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At least 433 records · Page 24Linked to original sources
PubMed2003

Intermediate effects of the ileocaecal urinary reservoir (Charleston pouch 1) on serum vitamin B12 concentrations: can vitamin B12 deficiency be prevented?

OBJECTIVE: To assess the long-term effects of a form of ileocolic urinary reservoir (Charleston Pouch 1) on vitamin B12 serum levels, as vitamin B12 deficiency may be an important long-term risk after urinary diversion by this method. PATIENTS AND METHODS: The study included 60 patients (mean age 52 years, range 27-77; 33 men and 27 women) who had a follow-up of >or= 36 months (36-132 months) after the construction of an ileocaecal urinary reservoir. Vitamin B12 serum levels were determined at the time of diversion and again when the patients were evaluated every 6 months. RESULTS: Fifty-eight patients had a normal serum vitamin B12 concentration before surgery (two patients were excluded from the study because they had low levels); the mean level was 464 pg/mL (normal range 247-1000). At 6 and 12 months, the mean vitamin B12 levels were 367.5 and 468.5 pg/mL; at 1.5, 2, 3, 4, 5, 6, 7, 8, 10 and 11 years, the mean levels were 305, 495.5, 436.5, 379.5, 423.5, 393, 529.5, 631, 333.5 and 340 pg/mL, respectively. CONCLUSION: Ileocaecal urinary reservoirs have no adverse effects on serum vitamin B12 levels for up to 10 years after surgery. Patients with vitamin B12 deficiency must be identified and given adequate parenteral doses for life. Because body stores of vitamin B12 may not be depleted for many years, problems with B12 may be masked for a long time. We recommend that vitamin B12 levels be obtained annually, that a modest supplement twice yearly (by injection) may be beneficial and that serum vitamin B12 must be sampled before giving vitamin B12 injections, to avoid false results.

Adult↗
PubMed1997

Effect of vitamin A on the oxidative stability of broiler meat during storage: lack of interactions with vitamin E.

1. An experiment was carried out with male broiler chicks to evaluate the combined effect of two concentrations of vitamin A (1.032 and 10.32 mg retinyl acetate/kg diet) and two concentrations of vitamin E (0 and 150 mg alpha-tocopheryl acetate/kg diet) on the oxidative stability of the drumstick meat of broiler chickens. The experimental diets were fed from 1 to 42 d of age. The oxidative stability, evaluated by thiobarbituric acid reactive substances (TBARS) values, was determined after 125 d of storage at -18 degrees C. 2. TBARS values were very low and not significantly affected by dietary vitamins A and E or their combinations. However, the TBARS values in the meat of birds fed on the vitamin E-free diets, but not on the vitamin E-supplemented diets, were markedly increased after using an accelerated test of oxidation of the meat lipids by incubation. This resulted in a significant (P<0.001) difference from vitamin E supplementation. Vitamin A, alone or in combination with vitamin E, did not affect TBARS values found after incubation. 3. It is concluded that vitamin A at the concentrations used had no effect on the oxidative stability of the meat, in contrast to the protective effect of vitamin E, and that there is no interaction between the effect of these two vitamins on meat stability.

Animal Feed↗
PubMed1998

Effect of B-group vitamins and antioxidant vitamins on hyperhomocysteinemia: a double-blind, randomized, factorial-design, controlled trial.

