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At least 1,351 records · Page 75Linked to original sources
PubMed1997

Salt concentration determines 1,25-dihydroxyvitamin D3 dependency of vitamin D receptor-retinoid X receptor--vitamin D-responsive element complex formation.

The electrophoretic mobility shift assay was used to determine in vitro formation of the vitamin D receptor-retinoid X receptor beta (VDR-RXR beta) heterodimer complex on vitamin D-response elements (VDREs) from rat osteocalcin, mouse osteopontin, rat 25-hydroxyvitamin D3 24-hydroxylase, and human parathyroid hormone (PTH) genes. Baculovirus-expressed rat VDR was used as VDR and the binding reactions were performed at salt concentrations ranging from 50 to 170 mM KCI. Without ligand, optimum complex formation was observed at 50 mM KCI and markedly decreased with increasing KCI for all VDREs. In the presence of 1,25-dihydroxyvitamin D3, optimum complex formation occurred between 110 and 130 mM KCI for positive (enhancer) VDREs. At low salt concentrations (50-70 mM KCI), 1,25-dihydroxyvitamin D3 did not increase complex formation and actually caused a slight decrease. However, above 90 mM KCI, 1,25-dihydroxy-vitamin D3 markedly increased complex formation and at 150-170 mM KCI, a concentration that presumably mimics physiologic nuclear levels, 1,25-dihydroxy-vitamin D3 appeared to be required for complex formation. With the suppressive cis-acting sequence, i.e., PTH-VDRE, optimum detection of VDR complexes in the presence of 1,25-dihydroxyvitamin D3 occurred at a lower salt concentration (90-110 mM KCI). Moreover, no specific complexes were formed at high salt concentrations, even when 1,25-dihydroxyvitamin D3 was added. Thus, when analyzing an effect of ligand on VDR-RXR-VDRE complex formation, it is essential that the reaction be carried out with a range of salt concentrations. Further, 1,25-dihydroxyvitamin D3 appears to be required for formation of the VDR-RXR beta-VDRE complex at salt concentrations approaching physiological.

Animals↗
PubMed1998

Studies on the interaction between the vitamin D receptor and the radiolabelled 20-epi vitamin D analogue GS 1500.

Previous studies have shown that the binding affinity of a vitamin D analogue for the vitamin D receptor (VDR) does not correlate with the biological potency of the compound. In the present investigation the vitamin D analogue GS 1500, which is characterised by an altered stereochemistry at carbon C-20 (20-epi) and an aromatic ring in the side chain, was studied with respect to its interaction with the VDR. Using [3H]-GS 1500 as tracer, the receptor binding properties of GS 1500 were investigated and compared to those of 1,25(OH)2D3. The binding studies did not reveal a different binding site for GS 1500 than the one already established, and the binding affinity was in accordance with previously found values. At the level of VDR interaction with the vitamin D responsive element, GS 1500 did induce a binding complex at a lower concentration than 1,25(OH)2D3, which may help explain the difference in potency.

Animals↗
PubMed2002

The water-soluble vitamin E analogue Trolox protects against ischaemia/reperfusion damage in vitro and ex vivo. A comparison with vitamin E.

We investigated the activities, both in vitro and ex vivo, of the water-soluble vitamin analogue Trolox in a model of isolated heart ischaemia-reperfusion and we compared them with those of alpha -tocopherol. Isolated rat hearts were perfused with Krebs-Henseleit solution. For in vitro experiments, the hearts were perfused with Trolox (20 micromol l (-1)) and were subsequently subjected to 20 min of global ischaemia and 40 min of post-ischaemic reperfusion. For ex vivo experiments, either Trolox or alpha -tocopherol (10 mg kg(-1) ) were administered by gastric gavage 60 min before excision of the heart. Various parameters of cardiac function were evaluated and oxidative damage was assessed by TBARS production. Trolox significantly enhanced cardiac recovery after ischaemia/reperfusion, both when it was perfused in vitro and after its oral administration. Vitamin E also favourably affected cardiac recovery but did so less effectively than Trolox. Further, the production of TBARS was significantly inhibited by Trolox, suggesting that its beneficial effects are due to its antioxidant activities. In conclusion, perfusion of isolated rat hearts with low concentrations of the water-soluble vitamin E analogue Trolox effectively enhances cardiac recovery after a 20 min ischaemic period and decreases reperfusion-induced oxidative damage. Interestingly, Trolox retains its activities after oral administration. Vitamin E, when administered per os, also increases functional recovery but does so less potently than Trolox. These differential effects are likely due to the scavenging, by Trolox, of reactive oxygen species generated in the water phase.

