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PubMed1989

[The vitamin A supply of laying hens including during rearing. 1. Testing of mixed feed with a varied vitamin A supplementation in chicks and young hens].

In seven experiments with 46,310 young animals from hatching to the 21st week the vitamin A supplement varied between 0 and 10,000 IU per kg mixed feed. Feed intake was significantly diminished in three out of seven experiments when chicken feed was given without vitamin A supplement. In the young chicken period 1,500 IU vitamin A supplement were sufficient for optimal body weight development, in the young hen period native carotene was sufficient. The variation of the body weight of the individual animals on the 126th day did not show any connection with vitamin A supply. The carotene content of the rations was sufficient to prevent deficiency symptoms. The livers and yolk sacs of one-day-old chickens on average contained 114 and 56 IU vitamin A/g substance when the parents had received mixed feed with 15,000 IU vitamin A/kg. There is a positive relation between the vitamin A supply of the young chickens and hens and the vitamin A content of the liver.

Animal Feed↗

PubMed2005

Ultraviolet exposure and vitamin D synthesis in a sun-dwelling and a shade-dwelling species of Anolis: are there adaptations for lower ultraviolet B and dietary vitamin D3 availability in the shade?

We compared the natural ultraviolet B (UV-B) exposure, dietary vitamin D, and skin-generated vitamin D synthesis for adult males of two species of Jamaican anoles. The more shade-tolerant and thermal-conforming Anolis lineotopus merope, rarely exposed to full sun, experienced less UV-B irradiation in its shady environment than the more heliophilic and thermophilic Anolis sagrei, which frequently basked in full sun during the morning hours (0800-1100 hours). Both species obtained detectable levels of vitamin D(3) in their diet, but the heliophilic A. sagrei obtained more. To compensate for less availability of UV-B and dietary vitamin D, the skin of A. lineotopus merope seems to have acquired a greater sensitivity than that of A. sagrei regarding UV-B-induced vitamin D(3) photobiosynthesis. We assessed this by observing a greater conversion of provitamin D to photoproducts in skin exposed to UV-B from a sunlamp. The reduced skin sensitivity of A. sagrei regarding vitamin D photobiosynthesis may reflect a correlated response associated with less need for vitamin D photobiosynthesis and greater need for UV-B screening capacity as an adaptation to a more damaging UV-B environment. However, the possibility that adaptations for photobiosynthesis of vitamin D and for protection from skin damage could involve independent mechanisms needs investigation. Also, the ability to behaviorally regulate UV-B exposure, as shown for the panther chameleon, would benefit both species of Anolis and should be investigated.

Adaptation, Physiological↗

PubMed1984

Interaction of dietary vitamin C and vitamin E on guinea pig immune responses to mitogens.

Guinea pigs were fed semipurified diets with 0.2 g/kg vitamin C and either 0, 30 or 200 mg/kg all-rac-alpha-tocopheryl acetate or 10 mg/kg vitamin C and either 0, 30 or 200 mg/kg all-rac-alpha-tocopheryl acetate for 4 weeks. Animals were killed, and blastogenic responses of splenocytes to T- and B-cell mitogens were measured. Both T- and B-cell responses were significantly depressed in vitamin E-deficient guinea pigs when compared to responses from guinea pigs fed diets containing vitamin E. The two dietary levels of vitamin C examined did not affect the magnitude of these responses. The higher dietary vitamin C, however, increased the vitamin E content of the lung at all levels of vitamin E intake.

Animals↗

PubMed1984

Dietary vitamin A, carotene, vitamin C and risk of lung cancer in Hawaii.

The authors conducted a case-control study among the multiethnic population of Hawaii to test the hypotheses that lung cancer risk is inversely associated with dietary intake of total vitamin A, carotene, and vitamin C. Detailed dietary interviews were completed between September 1979 and October 1982 for 364 primary lung cancer patients and 627 general population controls matched on age and sex. After adjusting for a number of potentially confounding variables, including ethnicity, smoking history, and occupation, evidence was found that total vitamin A intake (food sources plus supplements), vitamin A intake from food sources only, and carotene intake were each inversely associated with lung cancer risk in males, but not in females. Among males, a monotonic dose-response relationship was found only for total vitamin A intake. However, a comparison of the lowest and highest quartiles of intake gave similar results for each of the three measures of nutrient intake: total vitamin A (odds ratio (OR) = 1.8; 95% confidence limits (CL) = 1.1-3.1), vitamin A from foods (OR = 2.0; 95% CL = 1.2-3.5), and carotene (OR = 2.2; 95% CL = 1.3-3.7). Similar analyses revealed no significant association between dietary vitamin C intake and lung cancer risk.