Mild hyperhomocysteinemia is accepted as a risk factor for premature cardiovascular disease. In a population with a high prevalence of cardiovascular disease, we screened a group of clinically healthy working men aged 30-49 y (n = 509) for plasma homocysteine and 5,10-methylene tetrahydrofolate reductase (MTHFR) genotype status. Those with mildly elevated homocysteine concentrations (> or = 8.34 micromol/L) were selected for intervention. In a randomized, factorial-design, controlled trial we assessed the effects of B-group vitamins and antioxidant vitamin supplementation on homocysteine concentrations. The 132 men were randomly assigned to one of four groups: supplementation with B-group vitamins alone (1 mg folic acid, 7.2 mg pyridoxine, and 0.02 mg cyanocobalamin), antioxidant vitamins alone (150 mg ascorbic acid, 67 mg RRR-alpha-tocopherol, and 9 mg beta-carotene), B-group vitamins with antioxidant vitamins, or placebo. Intervention was double-blind. A total of 101 men completed the 8-wk intervention. When homocysteine concentrations were analyzed by group, significant (P < 0.001) decreases (32.0% and 30.0%, respectively) were observed in both groups receiving B-group vitamins either with or without antioxidants. The effect of B-group vitamins alone over 8 wk was a reduction in homocysteine concentrations of 27.9% (95% CI: 22.0%, 33.3%; P < 0.001) whereas antioxidants alone produced a nonsignificant increase of 5.1% (95% CI: -2.8%, 13.6%; P = 0.21). There was no evidence of any interaction between the two groups of vitamins. The effect of B-group vitamin supplementation seemed to depend on MTHFR genotype. Supplementation with the B-group vitamins with or without antioxidants reduced homocysteine in the men with mildly elevated concentrations, and hence may be effective in reducing cardiovascular risk.

Adult↗
PubMed2000

Bioconversion of plant carotenoids to vitamin A in Filipino school-aged children varies inversely with vitamin A status.

BACKGROUND: It is important to understand the factors affecting strategies to improve the vitamin A status of populations. We reported previously that a 3-d deuterated-retinol-dilution (DRD) procedure might be used to indicate total body stores of vitamin A. OBJECTIVE: We studied the ability of 3-d DRD to detect changes in the body pool size of vitamin A and the effect of vitamin A status on the bioconversion of plant carotenoids to vitamin A. DESIGN: Two separate, unrelated studies were conducted in 7-13-y-old children with poor or marginal serum retinol concentrations (0.32-0.93 micromol/L) by feeding them controlled diets daily for 5 d/wk for 12 wk, after treatment with an anthelmintic drug. In school 1 (n = 27), lunch and 2 snacks that were provided at school contained 2258 retinol equivalents/d (mostly from orange fruit and vegetables) and 5.3 MJ/d from 33 g fat, 37 g protein, and 209 g carbohydrates; in school 2 (n = 25), 2 snacks provided 2.5 MJ/d from 9.4 g fat, 9.6 g protein, and 119 g carbohydrates, but no carotenes. RESULTS: In school 1, mean serum beta-carotene increased from 0.12 to 0.62 micromol/L (P = 0.0001) and serum retinol increased from 0.68 to 1. 06 micromol/L (P = 0.0001). In school 2, serum beta-carotene increased from 0.06 to 0.11 micromol/L (P = 0.0001) and serum retinol increased from 0.66 to 0.86 micromol/L (P = 0.0001). In school 1, but not school 2, improvement in serum retinol varied inversely with baseline retinol (r = -0.38, P = 0.048). In both schools, 3-d DRD showed reductions in the ratio of serum deuterated to nondeuterated retinol (D:H retinol) postintervention, denoting improvements in vitamin A status; the higher D:H retinol (ie, the poorer the status) at baseline, the greater the reduction in D:H retinol postintervention (school 1: r = -0.99, P = 0.0001; school 2: r = -0.89, P = 0.0001). CONCLUSIONS: Three-day DRD can detect changes in the body pool size of vitamin A, although a predictive equation to quantitate total body stores of vitamin A with the use of 3-d data needs to be developed. Bioconversion of plant carotenoids to vitamin A varies inversely with vitamin A status; improvement in status after dietary interventions is strongly influenced by total body stores of vitamin A and is influenced little or not at all by serum retinol.

Adolescent↗
PubMed1977

Effect of high levels of dietary vitamin E on liver and plasma lipids and fat soluble vitamins in rats.