Administration, Oral↗
PubMed1978

[Methods for determination of vitamins by means of high performance liquid chromatography (HPLC). II. Determination of vitamin A (author's transl)].

A method is described for the rapid determination of vitamin A in vitamin-concentrates, precursors and mineral supplements. After saponification of the sample, the vitamin A is extracted with petroleum-ether. In this extract the vitamin A is determined spectrophotometrically by HPLC without further clean-up.

Chromatography, High Pressure Liquid↗
PubMed1990

In vitro calcium transport properties of skeletal muscle mitochondria from vitamin D-deficient and 1,25-dihydroxy-vitamin D3-treated chicks.

Previous work has shown that vitamin D3 or 1,25-dihydroxy-vitamin D3 affect calcium content and fluxes in mitochondria of chick skeletal muscle in situ. Studies were performed to investigate whether these effects are related to variations in the Ca2+ transport properties of mitochondrial membranes. Mitochondria isolated from skeletal muscle of vitamin D-deficient chicks and chicks dosed with 1,25(OH)2D3 for 3 or 7 days (50 ng/day) were employed. No changes in the rate and affinity for calcium of the Ruthenium Red-sensitive Ca2+ uptake system were detected after treatment with 1,25(OH)2D3. The metabolite did not cause either modifications in Ca2+ efflux from mitochondria preloaded with the cation induced by Na+ or blockage of mitochondria energy supply. Prior treatment of animals with vitamin D3 was also without effects. However, a significant stimulation of Ca2- uptake by intact muscle preparations from the same experimental animals was observed in response to treatment with 1,25(OH)2D3 in vivo (50 ng/day, 3 days) or in vitro (10(-10) M, 60 minutes). In addition, the Ca content of muscle mitochondria was markedly diminished in chicks treated with the sterol. It is suggested that the effects of 1,25(OH)2D3 on muscle mitochondrial Ca metabolism may be secondary to changes in cytoplasmic Ca2+.

Animals↗
PubMed2002

Diet supplementation with vitamin E, vitamin C and beta-carotene cocktail enhances basal neutrophil antioxidant enzymes in athletes.

Exercise increases oxygen consumption and causes a disturbance of intracellular pro-oxidant-antioxidant homeostasis. Few data are available as to the cumulative effects of exercise on the antioxidant defenses of the neutrophil. We studied the effects of 90 days' supplementation with placebo or an antioxidant cocktail of vitamin E (500 mg/day) and beta-carotene (30 mg/day) and the last 15 days also with vitamin C (1 g/day) on sportsmen's basal neutrophil antioxidant defenses. We analyzed the activities of catalase, glutathione peroxidase, glutathione reductase and the activities and levels of superoxide dismutase, glutathione and glutathione disulfide in neutrophils purified from antecubital vein blood of sportsmen before and after diet supplementation. Plasma vitamin E, beta-carotene and vitamin C concentrations in the antioxidant-supplemented group were approximately 1.6, 10, and 1.2 times higher respectively than those of the placebo group. The antioxidant-supplemented group presented a significantly higher glutathione versus glutathione disulfide ratio in neutrophils (about 20%) than the placebo one. Antioxidant supplementation enhances the antioxidant enzyme activity of superoxide dismutase and catalase in neutrophils.

Adult↗
PubMed1983

Individual quantitation of vitamin D2, vitamin D3, 25-hydroxyvitamin D2, and 25-hydroxyvitamin D3 in human milk.

