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PubMed2004

Influence of dietary vitamin E and C supplementation on vitamin E and C content and thiobarbituric acid reactive substances (TBARS) in different tissues of growing pigs.

To investigate the influence and possible interactions of dietary vitamin E and C supplementation on vitamin content of both vitamins and oxidative stability of different pork tissues 40 Large White barrows from 25 kg to 106 kg were allocated to four different cereal based diets: Basal diet (B), dl-alpha-tocopherylacetate + 200 mg/kg (E), crystalline ascorbic acid + 300 mg/kg (C) or both vitamins (EC). At slaughtering samples of liver, spleen, heart, kidney, backfat outer layer, ham and M. tongissimus dorsi were obtained. Growth performance of the pigs and carcass characteristics were not influenced by feeding treatments. Dietary vitamin E supplementation had a significant effect on the vitamin E and alpha-tocopherol concentration in all investigated tissues. Backfat outer layer, liver, spleen, kidney and heart had higher vitamin E concentrations than ham and M. longissimus dorsi. Dietary vitamin C supplementation tended towards enhanced vitamin E levels except for ham samples. Therefore, some synergistic actions without dietary vitamin E supplementation between the two vitamins could be shown. The vitamin C concentration and TBARS were increased or at least equal in all tissues due to vitamin C supplementation. Dietary alpha-tocopherol supplementation resulted in lower TBARS in backfat outer layer (malondialdehyde 0.35 mg/kg in B vs. 0.28 mg/kg in E), but increased in heart and ham. When both vitamins were supplemented (EC) TBARS were lower in M. longissimus dorsi and backfat outer layer, equal in heart and higher in liver and ham compared to a single vitamin C supplementation. Rancimat induction time of backfat outer layer was 0.3 h higher in C compared to B and 0.17 h higher in EC than in E. Correlations between levels of both vitamins were positive for kidney (r = 0.169), M. longissimus dorsi (r = 0.499) and ham (r = 0.361) and negative for heart (r = -0.350). In liver and spleen no interaction could be found. In backfat outer layer vitamin E was positively correlated with rancimat induction time (r = 0.550) and negatively with TBARS (r = -0.202), but provided no evidence that dietary vitamin E supply led to better oxidative stability.

Adipose Tissue↗
PubMed1990

Plasma vitamin A levels in cattle in response to large doses of vitamin A.

A dose response procedure was developed for evaluating vitamin A status and utilization in cattle. This could be useful for evaluating diets, vitamin A stores and homeostatic control of vitamin A. Three experiments were designed to determine: 1) size of vitamin A dose required to increase plasma vitamin A concentrations; 2) time after dosing when plasma vitamin A concentrations peak, and 3) if changes in plasma vitamin A concentrations are useful in assessing dietary vitamin A utilization. Using twenty-four steers and heifers, the first two experiments showed that 30X or 40X daily vitamin A requirement (daily requirement calculated as X = body weight in kilograms times 55 International Units of vitamin A) given orally was sufficient to cause plasma vitamin A concentrations to rise 20 hours after dosing. Plasma vitamin A concentrations increased (P less than .01) from 57 to 81 micrograms/dl and 64 to 84 micrograms/dl after a 30X or 40X treatment, respectively. Twenty-X daily requirement resulted in a slight increase after 20 hours (P greater than .05). Seventy-two feedlot steers were used in experiment three to determine if diet affects vitamin A dose response. Variations in feed intake, monensin in the diet or a single dose of vitamin E did not cause significant changes in plasma vitamin A response to vitamin A dosage. Steers receiving monensin had higher initial plasma vitamin A concentrations, but no differences were observed after dosing. Results indicate that dose responses may be useful in assessing dietary vitamin A utilization.

Administration, Oral↗
PubMed2000

Prophylactic vitamin K for vitamin K deficiency bleeding in neonates.