The effect of low, moderate and high dietary vitamin E (ranging from 0 to 25,000 IU/kg diet) on the levels of alpha-tocopherol, total lipids, cholesterol and vitamin A in liver and plasma of rats fed for 8 and 16 months was studied. A logarithmic relationship was observed between dietary levels of vitamin E and the concentrations of this vitamin in liver and plasma. The total alpha-tocopherol in whole liver of rats fed different levels of dietary vitamin E for 16 months was approximately double in comparison to rats fed for 8 months. Totoal lipids in liver were significantly increased by excess vitamin E supplementation in rats fed for 8 months, but not in rats fed for 16 months. There was no significant change observed in liver cholesterol level at 16 months. Plasma total lipids and cholesterol were lowered by vitamin E deficiency and also by dietary levels higher than 2,500 IU vitamin E/kg diet in rats fed for 16 months. Liver vitamin A storage was 4.5 times higher in rats supplemented with vitamin E than in rats without any supplement, but the effect of excess dietary vitamin E was no different from that of normal level (25 IU/kg diet). The findings of our long-term study are compared with the results of other short-term studies and the implications are discussed.

Animals↗
PubMed1993

Dietary vitamin A restriction produces marginal vitamin A status in young rats.

A model of marginal vitamin A deficiency was developed in young rats by limiting the vitamin A intake of dams and of offspring postweaning. Prior to and throughout pregnancy and lactation, female rats were fed diets in which the vitamin A concentration was either low marginal [0.18 retinol equivalent (RE)/g diet], high marginal (0.4 RE/g) or sufficient (4 RE/g). Vitamin A restriction had no effect on dams' reproduction or litter sizes, but total retinol in liver was depleted by the end of lactation. Pups fed all diets grew steadily from birth through 35 d. The milk curd total retinol concentration of 9-d-old pups' stomachs was significantly different among the low marginal, high marginal and vitamin A-sufficient groups. By 35 d, plasma retinol concentrations of pups in the low marginal group were less than half of those in the high marginal and vitamin A-sufficient groups. The liver total retinol concentrations and lecithin retinol:acyltransferase activity of 35-d-old pups in the low and high marginal groups were much lower than those of vitamin A-sufficient pups. When pups from dams fed low marginal diet were weaned onto vitamin A-free diet, frank vitamin A deficiency was evident by 33 d of age as judged by physical signs and biochemical alterations in vitamin A status. Thus, these dietary protocols are useful in inducing early onset of either marginal or frank vitamin A deficiency.

Animals↗
PubMed2002

Hyperhomocysteinaemia, folate and vitamin B12 in unsupplemented haemodialysis patients: effect of oral therapy with folic acid and vitamin B12.

BACKGROUND: Hyperhomocysteinaemia, a risk factor for atherosclerosis, is common in dialysis patients and particularly in those homozygous for a common polymorphism in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene (C677T transition). B-complex vitamin supplements have been shown to lower plasma total homocysteine (tHcy) concentrations, but the respective effectiveness of folate and oral vitamin B12 is not yet known. Our objectives were: (i) to determine the status of folate and vitamin B12 in a cohort of unsupplemented dialysis patients (ii) to assess the homocysteine-lowering effect of a folate supplement and then of a folate supplement with added vitamin B12. The responses were analysed for the C677T genotypes of MTHFR. METHODS: Plasma tHcy, folate and vitamin B12 were measured in 51 haemodialysis patients genotyped for the C677T MTHFR mutation (homozygotes, TT; heterozygotes, CT; without mutation, CC). All patients were then given daily supplements of 15 mg of folic acid for 2 months. They were given daily supplements of 1 mg of vitamin B12 in addition to the folate supplements for a further 2 months. Plasma tHcy, folate and vitamin B12 were monitored after each intervention. RESULTS: At baseline folate and vitamin B12 deficiencies were found in 10% and 6% of the patients. Initial plasma tHcy concentrations were high in all patients (mean 38.1+/-15 micromol/l). CC patients tended to have a lower tHcy concentration than pooled CT and TT patients. After 2 months of folate therapy, tHcy concentration decreased significantly to 20.2+/-7 micromol/l (P<0.001) and no significant differences were observed between the different genotype subgroups (19.4+/-6 for CC, 21.3+/-8 for CT, 18.5+/-4 for TT). A significant positive relationship was found between the reduction of tHcy and its initial value (rho=0.615, P<0.0001). The impact of the added vitamin B12 was negligible since tHcy concentrations did not change for the patients as a whole (19.8+/-7 micromol/l, NS) or in any subgroup (19.1+/-5 for CC, 20.3+/-9 for CT and 20+/-7 micromol/l for TT). CONCLUSIONS: (i) Folate and vitamin B12 deficiencies were observed in 10% and 6% respectively of our unsupplemented dialysis patients. (ii) After folate therapy, tHcy levels decreased significantly in all patients and were identical between the three C677T MTHFR genotype subgroups. (iii) Vitamin B12 supplements are useful in folate treated patients to prevent cobalamin deficiency and its neurological consequences but they did not lower tHcy plasma levels for the patients as a group or for any of the MTHFR subgroups.