Extraction, lipid-reduction, and chromatographic methods suitable for the resolution and subsequent quantitation of vitamin D2, vitamin D3, 25-hydroxyvitamin D2, and 25-hydroxy-vitamin D3 from human milk are described. This procedure utilizes a methanol:methylene chloride extraction, precipitation of unwanted lipids with cold methanol and ether, backwash with alkaline buffer, silica Sep-Pak preparative chromatography, normal- and reverse-phase high-performance liquid chromatography with final quantitation of the antirachitic sterols by competitive protein binding assay. The described assay was used to determine these antirachitic sterols in milk from women receiving various supplements of vitamin D or undergoing ultraviolet phototherapy.

Cholecalciferol↗
PubMed1987

Stopped-flow investigation of the reaction between vitamin E radical and vitamin C in solution.

Kinetic study of the reaction between vitamin E radical and vitamin C has been performed. The rates of reaction of vitamin C (ascorbic acid 1, 6-0-stearyl ascorbic acid 2, and 2,6-O-dipalmitoyl ascorbic acid 3) with vitamin E radical (5,7-diisopropyl-tocopheroxyl) in benzene-ethanol (2:1, v/v) solution have been determined spectrophotometrically, using stopped-flow technique. The second-order rate constants obtained are 549 +/- 30 M-1s-1 for 1, 626 +/- 53 M-1s-1 for 2, and 4.84 +/- 1.41 M-1s-1 for 3 at 25.0 degrees C. The result shows that the ascorbic acid ester 2 having a long-alkyl-chain at 6-position is 1.14 times as reactive as the ascorbic acid 1, whereas the ascorbic acid ester 3 substituted at 2-position is only 0.01 times as reactive as the ascorbic acid 1.

Ascorbic Acid↗
PubMed1987

Vitamin K-dependent carboxylase. Possible role for thioredoxin in the reduction of vitamin K metabolites in liver.

In the liver vitamin K epoxide, which is produced during the posttranslational carboxylation of protein-bound glutamic acid residues, is recycled by the action of one or more dithiol-dependent reductases. In vitro synthetic dithiols may serve as a cofactor for these enzymes, but the physiological reductant has not yet been found. In this paper we report that in vitro the commercially available thioredoxin/thioredoxin reductase from E. coli can replace the synthetic dithiols during the various reactions of the vitamin K cycle. Based on the assumption that in vivo thioredoxin also plays a role in the regeneration of vitamin K hydroquinone from the epoxide, an extension of the generally accepted vitamin K cycle is proposed.

Animals↗
PubMed1991

Vitamin C and vitamin E status in the spontaneously diabetic BB rat before the onset of diabetes.

Ascorbic acid (AA), dehydroascorbic acid (DHAA), and vitamin E were measured in tissues and plasma of 30 control and 30 spontaneously diabetic BioBreeding rats (BBdp) during development and before the onset of diabetes. At weaning, rats were fed an AIN-76 semisynthetic diet for 30, 64, or 113 days, after which plasma and tissues from 10 rats of each group were collected and analysed for AA, DHAA, and vitamin E. AA and DHAA levels were significantly increased in plasma and spleen of the diabetes-prone rats compared with those of the control group at 30 and 64 days, but the difference disappeared by 113 days. No differences were observed in liver, adrenals, thymus, and pancreas at any of the time periods. However, lower levels of vitamin E were observed in adrenal gland, thymus, and pancreas of the diabetes-prone rats. It is concluded that BBdp rats have an altered metabolism of AA, DHAA, and vitamin E, before the onset of diabetes. These changes could be due to genetic and physiological factors operating during development of this rat strain.

Adrenal Glands↗
PubMed1981

Biosynthesis of vitamin B-12. Part I. Role of the ribosomal proteins in vitamin B-12 biosynthesis.

1. 70 S ribosomes isolated from strains of Escherichia coli 113-3, K12 and B take part in vitamin B-12 biosynthesis from AdoCbi-GDP, NAD and dimethylbenzimidazole in the presence of enzymes of the cytosol fraction. 2. 70 S ribosomes from E.coli 113-3 bind Ado[58Co]Cbi-GDP. This reaction is independent of fusidic acid. 3. Proteins from 5 S RNA complex as well as l3 protein isolated from E.coli 113-3 ribosomes catalyze vitamin B-12 biosynthesis. The main catalytic function in this reaction is preformed by protein L18. 4. Vitamin B-12 biosynthesis proceeding in the presence of isolated ribosomal proteins is inhibited by fusidic acid, chloramphenicol and vernamycin but not by erythromycin. 5. Vitamin B-12 synthesized in the presence of isolated ribosomal proteins is biologically active.

