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Subclinical vitamin D deficiency in neonates: definition and response to vitamin D supplements.

To determine the biological criteria for neonatal vitamin D deficiency, serum 25-hydroxyvitamin D (calcidiol), parathyroid hormone (PTH), calcium, phosphates, and alkaline phosphatase (ALP) activity were measured during the winter-spring period in 80 healthy neonates and their mothers 3-6 d after delivery. A longitudinal 3-mo survey of the serum biology of 52 of these neonates consuming formula was also performed to test the influence of their neonatal vitamin D status on the effects of two oral ergocalciferol supplements (500 and 1000 IU or 12.5 and 25 micrograms/d). At birth, 63.7% of the infants had calcidiol concentrations < or = 30 nmol/L. Most of them had no other biological sign evocative of vitamin D deficiency, but 14 neonates had low calcidiol concentrations and serum PTH concentrations > 60 ng/L, the upper limit of the adult normal range. They also had a significantly lower mean serum calcium concentration than did neonates with calcidiol concentrations > 30 nmol/L. On the basis of the association of low calcidiol concentrations (< or = 30 nmol/L) and high PTH concentrations (> 60 ng/L) as criteria for vitamin D deficiency, 24% of the neonates born to unsupplemented mothers were found to be vitamin D-deficient. Neonatal vitamin D status influenced the response of the infants to vitamin D supplements. Neonates with no sign of vitamin D deficiency showed similar changes in their serum calcidiol, calcium, phosphate, and PTH concentrations and ALP activity and no toxic effect (hypercalcemia or highly elevated calcidiol concentration) was observed whatever their vitamin D intake. In contrast, neonates with subclinical vitamin D deficiency had normalized serum PTH within 1 mo only when they were given 1000 IU ergocalciferol (25 micrograms)/d in addition to their formula.

Adult↗

Vitamin K requirement and the concentration of vitamin K in rat liver.

The concentration of vitamin K was determined in the liver of different strains of rats, and in male and female warfarin-resistant rats by feeding 3H-vitamin K in a purified diet. In each case, the level of vitamin K in the liver correlated approximately with the amount of vitamin K fed. The results indicate that differences in the requirement for vitamin K between the sexes and between strains of rats are due principally to different required concentrations of vitamin K in liver and not to differences in absorption or turnover of the vitamin. The results of the determination of vitamin K epoxide levels in male and female warfarin-resistant rats, and other data, suggest that the amount of vitamin K required in liver may be in part due to differences in the activity of the enzyme, vitamin K epoxide reductase.

Animals↗

Megadose effects of vitamin C on vitamin B-12 status in the rat.

Effects of ascorbic acid ingestion on the severity of vitamin B-12 deficiency were investigated by feeding weanling rats experimental diets containing 0-100 micrograms of vitamin B-12 activity per kg of diet, with or without 6.0 mg of ascorbic acid per ml supplied in drinking water for 15 wk. This daily consumption of up to 150 mg of ascorbic acid did not impair growth, but did result in significantly higher concentrations of ascorbic acid in plasma, liver, adrenal glands and feces. When rats were fed diets deficient or marginally deficient in vitamin B-12, liver concentrations of vitamin B-12 were markedly lower than in liver of rats fed adequate vitamin B-12. Ascorbic acid ingestion raised values significantly in the vitamin B-12-deficient diet group. Urinary methylmalonic acid was significantly elevated in the deficient rats. However, it was significantly reduced to more normal values by ascorbic acid in rats with both low and marginal vitamin B-12 status, as defined by dietary and liver concentrations of vitamin B-12 activity. Although coprophagy was not prevented, rats showed no increased consumption of feces with the higher ascorbic acid content. Thus, the results of this research indicate that vitamin C ingestion partially protects rats from vitamin B-12 deficiency.

Adrenal Glands↗

Determination of vitamin B-6 estimated average requirement and recommended dietary allowance for children aged 7-12 years using vitamin B-6 intake, nutritional status and anthropometry.