Aged↗

PubMed2002

Vitamin C, vitamin E, and beta-carotene in relation to common cold incidence in male smokers.

We evaluated the role of dietary vitamin C, vitamin E, and beta-carotene, as well as long-term vitamin E and beta-carotene supplementation, on the incidence of common cold episodes. A cohort of 21,796 male smokers was drawn from the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study, which examined the effects of 50 mg per day vitamin E and 20 mg per day beta-carotene on lung cancer. Diet and background characteristics were recorded at the study entry, and subjects were queried three times per year on common cold episodes. We modeled the total number of colds during a 4-year follow-up period with Poisson regression, adjusting for covariates of dietary intake. Dietary vitamins C and E and beta-carotene had no meaningful association with common cold incidence. Long-term vitamin E and beta-carotene supplementation had no overall effect.Among subjects 65 years of age or older, the incidence of colds was slightly lower in the vitamin E group (RR = 0.95; 95% CI = 0.90-1.00); this reduction was greatest among older city dwellers who smoked fewer than 15 cigarettes per day (RR = 0.72; 95% CI = 0.62-0.83). In this male smoking population, vitamins C and E and beta-carotene had no overall association with the incidence of common cold episodes.

Aged↗

PubMed1998

Vitamin E and vitamin C supplement use and risk of incident Alzheimer disease.

Oxidative stress may play a role in neurologic disease. The present study examined the relation between use of vitamin E and vitamin C and incident Alzheimer disease in a prospective study of 633 persons 65 years and older. A stratified random sample was selected from a disease-free population. At baseline, all vitamin supplements taken in the previous 2 weeks were identified by direct inspection. After an average follow-up period of 4.3 years, 91 of the sample participants with vitamin information met accepted criteria for the clinical diagnosis of Alzheimer disease. None of the 27 vitamin E supplement users had Alzheimer disease compared with 3.9 predicted based on the crude observed incidence among nonusers (p = 0.04) and 2.5 predicted based on age, sex, years of education, and length of follow-up interval (p = 0.23). None of the 23 vitamin C supplement users had Alzheimer disease compared with 3.3 predicted based on the crude observed incidence among nonusers (p = 0.10) and 3.2 predicted adjusted for age, sex, education, and follow-up interval (p = 0.04). There was no relation between Alzheimer disease and use of multivitamins. These data suggest that use of the higher-dose vitamin E and vitamin C supplements may lower the risk of Alzheimer disease.

Aged↗

PubMed2006

The Melbourne Atherosclerosis Vitamin E Trial (MAVET): a study of high dose vitamin E in smokers.

OBJECTIVE: Our aim was to evaluate whether vitamin E (500 IU) slowed the progression of carotid atherosclerosis in a population of chronic smokers over 4 years as measured by ultrasound determination of carotid intima-media thickness (IMT) and systemic arterial compliance (SAC). METHODS: The Melbourne Atherosclerosis Vitamin E Trial (MAVET) was a randomized, double-blind, placebo-controlled trial in which 409 male and female smokers aged 55 years and over were randomized to receive 500 IU per day of natural vitamin E or placebo. The primary endpoint was progression of carotid atherosclerosis determined by intima-media thickness of the right common carotid artery. Secondary outcomes were change in systemic arterial compliance and low-density lipoprotein (LDL) oxidative susceptibility over time. RESULTS: The mean increase in intima-media thickness over time in the vitamin E group was 0.0041 mm/year faster than placebo (95% confidence interval -0.0021 to 0.0102 mm/year, P = 0.20). Similarly, a non-significant difference between vitamin E and placebo was found for rate of change in systemic arterial compliance (P = 0.11). Vitamin E supplementation did, however, significantly reduce LDL oxidative susceptibility (P < 0.001). CONCLUSION: Vitamin E supplementation is ineffective in reducing the progression of carotid atherosclerosis as measured by intima-media thickness in chronic smokers. This finding extends our knowledge of lack of effectiveness of vitamin E supplementation in populations with high oxidant stress.