BACKGROUND: Vitamin K deficiency can cause bleeding in an infant in the first weeks of life. This is known as Hemorrhagic Disease of the Newborn (HDN). HDN is divided into three categories: early, classic and late HDN. Early HDN occurs within 24 hours post partum and falls outside the scope of this review. Classic HDN occurs on days one to seven; common bleeding sites are gastrointestinal, cutaneous, nasal and from a circumcision. Late HDN occurs from week 2-12; the most common bleeding sites are intracranial, cutaneous, and gastrointestinal. Vitamin K is commonly given prophylactically after birth for the prevention of HDN, but the preferred route is uncertain. OBJECTIVES: To review the evidence from randomized trials in order to determine the effectiveness of vitamin K prophylaxis in the prevention of classic and late HDN. Main questions are: Is one dose of vitamin K, given after birth, able to significantly reduce the incidence of classic and late HDN? Is there a significant difference between the oral route and the intramuscular route in preventing classic and late HDN? Are multiple oral doses of vitamin K, given after birth, able to significantly reduce the incidence of classic and late HDN? SEARCH STRATEGY: The standard search strategy of the Cochrane Neonatal Review Group was used. SELECTION CRITERIA: All trials using random or quasi-random patient allocation, in which methods of vitamin K prophylaxis in infants were compared to each other, placebo or no treatment, were included. DATA COLLECTION AND ANALYSIS: Data were extracted independently by each author and were analysed with the standard methods of the Cochrane Collaboration and its Neonatal Review Group, using relative risk, risk difference and weighted mean difference. MAIN RESULTS: Two eligible randomized trials, each comparing a single dose of intramuscular vitamin K with placebo or nothing, assessed effect on clinical bleeding. One dose of vitamin K reduced clinical bleeding at 1-7 days, including bleeding after circumcision, and improved biochemical indices of coagulation status. Eleven additional eligible randomized trials compared either a single oral dose of vitamin K with placebo or nothing, a single oral with a single intramuscular dose of vitamin K, or three oral doses with a single intramuscular dose. None of these trials assessed clinical bleeding. Oral vitamin K improved biochemical indices of coagulation status at 1-7 days. There was no evidence of a difference between the oral and intramuscular route in effects on biochemical indices of coagulation status. A single oral compared with a single intramuscular dose resulted in lower plasma vitamin K levels at two weeks and one month, whereas a 3-dose oral schedule resulted in higher plasma vitamin K levels at two weeks and at two months than did a single intramuscular dose. REVIEWER'S CONCLUSIONS: A single dose (1.0 mg) of intramuscular vitamin K after birth is effective in the prevention of classic HDN. Either intramuscular or oral (1.0 mg) vitamin K prophylaxis improves biochemical indices of coagulation status at 1-7 days. Neither intramuscular nor oral vitamin K has been tested in randomized trials with respect to effect on late HDN. Oral vitamin K, either single or multiple dose, has not been tested in randomized trials for its effect on either classic or late HDN.

Humans↗
PubMed2006

Dose response effects of long-acting injectable vitamin B12 plus selenium (Se) on the vitamin B12 and Se status of ewes and their lambs.

AIM: To determine the effect of increasing doses of long-acting injectable vitamin B12 plus selenium (Se) given pre-mating on the vitamin B12 and Se status of ewes and their lambs from birth to weaning. METHODS: Four groups of 24 Poll Dorset ewes each were injected 4 weeks pre-mating with different doses of a long-acting vitamin B12 + Se product, containing 3 mg vitamin B12 and 12 mg Se per ml. The treatment groups received 5 ml (15 mg vitamin B12 + 60 mg Se), 4 ml (12 mg vitamin B12 + 48 mg Se), 3 ml (9 mg vitamin B12 + 36 mg Se), or no vitamin B12 or Se (control). Twelve of the twin-bearing ewes per group were selected for the study. Efficacy of the product was evaluated from changes in the concentrations of vitamin B12 in serum and liver, and of Se in blood, liver and milk in the ewes during gestation and lactation, and in their lambs from birth to weaning. Pasture samples in paddocks grazed by the ewes and lambs were collected at about 2-monthly intervals from 200-m transects. RESULTS: The flock was Se-deficient, as the mean initial concentration of Se in the blood of ewes was 182 (SE 20.3) nmol/L. Compared with untreated controls, all doses significantly (p < 0.01) increased concentrations of Se in the blood of ewes for at least 300 days. Selenium concentrations in milk were likewise increased throughout lactation, as were those in the blood and liver of lambs. The mean concentration of vitamin B12 in the serum of ewes was initially > 1,000 pmol/L, but this decreased within 28 days to < 460 pmol/L. Treatment with the 5-ml and 4-ml doses raised serum vitamin B12 concentrations of ewes for at least 176 days (p < 0.01), while their lambs had significantly greater concentrations of vitamin B12 in serum and liver for less than 37 days after birth. Tissue concentrations and duration of elevation of both vitamin B12 and Se were proportional to the dose administered. The mean concentrations of Se and cobalt (Co) in the pastures were 32 and 74 microg/kg dry matter (DM), respectively. CONCLUSIONS: Injecting ewes from a Se-deficient flock 4 weeks prior to mating with 48 or 60 mg Se and 12 or 15 mg vitamin B12 increased and maintained the Se status of ewes for at least 300 days, and of their lambs from birth to weaning. The vitamin B12 status of ewes was increased for at least 176 days and that of their lambs for less than 37 days. Due to the proportional nature of the response to increasing dosage, the dose rate of the formulation tested can be adjusted according to the severity of Se and Co deficiency in a flock. CLINICAL SIGNIFICANCE: A single subcutaneous injection of vitamin B12 + Se administered pre-mating to Se-deficient flocks is likely to prevent Se deficiency in ewes and their lambs until weaning, as well as increase the vitamin B12 status of ewes and their lambs until 5 weeks after lambing.

Animals↗
PubMed2002

Effects of vitamin C and vitamin E on in vivo lipid peroxidation: results of a randomized controlled trial.

