues of does dosed with tritiated vitamin D3 than in tissues of those dosed with tritiated 25-hydroxyvitamin D3. Concentrations of radioactivity were greater in maternal tissues than in tissues of pups. On the 5th day following administration of tritiated vitamin D3 or 25-hydroxyvitamin D3, the major portion of the radioactivity in does plasma and liver was associated with tritiated 25-hydroxyvitamin D3. In pups from the tritiated vitamin D3 group, the concentration of plasma radioactivity associated with 25-hydroxyvitamin D3 (isolated by high pressure liquid chromatography) increased significantly with time, reaching 85% of the total vitamin D and metabolite radioactivity in the pups at the 5th day. Over 90% of the total recovered plasma radioactivity of pups of the tritiated 25-hydroxyvitamin D3 group was associated with the 25-hydroxyvitamin D3. Much more radioactivity was secreted in the milk of tritiated 25-hydroxyvitamin D3 dosed does than in milk of does dosed with tritiated vitamin D3.     

Effects of continuous administration of 1,25-dihydroxyvitamin D3 on plasma minerals and unoccupied colon mucosal 1,25-dihydroxyvitamin D3 receptor concentrations

Six mature nonlactating, nonpregnant Jersey cows were implanted with Alzet mini-osmotic pumps, which delivered 50 micrograms of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] each day for 7 d in an effort to mimic plasma concentrations of 1,25-dihydroxyvitamin D [1,25-(OH)2D] observed in cows at parturition. Plasma samples were obtained daily beginning 6 d prior to implantation and ending 8 d after removal of the implants. Six biopsies of the descending colon mucosa were obtained per rectum before and after implantation and assayed for unoccupied 1,25-(OH)2D3 receptor concentration. Plasma concentration of 1,25-(OH)2D increased from 37 pg/ml pretreatment to 294 pg/ml with the pumps implanted. Plasma Ca concentration increased within 2 d after implantation and remained elevated for 7 d after the pumps were removed. Unoccupied colon mucosa 1,25-(OH)2D3 receptor mean concentration prior to treatment was 14.6 fmol/mg protein and increased within 2 d following implantation to 30.5 fmol/mg protein. These data suggest that 1,25-(OH)2D3 upregulates its own receptor in the intestine of the cow.     

Reduced serum vitamin D concentrations in healthy early-lactation dairy cattle

Cattle obtain vitamin D by ingestion or cutaneous exposure to UV light. Dairy cattle diets are frequently supplemented with vitamin D to compensate for limited sun exposure or during times of increased metabolic demands, such as the periparturient period, to maintain calcium homeostasis. Whether housing and supplemental vitamin D practices supply adequate amounts of vitamin D to optimally support the transition from gestation to lactation in dairy cattle is unknown. Our objective was to determine how serum vitamin D concentrations of dairy cows change with season, age, parity, and stage of lactation. Clinically healthy cows (n = 183) from 5 commercial dairies were enrolled in the study. Serum samples were collected at dry off, within 7 d of entering the close-up group, and within 7 d after calving (calving+7). Vitamin D status was determined by measuring serum 25-hydroxyvitamin D [25(OH)D] by radioimmunoassay. We performed repeated-measures mixed-effects linear regression to determine the effects of season, age, parity, and lactation stage (dry off, close-up, and calving+7) on 25(OH)D concentrations in serum. Bivariable analysis indicated that parity, age, and season were not associated with serum 25(OH)D concentrations. Sample period affected 25(OH)D concentrations, with the highest 25(OH)D levels at dry off (99.7 ± 1.9 ng/mL) followed by close up (93.8 ± 2.1 ng/mL), with the lowest levels at calving+7 (82.6 ± 1.7 ng/mL). These data showed a large depletion of 25(OH)D in dairy cattle postpartum compared with late prepartum, although the biological significance of this change in these healthy cattle is unclear. Consumption of serum 25(OH)D by immune system functions and calcium homeostasis in early lactation likely caused the reduction in serum 25(OH)D concentrations after calving. These results suggest that determining whether serum 25(OH)D concentrations are associated with the incidence of transition period disease is an appropriate next step. Assessing the effects of enhanced vitamin D supplementation of cows in early lactation on postpartum diseases may be warranted.     

Pharmacokinetics and amounts of 25-hydroxycholecalciferol in sheep affected by osteodystrophy.

Amounts of 25-hydroxycholecalciferol in plasma were measured in two groups (A and B) of lambs (Experiment 1) and in two groups (C and D) of wethers (Experiment 2). Groups A (eight lambs) and C (nine wethers) consisted of animals born and raised in total confinement; these animals exhibited an osteodystrophic condition. Groups B (four lambs) and D (10 wethers) consisted of healthy animals born and raised in a conventional barn with free access to an open barn yard (i.e. exposure to sunshine). The 25-hydroxycholecalciferol in plasma of both groups of sick animals, Group A (12.9 ng/ml) and Group C (18.0 ng/ml), were lower than the amounts of the two corresponding groups of healthy animals. Group B (29.2 ng/ml and Group D (32.5 ng/ml). Pharmacokinetic analysis of 25-hydroxycholecalciferol in affected lambs following intramuscular injection of 1,000,000 IU vitamin D3 indicated that transport of vitamin D3 from the site of injection to the liver and its metabolism to 25-hydroxycholecalciferol were rapid. Peak 25-hydroxycholecalciferol occurred at .6 wk, and half-life was 3.1 wk.     

Effects of oral vitamin D(3) supplementation and supplement withdrawal on the accumulation of magnesium, calcium, and vitamin D in the serum, liver, and muscle tissue and subsequent carcass and meat quality of Bos indicus influenced cattle

Bos indicus crossbred cattle (n=79) were fed vitamin D(3) (0 or 3 million IU/hd/d) for 5d. Afterwards, half of each group was slaughtered immediately, while half was fed, without supplementation, for 7d before processing. Serum calcium concentration was increased (P<0.05) in cattle after supplement removal, but not immediately following supplementation. This also was observed in the M. longissimus lumborum and M. triceps brachii, but not in the M. semitendinosus. Liver biopsy vitamin D(3) concentrations were higher (P<0.05) in supplemented cattle immediately following supplementation, but were not different from controls after supplement removal. Vitamin D(3) did not affect tenderness at supplement removal day 0, but increased the tenderness of the M. longissimus lumborum and M. semitendinosus at supplement removal day 7. Vitamin D(3) supplementation improves muscle tenderness and may be more effective when supplementation is ceased 7d before slaughter, with minimum food safety concerns.