Antioxidants↗

PubMed2007

Blood vitamin concentrations in privately owned dogs fed non-standardized commercial diets and after intake of diets with specified vitamin concentrations.

The objective was to investigate in a survey study the blood vitamin concentrations in healthy dogs fed non-specified commercial complete diets and in an intervention study to determine the effects of defined dietary vitamin intakes on blood vitamin levels and hair and skin condition. Sixty-four privately owned dogs, aged from 1 to 8 years, without history of skin or coat problems were included. All animals were fed commercial complete diets with uncertain vitamin concentrations before enrolment. The animals were assigned, according to weight and gender, to four groups with graded vitamin intakes. The blood vitamin levels and skin and coat quality of the dogs were investigated at days 0 and day 122. Coat and hair condition was not influenced by the experimental diets. The retinol concentrations were reduced at the end of the experiment compared with the baseline levels, retinyl esters were not influenced. 25-Hydroxycholecalciferol decreased in all groups, alpha-tocopherol was constant or tended to decrease. Ascorbic acid, thiamine pyrophosphate and riboflavin concentrations were not affected by treatment, flavin adenine dinucleotide and pyridoxal-5'-phosphate were partially reduced on day 122. Cobalamin, pantothenate and biotin concentrations increased with higher dietary intakes, folate levels in tendency. In conclusion, this study gives a survey of blood vitamin concentrations in healthy dogs and provides a data base for the evaluation of the vitamin status in health and disease.

Animal Feed↗

PubMed2003

Vitamin E and vitamin C treatment improves fibrosis in patients with nonalcoholic steatohepatitis.

OBJECTIVE: Nonalcoholic steatohepatitis (NASH) is a common cause of liver disease. Although usually indolent, this disease can progress to cirrhosis in some patients. There is currently no proven medical therapy for the treatment of NASH. The aim of our study was to evaluate the efficacy of combination alpha-tocopherol (vitamin E) and vitamin C in reducing histologic inflammation and fibrosis. METHODS: This was a prospective, double-blind, randomized, placebo-controlled trial with a total enrollment of 49 patients; 45 patients completed the study. All patients were randomized to receive either vitamins E and C (1000 IU and 1000 mg, respectively) or placebo daily for 6 months, based on their initial histologic diagnosis of NASH. Additionally, all patients were given standard weight-loss counseling and encouraged to follow a low fat diet (<30 fat g/day). The pre- and posttreatment liver biopsies were reviewed by a single pathologist, who was blinded to the patient's medication. Biopsies were scored based on a modification of the scoring system published by Brunt et al. (Am J Gastroenterol 1999;94:2467-74). A score of 0-4 was possible for fibrosis, and a score of 0-6 was possible for inflammation and hepatocyte degeneration and necrosis. In addition, body mass index, glycohemoglobin, lipids, and liver enzymes were followed throughout the study. RESULTS: Forty-five patients completed 6 months of therapy without significant side effects. Vitamin treatment resulted in a statistically significant improvement in fibrosis score (p=0.002). No changes were noted in inflammation with treatment. Vitamin E and vitamin C, in the doses used in this study, were well tolerated and were effective in improving fibrosis scores in NASH patients. No improvement in necroinflammatory activity or ALT was seen with this combination of drug therapy. A larger, multicenter, longer-term trial with vitamin E and vitamin C seems to be warranted.

Analysis of Variance↗

PubMed1988

Serum vitamin A levels in mothers and their breast-fed term infants with or without supplemental vitamin A.

Serum concentrations of vitamin A were measured in term infants (n = 72) and their mothers at delivery and after 20 weeks of breast-feeding (n = 48). During the 20 weeks the infants received either no supplemental vitamin A (but the mothers were given 3,000 IU vitamin A daily) (n = 16) or a daily vitamin A supplementation of 600 (n = 17) or 1,500 IU (n = 15). After 20 weeks of breast-feeding the vitamin A levels in the unsupplemented infants were similar to those at birth. The infants supplemented either with 600 or 1,500 IU had higher vitamin A serum levels than at birth (p less than 0.01), however, there was no difference between the two supplemented groups. During lactation, the serum vitamin A concentrations of the mothers increased significantly in all groups with or without vitamin A supplementation.