BACKGROUND: Lipid peroxidation may be important in the pathogenesis of atherosclerosis, particularly in its earliest stages. Evidence predominantly from in vitro studies suggests that antioxidant vitamins can prevent lipid peroxidation and that vitamin C and vitamin E have synergistic effects. However, in vivo evidence in support of these hypotheses is sparse. OBJECTIVE: The objective was to determine the effects of vitamin C and vitamin E, alone or in combination, on in vivo lipid peroxidation. DESIGN: We conducted a placebo-controlled, 2 x 2 factorial trial of vitamin C (500 mg ascorbate/d) and vitamin E (400 IU RRR-alpha-tocopheryl acetate/d) supplementation in 184 nonsmokers. The mean duration of supplementation was 2 mo. The outcome measures were changes from baseline in urinary 8-iso-prostaglandin F(2alpha), urinary malondialdehyde + 4-hydroxyalkenals, and serum oxygen-radical absorbance capacity. RESULTS: The within-group mean changes (and 95% CIs) in urinary 8-iso-prostaglandin F(2alpha) (pg/mg creatinine) were 9.0 (-125.1, 143.1), -150.0 (-275.4, -24.6), -141.3 (-230.5, -52.1), and -112.5 (-234.8, 9.8) in the placebo, vitamin C alone, vitamin E alone, and vitamins C + E groups, respectively. No synergistic effect of these 2 vitamins on urinary 8-iso-prostaglandin F(2alpha) was observed (P = 0.12). Neither vitamin had an effect on urinary malondialdehyde + 4-hydroxyalkenals. Vitamin C, but not vitamin E, increased serum oxygen-radical absorbance capacity (P = 0.01). CONCLUSIONS: Supplementation with vitamin C or vitamin E alone reduced lipid peroxidation to a similar extent. Supplementation with a combination of vitamins C and E conferred no benefit beyond that of either vitamin alone.

Adult↗
PubMed2000

Vitamin K antagonists or low-molecular-weight heparin for the long term treatment of symptomatic venous thromboembolism.

BACKGROUND: Patients who have had an episode of symptomatic venous thromboembolism are usually treated for at least five days with intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin. Thereafter, they received a three month course of a vitamin K antagonist, with a dose adjusted to achieve an International Normalized Ratio between 2.0 and 3.0. Some patients have contraindications to vitamin K antagonists. In addition, treatment with vitamin K antagonists has the disadvantage of regular laboratory measurements. OBJECTIVES: The objective of this review was to evaluate the efficacy and safety of long-term treatment of symptomatic venous thromboembolism with low-molecular-weight heparins compared with vitamin K antagonists. SEARCH STRATEGY: Computerized searches of MEDLINE, EMBASE and Current Contents were made and relevant journals were hand-searched using the search strategy described by the Cochrane Peripheral Vascular Disease Group. In addition, randomized clinical trials were located through personal communication with colleagues. Where necessary, the reviewers contacted pharmaceutical companies for further information. SELECTION CRITERIA: Two reviewers evaluated studies independently for methodological quality. DATA COLLECTION AND ANALYSIS: Two reviewers reviewed and extracted data independently using a standard form. Primary analysis concerned all patients in the studies during the period of randomized treatment. Additional separate analyses were performed for category I and category II studies; studies that used similar initial treatments in both study arms and those that used different treatment regimes during the initial treatment; and the total period of follow-up in the different studies. MAIN RESULTS: Five studies were identified that fulfilled our predefined criteria (three category I and two category II studies). When all five studies were combined, a statistically non-significant reduction of the risk of recurrent symptomatic venous thromboembolism in favor of low-molecular-weight heparin treatment (OR 0.72; 95% CI [0.42, 1.23]) was found. In category I studies, analysis of the pooled data showed a statistically non-significant reduction of the risk of recurrent symptomatic venous thromboembolism in favor of low-molecular-weight heparin treatment (OR 0.75; 95% CI [0.40, 1.39]). This OR was mainly due to one possibly confounded study, and after omitting this study from the analysis a statistically non-significant reduction of the risk of recurrent symptomatic venous thromboembolism in favor of vitamin K antagonist treatment remained (OR 1.95; 95% CI [0.74, 5.19]). No differences in the risk of bleeding (OR 0.63; 95% CI [0.21, 1.88]) and mortality (OR 1.13; 95% CI [0.47, 2.69] were observed. REVIEWER'S CONCLUSIONS: Low-molecular-weight heparins are possibly as effective and safe as vitamin K antagonists in the prevention of recurrent symptomatic venous thromboembolism after an episode of symptomatic deep venous thrombosis, but have the disadvantage of much higher medicinal costs. Treatment with low-molecular-weight heparin is possibly a safe alternative in some patients; for example patients who live in geographically inaccessible places; patients who are reluctant to go to the thrombosis service on a regular basis; and patients with contraindications to vitamin K antagonists (e.g. pregnant women). Therefore, in the absence of definitive evidence on the safety and efficacy of low-molecular-weight heparins compared with vitamin K antagonists, we believe that treatment with vitamin K antagonists is still the treatment of choice in the prevention of recurrent symptomatic venous thromboembolism after an episode of deep venous thrombosis, in the majority of patients.

Anticoagulants↗
PubMed1996

Vitamin K2 promotes 1alpha,25(OH)2 vitamin D3-induced mineralization in human periosteal osteoblasts.