Administration, Oral↗
PubMed1982

The effect of vitamin E on warfarin-induced vitamin K deficiency.

Vitamin K-deficient animals and humans developed a more severe coagulopathy when treated with vitamin E, which was due to further reduction in the vitamin K-dependent coagulation factors (II, VII, IX, and X). This phenomenon was not seen in normal vitamin K-sufficient animals or human subjects. The mechanism by which vitamin E causes this effect is not known. These coagulation factors are produced by the liver in precursor forms and are converted to functional proteins by a vitamin K-dependent reaction. Analysis of one of these coagulation factors, prothrombin (factor II), in plasma of vitamin K-deficient animals and humans treated with vitamin E was done in this study. The precursor of factor II is antigenically similar to biologically active factor II and can be activated to form thrombin by Echis carinatus venom. The data showed that functional factor II coagulant activity was reduced below base in warfarin-treated humans and animals given vitamin E. Factor II antigen as determined by electroimmunoassay in humans and factor II coagulant activity as measured using Echis venom in animals were unchanged and no different from untreated controls. The data suggest that vitamin E acts at the vitamin K-carboxylase step of carboxylation of precursor prothrombin and not in the synthesis of the precursor protein.

Animals↗
PubMed1994

[Influence of vitamin D3 on inhibitory effect of vitamin K2 on bone loss in ovariectomized rats].

To evaluate whether the vitamin D3 level in the plasma influences the inhibitory effect of vitamin K2 on bone loss, vitamin K2 (25 mg/kg/day) was administered to ovariectomized (OVX) rats fed a diet containing vitamin D3 (V.D.(+)) or a diet deficient in vitamin D3 (V.D.(-)). After 3 months of treatment, the plasma 25-OH-vitamin D3 (25-OH-D3) level in the V.D(-)-sham group was about 1/3 of that in the V.D(+)-sham group. The plasma calcium level and alkaline phosphatase activity were also significantly lower in the V.D(-)-sham group than in the V.D(+)-sham group. In the V.D(+) group, the plasma 25-OH-D3 level in the vitamin K2 group was about 1.5 times higher than that in the OVX-control group. Ovariectomy resulted in a significant decrease in bone density, bone mineral content (BMC) and bone mineral density (BMD) of femurs in both the V.D(+) and V.D(-) groups. In the V.D(-) group, vitamin K2 had no marked effect on the bone loss. In the V.D(+) group, the bone density and BMD in the mid portion of the femur were significantly increased by vitamin K2 treatment. These findings suggest that the effect of vitamin K2 on bone loss is affected by the vitamin D3 level in the plasma.

Animals↗
PubMed1987

Effect of ascorbic acid and vitamin E on biochemical changes associated with vitamin E deficiency in rats.

Weanling male Sprague Dawley rats were fed a vitamin E and C-free basal diet with or without supplementation of 100 IU vitamin E per kg diet. After 20 weeks, the vitamin E-deficient rats were divided into four groups, six in each group, and received supplemental ascorbic acid and/or vitamin E by tube feeding daily for 7 days: Group I, 30 mg ascorbic acid/100 g body wt.; Group II, 0.03 mg RRR-alpha-tocopheryl acetate/100 g body wt.; Group III, 30 mg ascorbic acid and 0.03 mg RRR-alpha-tocopheryl acetate/100 g body wt.; and Group IV, placebo. The six control rats (Group V) received placebo. The rats were sacrificed, blood and liver samples were collected for biochemical determinations. Vitamin E deficiency significantly increased erythrocyte (RBC) spontaneous hemolysis, liver thiobarbituric acid (TBA) value, activities of glutamateoxaloacetate transaminase (GOT), pyruvate kinase (PK), and creatine phosphokinase (CPK) in plasma, and significantly lowered plasma vitamin E levels and glutathione peroxidase (GPX) activities. Tube-feeding ascorbic acid for 7 days produced partial reversal effect on liver TBA values, activities of plasma PK, GOT, CPK, and plasma vitamin E levels but not on RBC hemolysis and plasma GPX activity. Tube feeding both ascorbic acid and vitamin E showed similar partial reversal effect as feeding vitamin E alone on all the parameters stated above. The results suggest that ascorbic acid may spare the metabolism of vitamin E and partially reverse the changes in some of the biochemical parameters characteristic of vitamin E deficiency.