The Estimated Average Requirement (EAR) and Recommended Dietary Allowance (RDA) of vitamin B-6 for children were recently estimated by extrapolating from adult values because of limited available information. To determine vitamin B-6 requirements and provide recommendations for intakes, vitamin B-6 intake, nutritional status and anthropometry of 168 healthy children (79 boys and 89 girls) were studied in Tainan, Taiwan. Direct and indirect vitamin B-6 status indicators were measured in plasma, erythrocytes and urine. Anthropometric data of children in this study were similar to those of the first Nutrition and Health Survey in Taiwan (NAHSIT) conducted in 1993-1996. The plasma pyridoxal phosphate (PLP) concentration of each child was >/=30 nmol/L, indicating an adequate vitamin B-6 status. Daily dietary vitamin B-6 intakes of boys and girls were 0.80 +/- 0.16 and 0.74 +/- 0.16 mg/d, respectively. Daily dietary vitamin B-6 intakes of children who had adequate urinary 4-pyridoxic acid (4-PA) (>3.0 micro mol/L), erythrocyte alanine aminotransferase activity coefficient (EALT-AC) (<1.25) and aspartate aminotransferase activity coefficient (EAST-AC) (<1.8) were not different from those of children who had adequate plasma PLP, although the percentages of adequacy for urinary 4-PA, EALT-AC and EAST-AC ranged from 20 to 91%. Vitamin B-6 status indicators were strongly correlated with vitamin B-6 intake. Adequate values of PLP, EALT-AC, EAST-AC and urinary 4-PA were used to determine the EAR according to Dietary Reference Intake (DRI) committee methodology. We determined the vitamin B-6 EAR (RDA) for boys and girls aged 7-12 y to be 0.84 (1.01) and 0.75 (0.89) mg/d, respectively.

Administration, Oral↗

Vitamin A and iron status are improved by vitamin A and iron supplementation in pregnant Indonesian women.

In Indonesia, deficiencies of vitamin A and iron are of public health concern during pregnancy. We sought to determine the effects of vitamin A and iron supplementation on the vitamin A and iron status of pregnant Indonesian women. The women (n = 27) were randomly assigned to four groups. The modified relative dose response (MRDR) test for vitamin A status and hemoglobin, hematocrit and ferritin values were determined at baseline. Thereafter, daily supplements were administered: placebo [Pl] (n = 7), 8.4 micromol vitamin A [A] (n = 7), 1.07 mmol iron [Fe] (n = 5), and 8.4 micromol vitamin A plus 1.07 mmol iron [A + Fe] (n = 8). Post-treatment tests were performed after 8 wk. The MRDR value was reduced, i.e., vitamin A status improved, more markedly by the combination of vitamin A and iron than by either nutrient alone (P = 0.034). The decrease in the MRDR relative to baseline was significant in the A + Fe group (P = 0.008). Iron status was also significantly improved in these women (P < 0.05) with both iron and vitamin A supplementation. The mechanism of the enhancing effect of iron on the vitamin A-induced reduction in the MRDR is not known.

Adult↗

Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk.

BACKGROUND: Vitamin E, beta-carotene, and vitamin C are micronutrient antioxidants that protect cells from oxidative damage involved in prostate carcinogenesis. In separate trials, supplemental vitamin E was associated with a decreased risk of prostate cancer among smokers and supplemental beta-carotene was associated with a decreased risk of prostate cancer among men with low baseline plasma beta-carotene levels. METHODS: We evaluated the association between intake of these micronutrient antioxidants from foods and supplements and the risk of prostate cancer among men in the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. At baseline, trial participants completed a 137-item food frequency questionnaire that included detailed questions on 12 individual supplements. Cox proportional hazards models were used to estimate relative risks (RRs) and 95% confidence intervals (CIs). All statistical tests were two-sided. RESULTS: We identified 1338 cases of prostate cancer among 29 361 men during up to 8 years of follow-up. Overall, there was no association between prostate cancer risk and dietary or supplemental intake of vitamin E, beta-carotene, or vitamin C. However, among current and recent (i.e., within the previous 10 years) smokers, decreasing risks of advanced prostate cancer (i.e., Gleason score > or = 7 or stage III or IV) were associated with increasing dose (RR for > 400 IU/day versus none = 0.29, 95% CI = 0.12 to 0.68; Ptrend = .01) and duration (RR for > or = 10 years of use versus none = 0.30, 95% CI = 0.09 to 0.96; Ptrend = .01) of supplemental vitamin E use. Supplemental beta-carotene intake at a dose level of at least 2000 microg/day was associated with decreased prostate cancer risk in men with low (below the median of 4129 microg/day) dietary beta-carotene intake (RR = 0.52, 95% CI = 0.33 to 0.81). Among smokers, the age-adjusted rate of advanced prostate cancer was 492 per 100,000 person-years in those who did not take supplemental vitamin E, 153 per 100,000 person-years in those who took more than 400 IU/day of supplemental vitamin E, and 157 per 100,000 person-years in those who took supplemental vitamin E for 10 or more years. Among men with low dietary beta-carotene intake, the age-adjusted rate of prostate cancer was 1122 per 100,000 person-years in those who did not take supplemental beta-carotene, and 623 per 100,000 person-years in those who took at least 2000 microg/day of supplemental beta-carotene. CONCLUSIONS: Our results do not provide strong support for population-wide implementation of high-dose antioxidant supplementation for the prevention of prostate cancer. However, vitamin E supplementation in male smokers and beta-carotene supplementation in men with low dietary beta-carotene intakes were associated with reduced risk of this disease.