The effect of vitamin K on mineralization by human periosteal osteoblasts was investigated in the absence and presence of 1alpha, 25 dihydroxyvitamin D3 (1,25(OH)2D3). Vitamin K1 and K2, but not vitamin K3, at 2.5 microM enhanced in vitro mineralization when cells were cultured with vitamin K for 20 days after reaching confluence in vitro. Vitamin K2 (2-methyl-3-all-trans-tetraphenyl-1, 4-naphthoquinone : menatetrenone) was the most potent of these vitamin K analogs; it slightly inhibited alkaline phosphatase (ALP) activity. Human osteoblasts were mineralized and showed the enhanced ALP activity on treatment with 10(-9) M of 1,25(OH)2D3 for 20 or 25 days after confluence. Vitamin K2 promoted the 1,25(OH)2D3-induced mineralization, but slightly inhibited the 1,25(OH)2D3-induced ALP activity. Moreover, vitamin K2 enhanced the 1,25(OH)2D3-induced osteocalcin accumulation in the cells and the extracellular matrix (cell layer), but inhibited the osteocalcin content in the medium produced by the 1,25(OH)2D3 treatment. However, vitamin K2 alone did not induce osteocalcin production in the human osteoblasts. On Northern blot analysis, osteocalcin mRNA expression on 1, 25(OH)2D3-treated cells was enhanced by vitamin K2 treatment, but vitamin K2 alone did not induce osteocalcin mRNA expression. Warfarin blocked both the 1,25(OH)2D3-induced osteocalcin production and the accumulation in the cell layer, and also blocked the 1, 25(OH)2D3 plus vitamin K2-induced osteocalcin production and the accumulation in the cell layer. The 1,25(OH)2D3-induced mineralization promoted by vitamin K2 was probably due to the enhanced accumulation of osteocalcin induced by vitamin K2 in the cell layer. However, we concluded that the mineralization induced by vitamin K2 alone was due to the accumulation of osteocalcin in bovine serum on the cell layer, since osteocalcin extracted from the cell layer was not identified by specific antiserum against human osteocalcin, which does not cross-react with bovine osteocalcin. These results suggest that the mechanism underlying the mineralization induced by vitamin K2 in the presence of 1,25(OH)2D3 was different from that of vitamin K2 alone, and that osteocalcin plays an important role in mineralization by osteoblasts in vitro.

Adult↗
PubMed1998

Effect of supplementing the hen's diet with vitamin A on the accumulation of vitamins A and E, ascorbic acid and carotenoids in the egg yolk and in the embryonic liver.

1. The effect of a range of supplementations of vitamin A to the laying hen on the concentration of vitamins A, E, ascorbic acid and carotenoids in the maternal liver, the egg yolk and the embryonic liver were investigated. 2. Four groups of 25 Rhode Island Red hens were fed on standard layer-breeder diets with concentrations of supplemented vitamin A ranging from 0 to 120 micrograms/g retinol equivalents from 28 weeks of age. After 3 months, the concentration of vitamin A in the maternal liver was found to be greatly enhanced in proportion to the increasing rates of supplementation with the vitamin. However, the concentration of vitamin E in the maternal liver was markedly reduced by high dietary contents of vitamin A. 3. The concentration of vitamin A in the yolk of the hens' eggs was markedly increased by the dietary supplementation. However, the concentration of both vitamin E and carotenoids in the yolks were significantly reduced by high dietary contents of vitamin A. 4. The concentration of vitamin A in the liver of the embryo and the day old chick was greatly increased by the high concentrations of maternal vitamin A provision. However, the concentration of vitamin E, carotenoids and ascorbic acid in the embryonic/neonatal liver were significantly reduced by high contents of vitamin A in the maternal diet. 5. The susceptibility of the embryonic/neonatal liver to lipid peroxidation was significantly increased as a result of high provisions of maternal vitamin A. 6. It is concluded that excessive provision of vitamin A to the laying hen results in an adverse effect on vitamin E, carotenoids and ascorbic acid in the embryonic/neonatal liver and can compromise the antioxidant status of the progeny.

Animal Feed↗
PubMedDate not supplied

Maternal vitamin D deficiency and vitamin D supplementation in healthy infants.