Animals↗
PubMed1985

Comparative hepatic response to bromobenzene and allyl alcohol in the vitamin D-replete and vitamin D-depleted rat.

Vitamin D-depleted and vitamin D-replete rats were treated with allyl alcohol (AA) or bromobenzene (BB). The severity of the hepatotoxicity was evaluated by the serum concentrations of aspartate aminotransferase, alanine aminotransferase and sorbitol dehydrogenase, the histomorphological appearance of the lesions, and the amount of cytochrome P-450 destroyed. The activity of the monooxygenases was also evaluated. All parameters indicated that vitamin D depletion alone did not lead to any signs of liver toxicity nor did it modify the pattern of toxicity of either AA or BB. However, the intensity of the response in the periportal (AA treatment) and in the centrilobular (BB treatment) zones was modified by the depletion. Vitamin D depletion was accompanied by increased hepatic damage due to AA while BB resulted in less hepatic damage in vitamin D-depleted compared to vitamin D-replete animals. The metabolic profile of the liver mixed function oxidases indicated that its intraacinar distribution was modified by the depletion. Although the overall activity toward the substrates studied was not changed by vitamin D depletion, two out of the three enzyme activities studied suggested that vitamin D-depleted rats were poorer "centrilobular metabolizers" and better "periportal metabolizers" than vitamin D-replete rats. These observations correspond to increased periportal and decreased centrilobular toxicity in vitamin D-depleted animals. These results suggest that vitamin D depletion associated with severe hypocalcemia may be associated with an intraacinar modulation of enzyme systems as well as with an intraacinar difference in the susceptibility of the liver to certain chemicals.

1-Propanol↗
PubMed1977

Effects of intramuscular injections of selenium and vitamin E on selenium-vitamin E deficiency in young pigs.

Effects of intramuscular injections of selenium and vitamin E on lesions in pigs with selenium-vitamin E deficiency syndrome were determined in 2 factorial experiments, using a total 69 pigs. The pigs were fed a selenium-vitamin E deficient, 22.3% protein ration, supplemented with methionine, minerals, and vitamins. Weekly intramuscular injections of isotonic saline solution, vitamin E, selenium, or vitamin E and selenium were given to the respective treatment groups. Selenium-vitamin E deficiency lesions occurred only in pigs that were given saline injections. Weekly intramuscular injections of either selenium (as selenous acid buffered to pH (7.3) at the rate of 0.05 mg/kg of body weight or vitamin E at the rate of 20 IU/kg of body weight or the combination of selenium and vitamin E prevented cardiac and skeletal myodegeneration, hepatic necrosis, and death. Significant increases of serum aspartate aminotransferase activity values were noted in pigs with liver, heart, or skeletal muscle lesions, but these increases were not correlated with the extent of the lesions. Vascular lesions, epicardial and endocardial hemorrhages, and yellow discoloration of body fat were not features of this experimentally induced disease. These lesions may be related to factors other than the deficiency of selenium, vitamin E, or selenium and vitamin E in rations previously used in reported studies.

Animals↗
PubMed1992

Hepatic concentration of vitamin K active compounds after application of phylloquinone to chickens on a vitamin K deficient or adequate diet.