Adult↗

Randomized trial testing the effect of vitamin A supplementation on pregnancy outcomes and early mother-to-child HIV-1 transmission in Durban, South Africa. South African Vitamin A Study Group.

OBJECTIVE: Poor vitamin A status has been associated with a higher risk for mother-to-child transmission of HIV-1 and there is contradictory evidence on the impact of vitamin A on perinatal outcome. We therefore assessed the effect of vitamin A supplementation to mothers on birth outcome and mother-to-child transmission of HIV-1. DESIGN AND METHODS: In Durban, South Africa 728 pregnant HIV infected women received either vitamin A (368) or placebo (360) in a randomized, double-blind trial. The vitamin A treatment consisted of a daily dose of 5000 IU retinyl palmitate and 30 mg beta-carotene during the third trimester of pregnancy and 200000 IU retinyl palmitate at delivery. HIV infection results were available on 632 children who were included in the Kaplan-Meier transmission analysis. Results are reported on mother-to-child transmission rates up to 3 months of age. RESULTS: There was no difference in the risk of HIV infection by 3 months of age between the vitamin A [20.3%; 95% confidence interval (CI), 15.7-24.9] and placebo groups (22.3%; 95% CI, 17.5-27.1), nor were there differences in foetal or infant mortality rates between the two groups. Women receiving vitamin A supplement were, however, less likely to have a preterm delivery (11.4% in the vitamin A and 17.4% in the placebo group; P = 0.03) and among the 80 preterm deliveries, those assigned to the vitamin A group were less likely to be infected (17.9%; 95% CI, 3.5-32.2) than those assigned to the placebo group (33.8%; 95% CI, 19.8-47.8). CONCLUSION: Vitamin A supplementation, a low-cost intervention, does not appear to be effective in reducing overall mother-to-child transmission of HIV; however, its potential for reducing the incidence of preterm births, and the risk of mother-to-child transmission of HIV in these infants needs further investigation.

Adult↗

Binding of vitamin B12--rat transcobalamin II and free vitamin B12 to plasma membranes isolated from rat liver.

When dialysed rat serum which contains a single, low molecular weight binder for vitamin B12, rat transcobalamin II (rat TC-II), was labelled in vitro with 57Co-vitamin B12 and then incubated at 30 degrees C (pH 7-5) with vesicles of highly purified plasma membranes separated from microsomal fractions of rat liver by density gradient centrifugation, the 57Co-vitamin B12-rat TC-II complex bound to high affinity sites on the vesicles via a specific (binding after correction for 'non-specific' binding in the presence of a large excess of the non-radioactive complex), saturable, and reversible interaction. The apparent affinity constant for the binding reaction was 5-5 X 10(9) M-1. Using the same incubation conditions, free vitamin B12 also bound to the vesicles of plasma membranes via a specific, saturable, but apparently irreversible interaction. Preincubation of the membranes with free vitamin B12 did not interfere with the subsequent binding of the vitamin B12-rat TC-II complex to the membranes; however, preincubation with the vitamin B12-rat TC-II complex did interfere, to some extent, with the subsequent binding of free vitamin B12. Dialysed rat serum, perhaps the free rat TC-II in the dialysed serum, also inhibited the binding of the vitamin B12-rat TC-II complex to the plasma membranes. The relationship of the binding sites identified in this report to the absorption of vitamin B12 by rat liver, and thus their physiological significance remains unknown until further work is done, perhaps using intact hepatocytes.