Breast Feeding↗

PubMed1985

The effects of different vitamin D-states on intestinal absorption of vitamin D3 and its metabolites in rats.

Rats were kept on a diet deficient in vitamin D for 2 months and were then randomly assigned to one of three groups with different supplies of vitamin D for 9 days. At the end of this period [3H]-cholecalciferol (5 microCi) was administered intragastrically and the serum radioactivity was recorded after various periods of time. The animals were kept in metabolic cages and urine and faeces were collected. After 3 days the animals were killed and the liver, kidney and fat tissue were investigated for radioactivity. The radioactivity was separated into different fractions of vitamin D by means of chromatography. The animals with vitamin D deficiency displayed higher levels of serum radioactivity, which were to a great extent confined to the fractions of the more polar metabolites (25(OH)D3 and 1,25(OH)2D3). There was significantly less radioactivity in the 3-day faecal collection from these animals. In general, there was a low urinary excretion of radioactivity. In the rats with sufficient vitamin D, most of the radioactivity remained as the parent substance and was also detected in increased amounts in the liver, kidney and fat tissue. The results suggest a discriminatory enterohepatic cycling of vitamin D and its more polar metabolites leading to an increased faecal loss of the pro-hormone in animals with a vitamin D surplus. It is proposed that the selectively effective enterohepatic reabsorption of the different metabolites may serve as a protective mechanism when body stores of vitamin D are overloaded.

Adipose Tissue↗

PubMed1979

Relevance of a borderline vitamin deficiency in relation to the question of vitamin requirement.

A definition is given for the terms of latent and borderline vitamin deficiency, and the vitamin requirement and optimal vitamin supply, respectively, are discussed in relation to these two terms. The upper limit of the latent vitamin deficiency status can be used to define the optimal intake of vitamins, whereas the lower limit indicates the minimum requirement. The impact on health of a latent vitamin deficiency lies in the risk of falling into a manifest vitamin deficiency during sudden stress, whereas, in borderline vitamin deficiency status, some health functions are affected so that a problem of public health may arise and countermeasures should be taken.

Adolescent↗

PubMed2001

Combined treatment with vitamin E and vitamin C decreases oxidative stress and improves fetal outcome in experimental diabetic pregnancy.

The aim was to investigate whether dietary supplementation of a combination of the two antioxidants, vitamin E and vitamin C, would protect the fetus in diabetic rat pregnancy at a lower dose than previously used. Normal and streptozotocin-induced diabetic rats were mated and given standard food or food supplemented with either 0.5% vitamin E + 1% vitamin C or 2% vitamin E + 4% vitamin C. At gestational d 20, gross morphology and weights of fetuses were evaluated. Vitamins E and C and thiobarbituric acid reactive substances were measured in maternal and fetal compartments. In addition, protein carbonylation was estimated in fetal liver. Maternal diabetes increased the rate of malformation and resorption in the offspring. High-dose antioxidant supplementation decreased fetal dysmorphogenesis to near normal levels. The low-dose group showed malformations and resorptions at an intermediate rate between the untreated and the high-dose groups. Thiobarbituric acid reactive substances were increased in fetal livers of diabetic rats and reduced to normal levels already by low-dose antioxidative treatment. Protein carbonylation rate was also increased in fetal liver of diabetic rats; it was normalized by high-dose treatment but only partially reduced by low-dose antioxidants. We conclude that combined antioxidative treatment with vitamins E and C decreases fetal malformation rate and diminishes oxygen radical-related tissue damage. However, no synergistic effect between the two antioxidants was noted, a result that may influence future attempts to design antiteratogenic treatments in diabetic pregnancy. Oxidatively modified proteins may be teratogenically important mediators in diabetic embryopathy.

Animals↗

PubMed1999

Vitamin D represses retinoic acid-dependent transactivation of the retinoic acid receptor-beta2 promoter: the AF-2 domain of the vitamin D receptor is required for transrepression.