Anti-Bacterial Agents↗
PubMed1986

The in vivo effects of acenocoumarol, phenprocoumon and warfarin on vitamin K epoxide reductase and vitamin K-dependent carboxylase in various tissues of the rat.

In rats the in vivo effects of a chronic low-dose treatment (+/- 60 micrograms/rat per day) with different coumarins (acenocoumarol, phenprocoumon and warfarin) on hepatic and non-hepatic vitamin K-dependent enzyme systems were compared. The plasma concentrations of the three coumarins differed largely but these differences were not reflected in the microsomal coumarin contents. The non-hepatic microsomes contained less than 20% of the coumarins found in liver microsomes. No substantial differences were observed between the following effects of the three anticoagulant treatments. The blood coagulation factor activities were about 10% of normal. The hepatic microsomal vitamin K epoxide reductase activity was diminished to about 35% of control values. The vitamin K epoxide reductase activities present in kidney, lung, spleen, testis and brain microsomes were less influenced by the coumarin treatments; activities ranged between 45 and 65% of normal. In the liver microsomes a 15-fold accumulation of non-carboxylated precursor proteins was found; in the non-hepatic microsomes this effect was less pronounced but still present. The hepatic vitamin K-dependent carboxylase activity was enhanced but the corresponding non-hepatic enzyme activities were slightly or not affected. In addition, the effects of a chronic low-dose warfarin treatment were compared with those after an acute high dose of the drug.

4-Hydroxycoumarins↗
PubMed1992

Rates of interactions of superoxide with vitamin E, vitamin C and related compounds as measured by chemiluminescence.

The rate constants for the interactions of superoxide with vitamin E (alpha-tocopherol), vitamin C (ascorbic acid) and their related compounds have been measured by a chemiluminescence method. A strong chemiluminescence of a constant intensity was observed when xanthine oxidase was added to an aqueous solution of hypoxanthine and a Cypridina luciferin analog, 2-methyl-6-phenyl-3-7-dihydroimidazo[1,2-a]pyrazin-3-one (CLA). Vitamin E, vitamin C and their related compounds competed with CLA to react with superoxide and reduced the chemiluminescence intensity. From a kinetic analysis of the effect of addition of these compounds on the chemiluminescence intensity, the rate constants for their interactions with superoxide were measured at 25 degrees C and pH 7.8. The rate constants were obtained as 3.3 x 10(5) and 1.7 x 10(4) M-1 s-1 for ascorbate and 2-carboxy-2,5,7,8-tetramethyl-6-chromanol, respectively, and also as 4.9 x 10(3) and 4.5 x 10(3) M-1 s-1 for alpha-tocopherol incorporated into soybean and dimyristoyl phosphatidylcholine liposomal membranes, respectively. It has been shown that this method is a sensitive and a quick method which can be applied for measurement of the reactivities of various natural and synthetic compounds toward superoxide. In addition it has been shown that this method can also be applied to the heterogeneous system as well as homogeneous solution, which makes it more versatile and useful for the study in biochemistry.

Ascorbic Acid↗
PubMed1987

A CIDEP and fluorescence study of the oxidation of vitamin E: the vitamin E radical cation.

The photochemical and thermal oxidations of vitamin E in trifluoroacetic acid were investigated by the combination of electron spin resonance, chemically induced dynamic electron polarization, and fluorescence techniques. Two independent thermal pathways led to the formation of the vitamin E radical cation in which one of the paths involved the intermediate neutral semiquinone radical. Photo-oxidation, however, did not involve the neutral radicals. The fluorescence spectra of both the neutral and the charged forms of the vitamin E radicals are reported here for the first time. Some model charge transfer reactions involving the vitamin E radical cation were reported.

Electron Spin Resonance Spectroscopy↗
PubMed2004

Cell cycle arrest and autoschizis in a human bladder carcinoma cell line following Vitamin C and Vitamin K3 treatment.