Animals↗

Formation of transcobalamin II--vitamin B12 complex by guinea-pig ileal mucosa in organ culture after in vivo incubation with intrinsic factor--vitamin B12.

The in vivo incubation of intrinsic factor--[57Co]vitamin B12 in an ileal loop of a guinea-pig followed by in vitro culturing of segments of the ileum for 180 min has been used to study the transepithelial transport of vitamin B12. Analysis of the solubilized supernate of mucosa following the in vivo phase demonstrated that 44% of the [57Co]vitamin B12 was bound to intrinsic factor (IF), 26% was free, and 16% was bound to transcobalamin II (TCII). Following culture, similar analysis demonstrated that 18% of the vitamin was now bound to IF, 49% was free, and 35% ws bound to TCII. In the culture medium, 54% of the [57Co]vitamin B12 was free and 37% was bound to TCII. The formation of TCII-[57Co]vitamin B12 did not occur if homogenized mucosa was incubated with free[57Co]vitamin B12, but it did form in cultures of ileal segments from animals given an excess of unlabelled vitamin to saturate all circulating TCH, and in the medium containing puromycin. Indirect immunofluorescence using chicken anti-TCII demonstrated that TCII was associated with the mucosal cells of both the ileum and jejunum. These studies demonstrate that following transepithelial flux of vitamin B12 through the ileal mucosa, the vitamin becomes coupled to TCII. This coupling requires a structurally intact mucosa and the source of the TCII appears to be the ileal mucosal cell rather than unsaturated TCII circulating in the blood.

Animals↗

Antioxidants vitamin C and vitamin e for the prevention and treatment of cancer.

OBJECTIVE: To evaluate the evidence of the supplements vitamin C and vitamin E for treatment and prevention of cancer. METHODS: Systematic review of trials and meta-analysis. DATA SOURCES AND MAIN RESULTS: Thirty-eight studies showed scant evidence that vitamin C or vitamin E beneficially affects survival. In the ATBC Cancer Prevention Study Group, no statistically significant effect of treatment was seen for any cancer individually, and our pooled relative risk (regardless of tumor type) for alpha-tocopherol alone was 0.91 (95% confidence interval [CI]: 0.74, 1.12). All cause mortality was not significant. In the Linxian General Population Trial, the relative risks for cancer death for vitamin C (combined with molybdenum) was 1.06 (95% CI: 0.92, 1.21) and for vitamin E (combined with beta-carotene and selenium) was 0.87 (95% CI: 0.76, 1.00). We identified only 3 studies that reported statistically significant beneficial results: vitamin C (in combination with BCG) was found to be beneficial in a single trial of bladder cancer and vitamin E (in combination with omega-3 fatty acid) increased survival in patients with advanced cancer. In the ATBC trial, in analyses of 6 individual cancers, the prevention of prostate cancer in subjects treated with alpha-tocopherol was statistically significant (RR=0.64, 95% CI: 0.44, 0.94). CONCLUSIONS: The systematic review of the literature does not support the hypothesis that the use of supplements of vitamin C or vitamin E in the doses tested helps prevent and/or treat cancer in the populations tested. There were isolated findings of benefit, which require confirmation.

Antioxidants↗

The protective effect of vitamin C, vitamin E and selenium combination therapy on ethanol-induced duodenal mucosal injury.

In this study, the effect of a combination of vitamin C, vitamin E and selenium on ethanol-induced duodenal mucosal damage in rats was investigated morphologically and biochemically. The duodenal mucosal injury was produced by oral administration of 1 mL of absolute ethanol to each rat. Animals received vitamin C (250 mg/ kg), vitamin E (250 mg/kg) and selenium (0.5 mg/kg) for 3 days and absolute ethanol 1 hour after last antioxidant administration and were sacrificed 1 hour after absolute ethanol. Extreme degeneration in intestinal mucosa of rats given ethanol was observed morphologically. In addition, an increase in neuronal nitric oxide synthase immunoreactive areas was observed in the rats of the group given ethanol. On the other hand, a normal morphological appearance and a decrease in neuronal nitric oxide synthase immunoreactive areas were detected in the rats given ethanol+vitamin C+vitamin E+ selenium. In the group to which ethanol was administered, an increase in serum cholesterol and a decrease in serum albumin levels were determined. On the other hand, in the group to which ethanol+vitamin C+vitamin E+selenium were administered, serum cholesterol value decreased, and the serum albumin level increased. As a result, we can say that the combination of vitamin C, vitamin E and selenium has a protective effect on ethanol-induced duodenal mucosal injury.