Retinoic acid (RA)-dependent activation of the RA receptor beta2 (RARbeta2) gene in embryonal carcinoma cells is mediated by binding of retinoid receptor heterodimers (RAR/RXR) to a RA response element (RARE) located closely to the TATA box. We have analyzed the effect of vitamin D on the response of the RARbeta2 promoter to RA in pituitary GH4C1 cells that coexpress receptors for retinoids and vitamin D. Incubation with vitamin D markedly reduced the response to RA caused by transcriptional interference of the vitamin D receptor (VDR) on the RARE. This DNA element binds VDR/RXR heterodimers with high affinity, and these inactive heterodimers can displace active RAR/RXR from the RARE. Overexpression of RXR in GH4C1 cells, as well as incubation with BMS649 (a RXR-specific ligand), increased the inhibitory effect of vitamin D, suggesting that the VDR/RXR heterodimer is the repressive species and that titration of RXR is not responsible for this inhibition. Although DNA binding could be required for full potency of the inhibitory activity of VDR, it is not absolutely required because a truncated receptor (VDR delta1-111), lacking the DNA binding domain, also displays repressor activity. Furthermore, the ability to mediate transrepression by vitamin D was strongly decreased when a mutant VDR in which the last 12 C-terminal aminoacids have been deleted (VDR deltaAF-2) was used. Because this region contains the domain responsible for ligand-dependent recruitment of coactivators, titration of common coactivators for VDR and RAR could be involved in the inhibitory effect of vitamin D. In agreement with this hypothesis, overexpression of E1A, which can act as a RARbeta2 promoter-specific coactivator, significantly reversed repression by vitamin D.

Cell Line↗

PubMed2003

The antioxidants--vitamin C,vitamin E, selenium, and carotenoids.

This is the second in a series of articles reviewing the recent revisions of the Recommended Dietary Allowances (RDA) and the resulting Dietary Reference Intakes (DRI). In April of 2000, the Food and Nutrition Board of the National Academy of Sciences released Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. The central premise of the report did not perpetuate the prevailing popular thought that large doses of antioxidants will prevent chronic diseases. Instead the panel concluded that at this time, insufficient scientific evidence exists to sustain claims that ingesting megadoses of dietary antioxidants can prevent certain chronic illnesses such as cardiovascular disease or cancer. In some instances recommended nutrient levels were reduced from the previous report in 1989; e.g., for the first time upper tolerable levels of ingestion (UL) were established to prevent the harmful effects of over consumption of essential nutrients, such as vitamin C, vitamin E, and selenium. Although dietary recommendations do exist for vitamin A, the panel did not set recommendations for beta-carotene or the other carotenoids due to lack of sufficient research to support recommended intakes or upper tolerable levels of intake. However, the panel advises the public to avoid intakes of provitamin A compounds, such as the numerous carotenoids, beyond the levels required to prevent vitamin A deficiency. Changes were also made with regard to estimating the amount of provitamin A carotenoids required to make a unit of retinal. The revised estimate suggests a twofold higher conversion rate than previously believed. Although this comprehensive report on the dietary reference intakes for vitamin C, vitamin E, selenium, and the carotenoids did not decisively confirm the role of antioxidants for the prevention of chronic diseases in humans, many research studies have generated new data to support this concept. Additional research is needed to define the attributes of antioxidants as studies progress from in vitro and animal studies to human nutrition.

Antioxidants↗

PubMed2006

Vitamin D-resistant rickets and type 1 diabetes in a child with compound heterozygous mutations of the vitamin D receptor (L263R and R391S): dissociated responses of the CYP-24 and rel-B promoters to 1,25-dihydroxyvitamin D3.

