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Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12.

AIMS: Chronic alcohol exposure leads to a deficiency of group B vitamins and increased risk of alcoholic cardiomyopathy characterized by impaired ventricular contractility. This study was designed to examine the effect of group B vitamin supplementation on short-term exposure of the main alcohol metabolite acetaldehyde (ACA)-induced cardiac contractile dysfunction in rat ventricular myocytes. METHODS: Mechanical contractile properties were evaluated by an IonOptix SoftEdge system. Protein damage and apoptosis were determined by protein carbonyl and caspase-3 assays, respectively. RESULTS: Short-term (4-6 h) culture of myocytes with ACA (10 microM) depressed peak shortening amplitude, maximal velocity of shortening/relengthening, shortened duration of shortening but not the duration of relengthening. ACA exposure also enhanced protein carbonyl formation and apoptosis in ventricular myocytes. The toxin-induced mechanical defects, protein damage and apoptosis were ablated by vitamin B1 (10 microM), an essential vitamin required for DNA synthesis and repair. Vitamin B6 (10 microM) attenuated ACA-induced impairment of shortening duration. Vitamin B12 (1 mM) attenuated ACA-induced reduction in maximal velocity of shortening/relengthening. Unlike vitamin B1, none of the other ACA-elicited alterations in myocyte mechanical function were affected by vitamin B6 or vitamin B12. Vitamin B6 and vitamin B12 partially, but significantly, attenuated the ACA-induced carbonyl formation without affecting ACA-induced apoptosis. CONCLUSIONS: These data provide evidence that vitamin B1 supplementation may be protective for ACA-induced cytotoxicity through protection against protein damage and apoptotic cell death in ventricular myocytes.

Acetaldehyde↗

Bioavailability and interaction of vitamin A and vitamin E in ruminants.

Recent interest in antioxidant vitamins and animal nutrition has resulted in the investigation of feeding levels of vitamin E which are considerably higher than NRC requirements. Relatively high levels of vitamin E are required to improve animal product quality such as extending beef color stability and minimizing off-flavors in milk due to lipid oxidation. Concerns regarding a negative effect of vitamin A on vitamin E utilization and the suitability of currently used standard activity values for vitamin E supplements for ruminants have been raised. High dietary levels of vitamin A have depressed vitamin E utilization in most animals studied. In the dairy cow, 675,000 IU of vitamin A acetate per head per day is required to significantly depress vitamin E utilization. This is approximately 10-fold greater than the highest levels currently fed to dairy or beef cattle and therefore should not cause a practical problem. Synthetic and naturally derived alpha-tocopherol, and their ester forms, are commonly used as vitamin E supplements. These various forms give rise to isomer differences, ester differences and formulation differences that can affect their absorption and subsequent utilization. The current research indicates that the commonly used standard activity values based on a value of 1.00 IU per mg of all-rac-alpha-tocopheryl acetate are probably too low for the ruminant. The roles of isomeric forms and gastrointestinal tract absorption have not been completely resolved regarding their effects on the bioavailability of vitamin E supplements.

Animal Nutritional Physiological Phenomena↗

Vitamin K prophylaxis to prevent neonatal vitamin K deficient intracranial haemorrhage in Shizuoka prefecture.

OBJECTIVE: To compare three methods of vitamin K prophylaxis for neonatal vitamin K deficient intracranial haemorrhage. DESIGN: We designed three strategies for vitamin K prophylaxis: 1. therapeutic administration of vitamin K in a mass screening system using the hepaplastin test; 2. routine oral administration of vitamin K to newborn infants; and 3. administration of vitamin K to lactating mothers during the late neonatal period in addition to the routine method. We evaluated the efficacy of these methods by determining hepaplastin test values at the first month of age. POPULATION: 66,076 full term healthy newborn infants without any complications. RESULTS: Of 55,513 infants in the mass screening system, 3068 infants received vitamin K therapeutically. At the first month of age, in the group where vitamin K was administered therapeutically, 56 infants (1.83%) exhibited low hepaplastin test values (< 40%) despite vitamin K administration. But extremely low values (< 20%), indicating a very high risk of neonatal intracranial haemorrhage, were observed in 34 (0.06%) of 52,445 infants who did not receive vitamin K. In the routine administration system, oral administration of vitamin K twice within the first week of life showed a lower incidence (0.19%) of low level cases than a single administration (1.56%). An additional administration of vitamin K to lactating mothers throughout the late neonatal period showed an effective result.