Animals↗

Plasma vitamin B6 vitamers before and after oral vitamin B6 treatment: a randomized placebo-controlled study.

BACKGROUND: Vitamin B(6) has attracted renewed interest because of its role in homocysteine metabolism and its possible relation to cardiovascular risk. We examined the plasma B(6) vitamers, pyridoxal 5'-phosphate (PLP), pyridoxal (PL), pyridoxine (PN), and 4-pyridoxic acid (4-PA) before and after vitamin B(6) supplementation. METHODS: Patients (n = 90; age range, 38-80 years) undergoing coronary angiography (part of the homocysteine-lowering Western Norway B-Vitamin Intervention Trial) were allocated to the following daily oral treatment groups: (A), vitamin B(12) (0.4 mg), folic acid (0.8 mg), and vitamin B(6) (40 mg); (B), vitamin B(12) and folic acid; (C), vitamin B(6); or (D), placebo. EDTA blood was obtained before treatment and 3, 14, 28, and 84 days thereafter. RESULTS: Before treatment, PLP (range, 5-111 nmol/L) and 4-PA (6-93 nmol/L) were the predominant B(6) vitamers identified in plasma. During the 84-day study period, the intraindividual variation (CV) in patients not treated with vitamin B(6) (groups B and D) was 45% for PLP and 67% for 4-PA. Three days after the start of treatment, the increases in concentration were approximately 10-, 50-, and 100-fold for PLP, 4-PA, and PL, respectively. No significant additional increase was observed at the later time points. The PLP concentration correlated to the concentrations of 4-PA and PL before treatment, but not after treatment. The PL concentration correlated with 4-PA before and after treatment. CONCLUSIONS: Vitamin B(6) treatment has an immediate effect on the concentrations and the forms of B(6) vitamers present in plasma, and the changes remain the same during prolonged treatment. Our results suggest that the B(6) vitamers in plasma reflect vitamin B(6) intake.

Adult↗

Markedly increased vitamin B12 concentrations attributable to IgG-IgM-vitamin B12 immune complexes.

BACKGROUND: High serum vitamin B12 concentrations have been reported in patients with hepatic disease, disseminated neoplasia, myeloproliferative disorders, and hypereosinophilic syndromes. We recently discovered an extraordinarily increased vitamin B12 concentration in a patient without these underlying conditions. METHODS: Affinity and size-exclusion chromatography, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and ELISA methods were used to determine the cause of the increased vitamin B12 concentrations in this patient's serum. RESULTS: The protein G column eluates from 2 apparently healthy volunteers and 2 patients with recent vitamin B12 treatment for anemia had vitamin B12 concentrations of <74 pmol/L, whereas the vitamin B12 concentration in the protein G column eluate from the patient was 7380 pmol/L. The elution profile from size-exclusion chromatography of vitamin B12-binding proteins in the patient's serum revealed an abnormal vitamin-B12-binding protein. SDS-PAGE analysis of the concentrated eluates from the protein G column, under reducing conditions, revealed an additional band with an apparent molecular mass of 76 kDa, which was not present in control column eluates. MALDI-TOF MS identified this band as an IgM heavy chain. By use of a modified ELISA, we determined that the IgM present in the patient's eluates was associated with the IgG to form IgG-IgM immune complexes. CONCLUSIONS: This case demonstrates the unusual circumstance of a patient with markedly increased vitamin B12 concentrations attributed to immune complexes composed of IgG, IgM, and vitamin B12 and illustrates techniques that can be used to identify this occurrence.

Amyotrophic Lateral Sclerosis↗

Biological activity of 1-alpha-hydroxy vitamin D3 in vitamin D dependency.

The biological activity of 1(OH) vitamin D3 was evaluated in 2 cases of vitamin D dependency. For the improvement of serum chemistry and increment of urinary excretion of calcium 1(OH) vitamin D3 was 500--1000 times more active than vitamin D2. The administration of 0.05 microg/kg/day and 0.1 microg/kg/day of 1(OH) vitamin D3 were equally effective to keep the serum chemistry within normal limits. However, urinary excretion of calcium increased to an abnormal height on 0.1 microg/kg/day of 1(OH) vitamin D3. On the other hand, administration of 0.05 microg/kg/day of 1(OH) vitamin D3 kept both serum level and urinary excretion of calcium normal. It is suggested that 0.05 microg/kg/day is close to the optimum requirement of 1(OH) vitamin D3 in vitamin D dependency and this should correspond to the essential requirement of 1(OH) vitamin D3 in man.