UNLABELLED: We report here the first association between vitamin D-resistant rickets, alopecia, and type 1 diabetes in a child with compound heterozygous mutations in the VDR gene. Transfection studies suggest dissociated effects of VDR gene mutations on the regulation of genes involved in vitamin D metabolism and dendritic cell maturation. INTRODUCTION: Whereas vitamin D may play a role in the immune tolerance process, no patient has been reported to associate hereditary vitamin D-resistant rickets (HVDRR) and an autoimmune disease, and no attempt has been made to delineate the outcome of mutations of the vitamin D receptor (VDR) on the transcription of genes controlling immune tolerance. MATERIALS AND METHODS: The VDR gene was analyzed in a child with vitamin D-resistant rickets, total alopecia, and early childhood-onset type 1 diabetes. Patient's fibroblasts and COS-7 cells transfected with wildtype or mutant VDRs were studied for ligand-binding capacity, transactivation activity using two gene promoters [CYP-24, a classical 1,25(OH)2D3-responsive gene, and relB, a critical NF-kappaB component for regulation of dendritic cell differentiation], VDR-RXR heterodimers association to CYP 24 VDREs by gel mobility shift assays, and co-activator binding by Glutathione-S-transferase pull-down assays. RESULTS: Two novel compound heterozygous mutations (L263R and R391S) were identified in the VDR ligand-binding domain in this child. Both mutations significantly impaired VDR ligand-binding capacity but had dissociated effects on CYP-24 and RelB promoter responses to vitamin D. CYP 24 response binding to SRC-1 and RXR-heterodimer binding to CYP24 VDREs were abolished in L263R mutants but normal or partially altered in R391S mutants. In the opposite, RelB responses to vitamin D were close to normal in L263R mutants but abolished in R391S mutants. CONCLUSIONS: We report the first clinical association between HVDRR, total alopecia, and early childhood-onset type 1 diabetes. Mutations in the VDR ligand-binding domain may hamper the 1,25(OH)2D3-mediated relB responses, an effect that depends on the site of the VDR mutation and cannot be anticipated from VDR ligand-binding ability or CYP-24 response. Based on these results, we propose to survey the immune function in patients with HVDRR, including those with moderate features of rickets.

Animals↗

PubMed1979

Effect of vitamin B6 deficiency on the levels of several water-soluble vitamins in tissues of germ-free and conventional rats.

The influence of vitamin B6 deficiency on the levels of several water-soluble vitamins and on acetyl-coenzyme A carboxylase activity was investigated using of germ-free and conventional rats. Judging from the vitamin B6 levels in tissues and the percent of decrease, the degree of vitamin B6 deficiency was more severe in the tissues of deficient germ-free rats than in deficient conventional rats. Nicotine acid, pantothenic acid and biotin levels per wet weight significantly decreased in the liver of vitaminB6-deficient germ-free rats, and nicotine acid levels per wet weight significant decreased in the liver of deficient conventional rats. In the kidney of vitamin B6-deficient germ-free rats, a significant decrease in riboflavin and biotin levels was observed, although there was no observable difference in riboflavin, nicotinic acid, biotin and patothenic acid levels in the kidney of deficient conventional rats. From an enzymatic standpoint, acetyl-coenzyme A carboxylase activity was especially significantly decreased in both germ-free and conventional rats fed a vitamin B6-deficient diet, and the percent od decrease was more in germ-free rats than in conventional ones. These findings suggest that vitamin B6 deficiency had stronger effects on the levels of water-soluble vitamins in germ-free rats compared with conventional rats.

Acetyl-CoA Carboxylase↗

PubMed2001

Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia.

In the present study, the effects of vitamins E and C on the levels of neurotransmitters and acetylcholinesterase activity in the brains of rats treated with scopolamine, an inducer of dementia, were examined. Fifty male Sprague-Dawley rats at the age of 5 wk were divided into five groups after 1 wk of adaptation and fed five different diets for 6 wk: a no-scopolamine group, which was a scopolamine-untreated group fed only a basal diet: a scopolamine-treated group fed a basal diet; a vitamin E-supplemented scopolamine-treated group: a vitamin C-supplemented scopolamine-treated group; and a vitamins E and C-supplemented scopolamine-treated group. Scopolamine was twice administered by intraperitoneal injection (300 mg/kg, body weight), 3 d and 20 min prior to sacrifice. Brain acetylcholinesterase activity was markedly reduced by scopolamine injection. However, the supplementation of vitamins E and C in the diet significantly increased the reduced brain acetylcholinesterase activity up to the level of the scopolamine-untreated group. Brain serotonin concentration in the vitamin C-supplemented scopolamine-treated group was significantly higher than that in the scopolamine-treated group. However, there were no significant differences in brain dopamine and norepinephrine concentrations among all groups. In conclusion, supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase activity at the normal level and serotonin concentration for some extent under the condition to induce dementia by scopolamine administration.

Acetylcholinesterase↗