Administration, Oral↗

Differential effect of vitamin K and vitamin D supplementation on bone mass in young rats fed normal or low calcium diet.

The purpose of this study was to clarify the differential effect of vitamin K and vitamin D supplementation on bone mass in young rats fed a normal or low calcium diet. Ninety female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into nine groups with 10 rats in each group: baseline control, and 0.5% (normal) or 0.1% (low) calcium diet, either alone, or with vitamin K (30 mg/100g, food intake), vitamin D (25 micro g/100 g, food intake), or vitamin K + vitamin D. After 10 weeks of feeding, bone histomorphometric analyses were performed on cortical bone of the tibial shaft and cancellous bone of the proximal tibia. Vitamin K supplementation increased the maturation-related cancellous bone gain and retarded the reduction in the maturation-related cortical bone gain in rats fed a low calcium diet, and increased the maturation-related cortical bone gain in rats fed a normal calcium diet. Vitamin D supplementation reduced the maturation-related cancellous bone gain, prevented the reduction in periosteal bone gain, and enhanced the enlargement of the marrow cavity, with no significant effect on the reduction in the maturation-related cortical bone gain in rats fed a low calcium diet, and increased the maturation- related cancellous and cortical bone gains with increased periosteal bone gain in rats fed a normal calcium diet. An additive effect of vitamin K and vitamin D on the maturation- related cortical bone gain was found in rats fed a normal calcium diet. This study shows the differential effects of vitamin K and vitamin D supplementation on cancellous and cortical bone mass in young rats fed a normal or low calcium diet, as well as the additive effect on cortical bone under calcium sufficient condition.

Age Factors↗

Vitamin D intake and vitamin D status of Australians.

The main source of vitamin D for Australians is exposure to sunlight. Thus, levels of serum 25-hydroxyvitamin D(3), the indicator of vitamin D status, vary according to the season and are lower at the end of winter. In Australia and New Zealand, the prevalence of vitamin D deficiency varies, but is acknowledged to be much higher than previously thought. One study found marginal deficiency in 23% of women, and another frank deficiency in 80% of dark-skinned and veiled women. The groups at greatest risk of vitamin D deficiency in Australia are dark-skinned and veiled women (particularly in pregnancy), their infants, and older persons living in residential care. Only a few foods (eg, fish with a high fat content) contain significant amounts of vitamin D. In Australia, margarine and some milk and milk products are currently fortified with vitamin D. The average estimated dietary intake of vitamin D for men is 2.6-3.0 g/day and for women is 2.0-2.2 g/day. The estimated dietary requirement of vitamin D is at least 5.0 g/day and may be higher for older people. Adequate intake of vitamin D is unlikely to be achieved through dietary means, particularly in the groups at greatest risk, although vitamin D-fortified foods may assist in maintaining vitamin D status in the general population. An appropriate health message for vitamin D needs to balance the need for sunshine against the risk of skin cancer.

Adult↗

Experimental vitamin A deficiency in mallards (Anas platyrhynchos): lesions and tissue vitamin A levels.

Captive mallards (Anas platyrhynchos), fed an all-grain diet for up to 5 months during the winters of 1991 to 1992 and 1992 to 1993, developed lesions of squamous metaplasia; some had no detectable hepatic vitamin A. Vitamin A deficiency in mallards was defined as hepatic levels of retinyl palmitate < 2 micrograms/g liver. Lesions were found only in ducks with low levels of hepatic vitamin A, but not all ducks with these low levels of hepatic vitamin A had histological lesions. The prevalence of lesions in the esophagus was greatest cranially and caudally and less common in the central region. Palatine salivary glands rarely were affected. Mallards with liver stores > 600 micrograms of hepatic retinyl palmitate per g liver, fed a diet deficient in vitamin A were unlikely to become deficient over a 5 month period. Birds fed an all-grain diet had significantly lower vitamin A concentrations in their liver compared to those fed an all-grain diet with vitamin A added. Liver weight, when corrected for body size, did not affect vitamin A concentration. Serum retinol levels were conserved over a large range of hepatic vitamin A levels but levels below 300 micrograms retinol/l were useful in detecting vitamin A deficiency in captive mallards. Based on the findings, the presence of lesions provides a conservative measure of vitamin A status in ducks and tissue levels should be measured in instances when mallards have questionable vitamin A status.