The objective of this study was to evaluate the common effects of maternal vitamin D deficiency, various doses of vitamin D given to newborns and the effects of these on vitamin D status in early childhood. Seventy-eight pregnant women and 65 infants who were followed up in various health centers were included in the sudy. 25-hydroxyvitamin-D (25-OHvitD), calcium (Ca), phosphorus (P) and alkaline phosphatase levels were measured in blood samples drawn from pregnant women in the last trimester. Infants born to these mothers were given 400 or 800 IU of vitamin D subsequently at the start of the second week. 25-OHvitD, Ca, P and alkaline phosphatase levels of the 65 infants who were brought in for controls (May-September 2000) were measured and hand-wrist X-rays were evaluated. We analyzed the relationship between vitamin D status of the mothers and infants and socio-economic status; mothers' dressing habits (covered vs uncovered), educational level, and number of pregnancies; and sunlight exposure of the house. Covered as a dressing habit meant covering the hair and sometimes part of the face and wearing dresses that completely cover the arms and legs. In 40 infants who were breast-fed and received the recommended doses of vitamin D on a regular basis, the relationship between serum vitamin D levels and supplementation doses given was analyzed. Serum 25-OHvitD level of the mothers was 17.50 +/- 10.30 and 94.8% of the mothers had a 25-OHvitD level below 40 nmol/L (below 25 nmol/L in 79.5%). The risk factors associated with low maternal 25-OHvitD were low educational level (p = 0.042), insufficient intake of vitamin D within diet (p = 0.020) and "covered" dressing habits (p = 0.012). 25-OHvitD level of the infants was 83.70 +/- 53.70 nmol/L, and 24.6% of the infants had 25-OHvitD levels lower than 40 nmol/L. Risk factors for low 25-OHvitD levels in infants were a) not receiving recommended doses of vitamin D regularly (p = 0.002) and b) insufficient sunlight exposure of the house (p = 0.033). There was a pour but significant correlation between maternal vitamin D levels and infants' 25-OHvitD levels at four months (r = 0.365, p < 0.05). No significant correlation was found between 25-OHvitD levels and supplementation doses of vitamin D (19 infants were supplemented with 400 IU/day and 21 with 800 IU/day of vitamin D) (p = 0.873). Severe maternal vitamin D deficiency remains a commonly seen problem in Turkey. However, vitamin D deficiency can be prevented by supplementation of vitamin D to newborns (at least 400 IU). Supplementation of 800 IU vitamin D in the areas of maternal vitamin D deficiency has no greater benefits for the infants.

Adult↗
PubMed1986

Effect of moderate vitamin A supplementation and lack of dietary vitamin A on the development of mammary tumors in female rats treated with low carcinogenic dose levels of 7,12-dimethylbenz(a)anthracene.

We examined the effect of moderately increased and of marginal continued dietary supplementation of vitamin A (retinyl acetate) and the effect of lack of dietary vitamin A on the initiation and promotion stages of mammary tumorigenesis in female Sprague-Dawley rats treated with a single low (0.5 mg/100 g body weight) or very low (0.1 mg/100 g body weight) dose of i.v.-administered 7,12-dimethylbenz(a)anthracene. The number of mammary tumors was significantly (P less than 0.05) reduced if prior to and during initiation with 7,12-dimethylbenz(a)anthracene the rats were fed a moderately increased (30 micrograms/day) or marginal (3 micrograms/day) amount of vitamin A, compared to rats fed an adequate (10 micrograms/day) amount of vitamin A. The number of mammary tumors was also significantly (P less than 0.05) reduced when a moderately increased or marginal amount of vitamin A was provided during the tumor promotion phase. In addition, the number of mammary tumors was significantly (P less than 0.05) reduced by the lack of dietary vitamin A during both the initiation and promotion stages of this tumorigenic process, when compared to vitamin A adequate, ad libitum-fed rats, but not when compared to vitamin A adequate, food-restricted controls. The reduction in numbers of mammary tumors observed in these studies was reflected primarily in significant (P less than 0.05) decreases in mammary fibroadenomas; the number of mammary carcinomas was often reduced, but due to a low frequency of the carcinomatous lesions, this reduction did not reach the 5% level of statistical probability. Plasma and liver vitamin A levels were determined during both the initiation and promotion stages. As the dietary supplementation of vitamin A increased from 0 to 30 micrograms/day, there was an increase in mean liver and plasma vitamin A levels. No consistent correlation between plasma and liver vitamin A levels and the occurrence of mammary tumors was observed, except with the moderately increased (30 micrograms/day) intake of vitamin A, that resulted in a small, but statistically significant (P less than 0.05) increase of serum retinol at initiation; this may account for the observed reduction in mammary tumors. These results provide evidence that moderate alterations in vitamin A consumption can modulate low-dose chemically induced mammary gland tumorigenesis. Most importantly, suppression of mammary gland tumorigenesis can be achieved by moderately increased, frequent, and regular consumption of vitamin A; prolonged consumption of vitamin A-deficient diets or diets marginal in vitamin A does not enhance the risk of mammary tumor development.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

[Vitamin deficiency and marginal vitamin deficiency].

Fat-soluble vitamin deficiency and marginal deficiency of this type of vitamin will be discussed. The trias of vitamin A deficiency is composed of nyctalopia, xerophthalmia and hyperkeratosis follicularis. Vitamin D deficiency causes rachitis and osteomalacia. In Japan, vitamin D deficiency is more often caused by impaired vitamin D activation due to renal failure, than by a lack of sunbathing or insufficient ingestion of vitamin D from diet. At present, it is quite rare that the physician encounters patients with deficiency of vitamin E or other vitamins. According to surveys of occult vitamin deficiency, the prevalence of marginal fat-soluble vitamin deficiency was lower than that of marginal water-soluble vitamin deficiency. Marginal vitamin deficiency seems to be absent or very rare among healthy individuals. In patients, however, marginal vitamin deficiency is sometimes observed. Since marginal vitamin deficiency can modify the underlying disease or trigger complications, the physician should take adequate measures to prevent the onset of marginal vitamin deficiency in managing patients with various diseases.