Liver and serum concentrations of vitamin K active compounds were measured in two groups of (deficient and normal) broilers after administration of phylloquinone 1 mg/kg. Assays were performed by HPLC after extraction and purification of these compounds. The only menaquinone found in the chicken was menaquinone-4. In the deficient group, the chickens exhibited hepatic concentrations of vitamin K1, vitamin K1 epoxide and menaquinone-4 markedly lower than those of the control group. After administration of phylloquinone, vitamin K and vitamin K epoxide levels fell sharply. There is no hepatic storage of vitamin K comparable to that of vitamin A. However, while menaquinone levels were found to be stable in the control group, they rose significantly in the deficient group after vitamin K injection. The question is: is there a transformation of vitamin K into menaquinone and/or is there a preferential utilization of one of the vitamin K active compounds?

Animals↗
PubMed1993

Subacute combined degeneration with high serum vitamin B12 level and abnormal vitamin B12 binding protein. New cause of an old syndrome.

Subacute combined degeneration of the spinal cord due to vitamin B12 deficiency invariably has been associated with a low serum vitamin B12 level. We describe a young man who presented with a unique syndrome of subacute combined degeneration associated with high serum vitamin B12 level, low red blood cell vitamin B12 level, and an abnormal plasma vitamin B12-binding protein. Uptake of cobalamin by his leukocytes in vitro was inhibited by his own but not by normal control plasma. Intensive hydroxocobalamin (vitamin B12) treatment was associated with clinical and electrophysiologic recovery accompanied by normalization of mean corpuscular volume, red blood cell vitamin B12 level, plasma homocysteine, and urinary methylmalonic acid. The subacute combined degeneration was probably precipitated by treatment with folic acid as the significance of his high serum vitamin B12 level was not apparent when he first presented with megaloblastic anemia 3 years earlier. To our knowledge, this is the first example of neurologic disease associated with high serum vitamin B12 level and provides further evidence that sometimes a serum vitamin B12 level may not be a reliable guide to vitamin B12 deficiency.

Adult↗
PubMed1983

Vitamin deficiencies in rice-eating populations. Effects of B-vitamin supplements.

Rice is the staple food in many countries of Asia. Recent nutrition surveys in eight states, conducted by the National Nutrition Monitoring Bureau of India, show that though the average energy intake is adequate, more than 50% of the households surveyed consumed less than the Recommended Dietary Allowance (RDA) of energy. These households generally had per capita incomes of less than Rupees 2/- (US+ 0.25) per day. The average intake of vitamin A was only 42% of the RDA and that of riboflavin, 70% of the RDA. The average intake of other nutrients such as thiamin, niacin, ascorbic acid, iron and calcium was adequate, although thiamin deficiency was present in populations where rice was the main cereal, but not in populations where rice was the main cereal, but not in populations that consumed mixed cereal or cereal-millet diets. The magnitude of the riboflavin deficiency (after correction or energy) was also more marked in the former. Vitamin A intake was not related to the type of cereal, but had some relationship to the quantity of vegetables consumed. Nutrition surveys from Japan also reveal deficiencies in intake of energy, vitamin A, thiamin and riboflavin. The Japanese diet tends to be deficient by 20% in vitamin A and riboflavin, but not thiamin. Thus, vitamin A, riboflavin and energy (in that order) are the major nutritional constraints in rice-eating populations. Clear-cut correlations between the magnitude of dietary deficiency and the prevalence of signs and symptoms of vitamin deficiency were not apparent in the comparisons between populations, suggesting that as well as dietary deficiency other environmental factors play a role in the development of clinical deficiency. Attempts to correlate clinical deficiency with the magnitude of biochemical deficiency have also failed. Recent studies aimed at examining the effects of food supplements (rural Gambian women) or vitamin supplements (rural Indian boys) on vitamin status suggest that in some communities, vitamin intakes close to the RDA fail to saturate the tissues, as judged by biochemical tests. In the Indian boys, there was a marked rise in urinary excretion of riboflavin during winter when the incidence of respiratory infections was high. Metabolic losses of vitamins due to infections may preclude tissue saturation despite adequate dietary intake. Administration for 1 year of B-vitamins at levels close to the RDA failed to reduce the prevalence of clinical deficiency signs, but did produce some improvement in hand steadiness - a psychomotor test.(ABSTRACT TRUNCATED AT 400 WORDS)

Asia↗
PubMed1992

[Determination of vitamin D in food using high performance liquid chromatography (HPLC). Results of collaborating studies of the working group "Vitamin Analysis" according to section 35 of the German Food Act].