Animals↗

[Vitamin D and calcium metabolism in relation to different levels of vitamins B6 and D].

The influence of vitamin B6 deficiency on some vitamin D-dependent processes was studied in animals. The following parameters changing in relation to the level of vitamin D providing were investigated: activity of alkaline phosphatase in the serum and small intestine mucosa, the levels of Ca, P and parathormone, concentration of vitamin D metabolites and enzyme activity; and only 25-hydroxyvitamin D (25-OVD) concentration in the blood serum, under conditions of combined vitamin B6 and D deficiency was significantly lower as compared to cases with vitamin D deficiency alone. In the presence of vitamin B6 deficiency recovery of 25-OVD level in the blood serum, after vitamin D administration to the animals, had a tendency to delay as compared to that in the animals provided with vitamin B6. Vitamin B6 deficiency produced similar effect on 25-OVD 1-hydroxylase activity. The data obtained have evidenced a possibility of vitamin B6 influence on vitamin D metabolism.

Alkaline Phosphatase↗

Metabolism of vitamin K and prothrombin synthesis: anticoagulants and the vitamin K--epoxide cycle.

Vitamin K is primarily located in hepatic microsomes, where the vitamin K-dependent carboxylation in prothrombin synthesis occurs. Recent evidence supports the idea that the carboxylation is linked to the metabolism of the vitamin--specifically the cyclic interconversion of vitamin K and vitamin K epoxide. The primary site of action of coumarin and indandione anticoagulants appears to be an inhibition of the epoxide-to-vitamin K conversion in this cycle. There is a correlation between the inhibition of prothrombin synthesis and the regeneration of vitamin K from the epoxide by anticoagulants. In hamsters and warfarin-resistant rats prothrombin synthesis and the epoxide-K conversion are less sensitive to warfarin than in the normal rat. The epoxide-K conversion is impaired in resistant rats, which may explain their high vitamin K requirement. There is also a correlation between vitamin K epoxidation and vitamin K-dependent carboxylation, but the apparent link may be because vitamin K hydroquinone is an intermediate in the formation of the epoxide and also the active form in carboxylation. The vitamin K-epoxide cycle is found in extrahepatic tissues such as kidney, spleen, and lung and is inhibited by warfarin.

1-Carboxyglutamic Acid↗

Vitamin A and vitamin E content of infant formulas produced in the United States.

Vitamin A (vitamin A palmitate) and vitamin E (alpha-tocopheryl acetate) levels were determined in 77 samples of fortified infant formulas manufactured by 4 firms in the United States from 1981 to 1983 and were compared by formulation base (soy, milk) and manufacturing firm. For vitamin A and vitamin E, the mean values (IU/100 kcal) were 454 +/- 95 (range 248-614) and 2.0 +/- 0.7 (range 1.1-5.0), respectively. No significant differences (alpha = 0.05) were found in levels (IU/100 kcal) of vitamin A and vitamin E between milk- and soy-based formulas. When the mean vitamin A and vitamin E levels of formulas produced by the various firms were compared on an IU/100 kcal or percent of label declaration basis, significant differences (alpha = 0.05) were found among firms. Mean vitamin A levels for the various products compared to label declarations ranged from 126% of declared for the ready-to-use formulas to 139% of declared for the powders. Mean vitamin E levels ranged from 97% of declared for ready-to-use formulas to 118% of declared for concentrates. Except for one sample that contained 248 IU vitamin A/100 kcal, the formulas met the requirements of the 1980 Infant Formula Act.

Chromatography, Liquid↗

Randomised trial to assess benefits and safety of vitamin A supplementation linked to immunisation in early infancy. WHO/CHD Immunisation-Linked Vitamin A Supplementation Study Group.