Humans↗
PubMedDate not supplied

[The vitamin A requirement and the vitamin A status of growing cattle. 1. Studies of calves].

Five experiments with 18 to 36 male calves each of the black and white dairy cattle breed (age: 14-21 days, initial live weight: approximately 45 kg per animal) were carried out in order to investigate the influence of various vitamin A supply (0-80,000 IU per 100 kg LW and day) on dry matter intake and weight gain as well as the vitamin A status of liver and blood plasma over 84 days. The calves consumed a diet free of carotene and vitamin A consisting of milk replacer, concentrate and chopped wheat straw. The calves were fed in three experiments for a longer time in order to observe the further vitamin A depletion. Nine animals consumed an unsupplemented ration, nine other one got 10,000 IU vitamin A per 100 kg LW and day. Biopsies of liver and plasma samples were taken from 4 animals per group every four weeks. The various vitamin A supplementation did not significantly influence the dry matter intake (Mean: 1.67; 1.48 to 1.80 kg DM per animal and day) and the weight gain of calves (Mean: 702, 599 to 770 g per animal and day). First vitamin A deficiency symptoms (reduced feed intake, decreased weight gain, diarrhoea etc.) were observed in animals of unsupplemented group after 100 days of experiments. After 84 days the vitamin A concentration of liver of animals of unsupplemented groups decreased to 1.3-32.2% compared with the begin of experiments (60.6-155.7 mumol/kg fresh matter). Up to 51% of initial concentration were found when 10,000 IU vitamin A per 100 kg LW and day were fed. About 25,000 IU vitamin A per 100 kg LW and day were required in order to keep the initial level of vitamin A concentration of liver. The plasma vitamin A concentration is unsuitable for estimation of vitamin A status of calves. The concentration of vitamin A of liver and plasma amounted to 114 mumol per kg and 0.25 mumol per litre at the begin of experiments. The vitamin A concentration of liver of unsupplemented group decreased to 20 mumol per kg, that of plasma increased to 0.28 mumol per 1 at the end. A strong vitamin A deficiency (liver concentration: less than 10 mumol/kg) may cause a decrease of vitamin A concentration of blood.

Animal Feed↗
PubMed1984

Inhibition of oxidation of methyl linoleate in solution by vitamin E and vitamin C.

The oxidation of methyl linoleate in solution initiated with azo compounds has been studied in the absence and presence of vitamin E and vitamin C. Both vitamin E and vitamin C acted as a chain-breaking antioxidant and they suppressed the oxidation and produced an induction period. The inhibition rate constant for the scavenging of peroxy radical was calculated at 37 degrees C as kinh = 5.1 X 10(5) M-1 s-1 and 7.5 X 10(4) M-1 s-1 for vitamin E and vitamin C, respectively. It was suggested that each vitamin E could trap two peroxy radicals, whereas vitamin C could trap only one peroxy radical under the reaction conditions employed in this study. When both vitamin E and vitamin C were present, the oxidation was suppressed quite efficiently and the apparent inhibition rate constant was obtained as kinh = 4.0 X 10(5) M-1 s-1. Furthermore, vitamin E remained almost unchanged and only vitamin C was consumed at the initial stage and vitamin E was consumed after vitamin C was exhausted. It was concluded that vitamin E trapped the peroxy radical and the resulting alpha-chromanoxy radical reacted with vitamin C to regenerate vitamin E.

Ascorbic Acid↗
PubMed2006

Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron.

BACKGROUND: Vitamin A deficiency impairs iron metabolism; vitamin A supplementation of vitamin A-deficient populations may reduce anemia. The mechanism of these effects is unclear. In vitro and in animal models, vitamin A treatment increases the production of erythropoietin (EPO), a stimulant of erythropoiesis. OBJECTIVE: We measured the effect of vitamin A supplementation on hemoglobin, iron status, and circulating EPO concentrations in children with poor iron and vitamin A status. DESIGN: In a double-blind, randomized trial, Moroccan schoolchildren (n = 81) were given either vitamin A (200,000 IU) or placebo at baseline and at 5 mo. At baseline, 5 mo, and 10 mo, hemoglobin, indicators of iron and vitamin A status, and EPO were measured. RESULTS: At baseline, 54% of children were anemic; 77% had low vitamin A status. In the vitamin A group at 10 mo, serum retinol improved significantly compared with the control group (P < 0.02). Vitamin A treatment increased mean hemoglobin by 7 g/L (P < 0.02) and reduced the prevalence of anemia from 54% to 38% (P < 0.01). Vitamin A treatment increased mean corpuscular volume (P < 0.001) and decreased serum transferrin receptor (P < 0.001), indicating improved iron-deficient erythropoiesis. Vitamin A decreased serum ferritin (P < 0.02), suggesting mobilization of hepatic iron stores. Calculated from the ratio of transferrin receptor to serum ferritin, overall body iron stores remained unchanged. In the vitamin A group at 10 mo, we observed an increase in EPO (P < 0.05) and a decrease in the slope of the regression line of log10(EPO) on hemoglobin (P < 0.01). CONCLUSION: In children deficient in vitamin A and iron, vitamin A supplementation mobilizes iron from existing stores to support increased erythropoiesis, an effect likely mediated by increases in circulating EPO.