A standardized method to determine the vitamin D content of food by means of HPLC is described. After the test material was homogenized and saponified with ethanolic aqueous potassium hydroxide solution, vitamin D was extracted using n-hexane. Using HPLC on a silica gel column, the fraction containing vitamin D is separated from the nonsaponifiable residue. After the fraction was reduced, the residue was dissolved in methanol and the vitamin D content determined after HPLC separation on an RP-C18 column. For evaluation, either a conventional external standard method using laboratory and matrix specific recovery rates as correction factors, or an internal standard method using vitamin D2, and D3, respectively as internal standards were employed. The method was developed and standardized by the working group "Vitamin Analysis" in accordance with section 35 LMBG (German Food Act). Repeatability and comparability of the results were checked in collaborative studies (14 laboratories) in milk powder and gruel that had been enriched with vitamin D3. Applicability of the method to other food (eggs, milk, fish, margarine) was checked separately. The statistical evaluation of the results of the collaborative studies has shown that the method is reliable enough to be included into the "Amtliche Sammlung" (official collection of analytical methods) according to section 35 LMBG. The present method may be used to determine the content of vitamin D2 and D3 in natural and vitaminized food. It is specific for the vitamins D2 and D3 released during saponification of food, but does not allow separate determination of the pre-vitamins D already present in the sample.

Chromatography, High Pressure Liquid↗
PubMed2001

In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats.

Reactive oxygen species (ROS) may be involved in the toxicity of chlorpyrifos-ethyl (CE) [O,O-diethyl-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate]. We have, therefore, examined the in vivo effects of CE on the rat erythrocyte antioxidant system and evaluated the ameliorating effects of melatonin and a combination of vitamin E and vitamin C on the oxidative damage induced by CE. The experimental groups were: (1) control group, (2) CE-treated group (CE), (3) vitamin E plus vitamin C treatment group (Vit), (4) melatonin-treated group (Mel), (5) vitamin E plus vitamin C plus CE treatment group (Vit + CE), and (6) melatonin plus CE treatment group (Mel + CE). Vitamin E and vitamin C were administered intramuscularly once a day for 6 consecutive days at 150 and 200 mg/kg, respectively, in the Vit and Vit + CE groups. Melatonin was administered intramuscularly at 10 mg/kg per day for 6 consecutive days in the Mel and Mel + CE groups. At the end of the fifth day, the rats of CE, Vit + CE and Mel + CE groups were treated orally with the first of two equal doses of 41 mg/kg CE, the second oral dose being given 21 h later. Blood samples were taken 24 h after the first CE administration. Levels of thiobarbituric acid reactive substance (TBARS), antioxidant defence potential (AOP), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were determined in erythrocytes. In comparison with the control group, oral administration of CE significantly (P < 0.05) stimulated TBARS activity while significantly (P < 0.05) inhibiting AOP and the activities of SOD and CAT. However, GSH-Px activity remained unchanged by CE treatment. Treatment with melatonin and vitamins E plus C significantly (P < 0.05) reduced the CE-induced increase of TBARS, and overcame the inhibitory effect of CE on SOD and CAT, but not on AOP. Melatonin treatment significantly (P < 0.05) increased only GSH-Px activity, irrespective of the effect of CE. These results suggest that CE treatment increases in vivo lipid peroxidation and decreases antioxidant defence by increasing oxidative stress in erythrocytes of rats, and melatonin and a combination of vitamin E and vitamin C can reduce this lipoperoxidative effect.

Administration, Oral↗
PubMed2006

Evaluation of the vitamin status in nursing women by vitamin content in breast milk.

The dependence of daily vitamin excretion with breast milk on dietary vitamin content and blood vitamin level was studied in nursing women. Breast mils vitamins were assayed in women supplied with vitamins. We identified the criteria for adequate vitamin supply in nursing women over the 1st month after labor (vitamins A, 130 microg; vitamin B1, 100 microg; vitamin B2, 130 microg; vitamin E, 750 microg; vitamin B6, 60 microg).

Adult↗