BACKGROUND: The benefits and safety of vitamin A supplementation linked to immunisation in infancy need to be assessed before it can be widely recommended. We assessed the safety and benefits of maternal postpartum and infant vitamin A supplementation administered with each of the three diphtheria-tetanus-pertussis (DPT) and poliomyelitis immunisations and with a fourth dose with measles immunisation. METHODS: From January, 1995, we enrolled 9424 mother-infant pairs from Ghana, India, and Peru in this randomised, double-blind, placebo-controlled trial. 4716 mothers of infants in the vitamin A group received 200000 IU vitamin A, and their infants were given 25000 IU vitamin A with each of the first three doses of DPT/poliomyelitis immunisation at 6, 10, and 14 weeks. In the control group, 4708 mothers and their infants received placebo at the same times. At 9 months, with measles immunisation, infants in the vitamin A group were given a further dose of 25000 IU and those in the control group received 100000 IU vitamin A. Infants were followed up to age 12 months. The primary outcome measures were vitamin A status, signs of acute toxic effects, anthropometric indicators, and severe morbidity. Analysis was by intention to treat. FINDINGS: 3933 (93%) of the eligible 4212 infants on vitamin A and 3938 (93%) of the eligible 4227 controls received all four study doses. At the 6-month follow-up, there was a small decrease in vitamin A deficiency in the vitamin A group compared with controls (serum retinol < or =0.70 micromol/L 101 [29.9%] vs 122 [37.1%; 95% CI of the difference -14.3% to -0.2%]). This effect was no longer apparent at 9 and 12 months. There were no significant between-group differences in mortality throughout the study. The rate ratio to compare all deaths up to age 9 months in the two groups was 0.96 (95% CI 0.73 to 1.27). Fewer than 1% of the infants had bulging fontanelle. The intervention had no effect on anthropometric status, or on overall or severe morbidity. INTERPRETATION: The trial confirmed the safety of the intervention, but shows no sustained benefits in terms of vitamin A status beyond age 6 months or infant morbidity.

Adult↗

Difference in the metabolism of vitamin K between liver and bone in vitamin K-deficient rats.

The difference between vitamin K metabolism in the liver and that in the bone of vitamin K-deficient rats was examined. After 17 d administration of vitamin K-deficient food, vitamin K in the liver was almost depleted, and prothrombin time (PT) was prolonged. Serum total osteocalcin level was slightly decreased by vitamin K deficiency, whereas serum undercarboxylated osteocalcin level did not change. The level of menaquinone (MK)-4 as well as that of phylloquinone was decreased, but approximately 40 % of the initial level still existed in the femur after the 17 d period. A single-dose administration of vitamin K (250 nmol/kg body weight) markedly increased vitamin K level in the liver but not in the femur. These results suggest that the turnover of vitamin K in the bone is slower than that in the liver, and bone metabolism may be little affected by the short period of intake of vitamin K-deficient food. However, intake of a larger amount of vitamin K is required for its accumulation in the bone than in the liver. Furthermore, the counteracting effect of MK-7 on prolonged PT in vitamin K-deficient rats was found to be higher than phylloquinone or MK-4.

Animals↗

The interaction of dietary vitamin A and vitamin D related to skeletal development in the turkey poult.

Large white male turkey poults were fed diets with different levels of vitamins A and D to study the interaction of these vitamins with regard to skeletal development. Poults fed a basal diet deficient in both vitamins A and D developed severe lameness, growth depression, mortality and lesions consistent with rickets. Birds fed a diet containing the required level of vitamin D (900 ICU/kg, NRC estimated requirement) and a high level of vitamin A (400,000 IU/kg) also developed severe lameness, growth depression and a rachiticlike condition, characterized by thicker than normal proximal tibial epiphyseal plates and lower than normal bone mineral content. When fed a diet containing the required level of vitamin A (4,000 IU/kg, NRC estimated requirement) and a high level of vitamin D (900,000 ICU/kg), poults developed hypervitaminosis D as evidenced by mild growth depression and renal tubular mineralization. When poults were fed a diet containing high levels of both vitamins A and D growth rate and bone mineral content were similar to control poults fed a diet containing the required levels of vitamins A and D. In addition, lameness and renal tubular mineralization were not apparent in the poults fed a diet containing high levels of both vitamins A and D. It was concluded that there is an antagonistic interaction between vitamins A and D.

Animals↗