Adolescent↗
PubMed1996

[The effect of different vitamin B6 supplies on the vitamin B6 status (pyridoxine, pyridoxal and pyridoxamine) of the liver and the body of lactating rats].

Eighty female Sprague-Dawley rats were fed a semisynthetic diet during gravidity which was supplemented with 5 mg vitamin B6 per kg diet. The daily food intake was 14 g. During the following lactation the rats were assigned to one of 10 vitamin B6 treatment groups (0, 3, 6, 9, 12, 15, 18, 36, 360 and 3,600 mg per kg diet). The feed was given ad libitum. At day 14 of lactation the rats were decapitated. Parameters for determination of the vitamin B6 status were concentration of pyridoxine, pyridoxal and pyridoxamine in liver and body analyzed by using HPLC. Body was defined without the gastroenteral tract that was divided into carcass (extrahepatic compartments without liver) and total body (extrahepatic compartments plus liver). The mean weight of liver was 13 g with a dry mass of 33%; there was no difference between the treatment groups. The vitamin B6 concentration was lowest in rats fed 0 mg vitamin B6/kg diet (5 micrograms/g fresh matter, FM) and highest in the rats fed 3600 mg vitamin B6/kg diet (10.9 micrograms/g FM). The total vitamin B6 consisted on the average of 38% pyridoxal and 62% pyridoxamine. This was only changed significantly at the highest supplementation level, where 20% pyridoxine were detected instead of pyridoxamine. The mean weight of carcass averaged 212 g at a dry matter content of 31%. The vitamin B6 concentration ranged in the treatment groups from 0 mg to 360 mg vitamin B6/kg diet between 2.1 micrograms/g FM and 2.8 micrograms/g FM. It was highest in the 3600 mg vitamin B6 treatment group at 7.5 micrograms/g FM. The total vitamin B6 consisted of 63% pyridoxal and 37% pyridoxamine. It was only significantly affected in the 3600 mg vitamin B6 treatment group, where also pyridoxine could be found in the amount of 56%. The results indicate that alimentary vitamin B6 supply had more influence on liver vitamin B6 concentration than on carcass concentration. Total body concentration is very similar carcass concentration, as 95% of vitamin B6 is located there. The suitability of the parameters by the evaluation of the vitamin B6 requirement was confirmed the comparison of two statistical methods. It is concluded that a vitamin B6 supply of 5 to 6 mg/kg diet is necessary to meet the requirements during lactation.

Animals↗
PubMed1998

Effects of high dose vitamin C treatment on Helicobacter pylori infection and total vitamin C concentration in gastric juice.

Low gastric juice total vitamin C concentration in the presence of Helicobacter pylori (H. pylori) infection probably plays a role in gastric carcinogenesis. In vitro vitamin C has been shown to inhibit the growth of H. pylori. The aims of this study were to determine the effect of high dose vitamin C administration on H. pylori infection and on gastric juice total vitamin C concentration in patients with H. pylori related chronic gastritis. Sixty patients with dyspeptic symptoms and proven chronic gastritis and H. pylori infection, who were undergoing routine endoscopy, entered the study after giving informed consent. They were randomly coded into two treatment groups. Group 1 (controls, n = 28) were treated with antacids for 4 weeks and Group 2 (n = 32) received vitamin C 5g daily also for 4 weeks. Nine patients did not complete the study and were excluded. Plasma and gastric juice total vitamin C levels were measured at baseline, at the end of 4 weeks treatment and again 4 weeks after treatment cessation. In the control group H. pylori infection remained unchanged in all 24 patients throughout as did the mean gastric juice total vitamin C concentration. However, in the vitamin C treated group eight of 27 patients (30%) who completed the treatment course the H. pylori infection was eradicated (P = 0.01). In these patients the mean gastric juice total vitamin C concentration rose significantly from 7.2 +/- 1.6 micrograms/ml after 4 weeks treatment (P < M 0.001) and 19.8 micrograms/ml 4 weeks after treatment was discontinued (P < 0.001). In the remaining 19 patients with persistent H. pylori infection, the mean gastric juice total vitamin C concentration rose less than in those with successful H. pylori eradication; 6.3 +/- 1.7 micrograms/ml before treatment, 10.8 +/- 1.5 micrograms/ml after 4 weeks treatment (P < 0.05) and a return to pre-treatment levels (7.1 +/- 2.7 micrograms/ml) 4 weeks after vitamin C intake stopped. There were no side effects of vitamin C treatment. This study has shown that 4 weeks daily high dose vitamin C treatment in H. pylori infected patients with chronic gastritis resulted in apparent H. pylori eradication in 30% of those treated. In those patients there was also a highly significant rise in gastric juice total vitamin C concentration which persisted for at least 4 weeks after the treatment ceased. A significant, though less marked, gastric juice total vitamin C concentration increase was observed during vitamin C treatment even in subjects with persistent H. pylori infection, though this was not maintained after treatment ended. The mechanism whereby vitamin C treatment appeared to result in H. pylori eradication is unclear. Further confirmatory studies are indicated.