Humans↗

Protective effects of vitamin C, alone or in combination with vitamin A, on endotoxin-induced oxidative renal tissue damage in rats.

This study was designed to investigate the protective effects of vitamin C and vitamin A on oxidative renal tissue damage. Male Wistar rats were given an intraperitoneal injection of 0.5 ml saline (control) or 0.5 ml solution of lipopolysaccharide (10 mg/kg), which caused endotoxemia. Immediately (within 5 min) after the endotoxin injection, the endotoxemic rats were untreated or treated with intraperitoneal injection of vitamin A (195 mg/kg bw), vitamin C (500 mg/kg bw) or their combination. After 24 hours, tissue and blood samples were obtained for histopathological and biochemical investigation. Endotoxin injection caused renal tissue damage and increased erythrocyte and tissue malondialdehyde (MDA) and serum nitric oxide (NO), urea and creatinine concentrations, but decreased the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities compared to the parameters of control animals. Treatment with vitamin C or with vitamins C and A significantly decreased the MDA levels and serum NO, urea and creatinine levels, recovered the antioxidant enzyme activities (SOD, GSH-Px and CAT), and prevented the renal tissue damage in endotoxemic rats. In contrast, vitamin A alone did not change the altered parameters except for creatinine levels. Notably, the better effects were observed when vitamins A and C given together. It is concluded that vitamin C treatment, alone or its combination with vitamin A, may be beneficial in preventing endotoxin-induced oxidative renal tissue damage and shows potential for clinical use.

Animals↗

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.

24,25-Dihydroxyvitamin D 3↗

Vitamin profiles of eggs as indicators of nutritional status in the laying hen: vitamin A study.

Laying hens were fed deficient diets, unsupplemented or supplemented with one, two, or four times the National Research Council requirement level of vitamin A for 27 wk. Vitamin A levels of egg yolk from hens fed the unsupplemented diet slowly declined but levels of vitamin A stabilized at 12 wk in the supplemented groups and were related to dietary level. Egg production of hens fed the unsupplemented diet declined significantly after 12 wk and egg yolk levels continued to decline to Week 27. Hatchability of eggs laid by the unsupplemented hens was significantly lower at Weeks 25 and 26 than hatchability for those hens receiving dietary vitamin A. Hen weight, egg weight, and shell thickness were not consistently changed by treatment. In a second experiment, hens were fed a diet with and without 9,000 IU vitamin A/kg of diet. With birds receiving the supplemented diet, egg yolk vitamin A levels were stable after 13 wk, whereas egg yolk levels from unsupplemented hens declined slowly. Egg production with the unsupplemented diet was significantly reduced after 16 wk but the magnitude of the reduction was less than that in the first experiment, although egg vitamin A levels were as low as those in the first experiment. Hatchability of eggs during Weeks 25 to 28 was greatly reduced. Egg weight, albumen score, and chick weight were not consistently altered by vitamin A status. Because declines in egg yolk vitamin A do not precede declines in egg production they are not useful to predict future vitamin A deficiency in laying hens.

Animals↗

Vitamin A alcohol and vitamin A palmitate transfer from ewes to lambs.

The effects of pre-partum intravenous injections of vitamin A alcohol and vitamin palmitate on vitamin A levels in the plasma and livers of newborn lambs and in colostrum were studied with twenty mature Romney ewes. Injecting ewes with 250000 IU of vitamin A alcohol significantly (P less than .05) increased vitamin A levels in the blood (77%) and livers (75%) of newborn lambs. Differences between effect of vitamin A alcohol and vitamin A palmitate on either blood or liver levels in lambs were not significant. Transfer of injected vitamin A to lamb liver was inefficient (0.37% for palmitate, 0.12% for alcohol). There was 52% more vitamin A in colostrum from alcohol-injected than from palmitate-injected ewes. Although consistent with a postulation of preferential mammary transfer of vitamin A alcohol, this difference was not statistically significant (P greater than .05).

Alcohols↗