Adolescent↗
PubMedDate not supplied

[Basis for the historical stages for studying the biochemistry of vitamins. Noncoenzymatic mechanisms of vitamin B1].

Biochemistry of vitamins is one of the leading trends in the fundamental researches of A. V. Palladin Institute of Biochemistry from the moment of its foundation in 1925. The Laboratory of Vitamins Biochemistry was organised in 1994, it was reorganized into the Department of Vitamins Biochemistry in 1966, and later it was renamed as the Department of Coenzymes Biochemistry. Now the investigations at the Coenzymes Biochemistry Department headed (from 1986) by G. V. Donchenko, Corr.-Member of the National Academy of Sciences of Ukraine, are directed to estimation of vitamins A, E, B1 and PP action molecular mechanisms. Investigation of specific protein-acceptors of vitamins and their biologically active derivatives is a contemporary and effective methodological approach to the estimation of some molecular mechanisms of vitamins action on cellular metabolism. Considering the challenging theoretical and practical aspects of the further fundamental investigation development in the molecular vitaminology the following items are currently being worked in the Department last time: 1. Study of some molecular mechanisms of thiamine and vitamin PP neurotropic action. These investigations are oriented to clearing some new aspects of noncoenzymic mechanism of its influence on the nervous cell functioning both in the norm and at some nervous diseases. 2. Study of some molecular mechanisms of regulation by means of fat-soluble vitamins A, E and their specific proteins-acceptors of DNA, RNA and protein biosynthesis in the nuclei and mitochondria of actively proliferous cells. These investigations are aimed to the estimation of molecular mechanisms of fat-soluble vitamins participation in the regulation of DNA-dependent synthesis of RNA, RNA-polymerase activity, mechanism of their anticancerogenous effect, vitamin E participation in the realisation of nuclear genetic information. 3. Study of intracellular protein-receptors, which take part in realisation of vitamins and their biologically active derivatives functions in the human and animals' organism. The investigations, directed to study of a role of retinol-binding proteins in exchange of the vitamin A and in biosynthesis of DNA, RNA and proteins, the role of tocopherol-binding proteins in realisation of biological action of vitamin E in cells and thiamine-binding proteins in realisation of neurotropic action of vitamin B1 are actively developed. 4. Investigation of mechanisms of antioxidizing and antiradical biological action of vitamin D3, ecdisterone and related biologically active compounds. Basing on the fundamental researches some vitamins preparations have been created, such as "Carotin-M", "Cardiovit", "Evit-1", "Soevit", "Metovit", "Caratel'ka" and others. The results of fundamental investigation of noncoenzymic thiamine function led us to elaboration of a new hypothesis about molecular mechanism of vitamin B1 neurotropic action. According to the hypothesis the thiamine high neuroactivity is a result of existence in the nervous ending a specific mobile thiamine pool and connection thiamine metabolism with nervous cell membrane potential and acetylcholine metabolism.

Academies and Institutes↗
PubMed1996

Influence of different dietary vitamin B6 supply during gravidity and lactation on total vitamin B6 concentration (pyridoxine, pyridoxal and pyridoxamine) in blood and milk.

In a two factorial trial with 80 (5 x 2 x 8) Sprague-Dawley rats weighing 257 g the influence of different dietary vitamin B6 supply on concentration in blood and milk was examined. The two factors were 5 doses of alimentary vitamin B6 supply during pregnancy (0.6, 3, 6, 18, and 180 mg vitamin B6 per kg diet) and 2 doses in lactation (3 and 6 mg vitamin B6 per kg diet). The rats were fed a semisynthetic diet. The daily food intake was 14 g during pregnancy and ad libitum during lactation. At day 7 and 13 of lactation the dams were milked and at day 14 the animals were killed by decapitation. Vitamin B6 concentration of milk at 7th and 13th day of lactation and vitamin B6 concentration of blood at 14th day of lactation were examined. The mean total vitamin B6 concentration in blood was 0.18 microgram/ml and consisted of 94.8% pyridoxal and 5.2% pyridoxamine. An elevation in vitamin B6 supply during pregnancy led to an increase in blood vitamin B6 concentration of 40% and the vitamin B6 treatment during lactation caused an increase of 50%. The mean total vitamin B6 concentration in milk at the 7th day of lactation was 0.35 microgram/ml and consisted of 79.5% pyridoxal, 15.6% pyridoxamine and 4.9% pyridoxine. An elevation in dietary vitamin B6 supply during pregnancy led to an increase in milk vitamin B6 concentration of 79% and vitamin B6 treatment during lactation led to an increase of 38%. The mean total vitamin B6 concentration in milk at the 13th day of lactation was 0.44 microgram/ml and consisted of 79.8% pyridoxal, 13.9% pyridoxamine and 6.3% pyridoxine. Milk vitamin B6 concentration was increased by 53% through the dietary supply during pregnancy and by 32% through the higher lactational supply. The experiments indicate that vitamin B6 concentration in blood and milk is a reflection of dietary supply, whereby in lactation milk concentration is less influenced than blood.

Analysis of Variance↗