Exponentially growing cultures of human bladder tumor cells (T24) were treated with Vitamin C (VC) alone, Vitamin K(3) (VK(3)) alone, or with a VC:VK(3) combination for 1, 2, or 4hr. Flow cytometry of T24 cells exposed to the vitamins for 1h revealed a growth arrested population and a population undergoing cell death. Cells in G(1) during vitamin treatment arrested in G(1) while those in S phase progressed through S phase and arrested in G(2)/M. DNA synthesis decreased to 14 to 21% of control levels which agreed with the percent of cells in S phase during treatment. Annexin V labeling demonstrated the majority of the cells died by autoschizis, but necrosis and apoptosis also were observed. Catalase treatment abrogated both cell cycle arrest and cell death which implicated hydrogen peroxide (H(2)O(2)) in these processes. Redox cycling of VC and VK(3) increased H(2)O(2) production and decreased cellular thiol levels and DNA content, while increasing intracellular Ca(2+) levels and lipid peroxidation. Feulgen staining of treated cells revealed a time-dependent decrease in tumor cell DNA, while electrophoresis revealed a spread pattern. These results suggest that Ca(2+) disregulation activates at least one DNase which degrades tumor cell DNA and induces tumor cell death.

Antioxidants↗
PubMed2005

Biosynthesis and uptake of thiamine (vitamin B1) in bloodstream form Trypanosoma brucei brucei and interference of the vitamin with melarsen oxide activity.

Bloodstream forms of Trypanosoma brucei brucei were cultivated in the presence and absence of thiamine (vitamin B1) and pyridoxine (vitamin B6). The vitamins do not change growth behaviour, indicating that Trypanosoma brucei is prototrophic for the two vitamins even though in silico no bona-fide thiamine-biosynthetic genes could be identified in the T. brucei genome. Intracellularly, thiamine is mainly present in its diphosphate form. We were unable to detect significant uptake of [3H]thiamine and structural thiamine analogues such as pyrithiamine, oxithiamine and amprolium were not toxic for the bloodstream forms of T. brucei, indicating that the organism does not have an efficient uptake system for thiamine and its analogues. We have previously shown that, in the fission yeast Saccharomyces pombe, the toxicity of melarsen oxide, the pharmacologically active derivative of the frontline sleeping sickness drug melarsoprol, is abolished by thiamine and the drug is taken up by a thiamine-regulated membrane protein which is responsible for the utilization of thiamine. We show here that thiamine also has weak effects on melarsen oxide-induced growth inhibition and lysis in T. brucei. These effects were consistent with a low affinity of thiamine for the P2 adenosine transporter that is responsible for uptake of melaminophenyl arsenicals in African trypanosomes.

Animals↗
PubMed2005

Mitochondrial damage induced by fetal hyperphenylalaninemia in the rat brain and liver: its prevention by melatonin, Vitamin E, and Vitamin C.

Abnormal oxidative stress was observed in hyperphenylalaninemia and other inborn errors of intermediary metabolism, owing to the accumulation of toxic metabolites, free radical production and increased LPO products. In our model of maternal hyperphenylalaninemia, pregnant rats were injected with 300 mg/kg BW l-phenylalanine (PHE) and 50 mg/kg BW p-chlorophenylalanine (PCPA) dissolved in saline. In this research study, we measured LPO-by-products, i.e., malonaldehyde (MDA) and 4-hydroxynonenal (4-HNE) and we demonstrated that maternal hyperphenylalaninemia increased both markers of oxidative stress in the brain and liver mitochondria of the pups. We also demonstrated that administration of melatonin, Vitamin E, and Vitamin C, in this order of potency, prevented the oxidative damage to the mitochondria, especially in the brain. We therefore conclude that maternal hyperphenylalaninemia induces a clear state of oxidative stress that is somehow directly involved in brain and liver impairment, which can be prevented by melatonin, Vitamin E, and Vitamin C.

Aldehydes↗
PubMed1998

Co-purification of microsomal epoxide hydrolase with the warfarin-sensitive vitamin K1 oxide reductase of the vitamin K cycle.

Vitamin K1 oxide reductase activity has been partially purified from rat liver microsomes. A three-step procedure produced a preparation in which warfarin-sensitive vitamin K1 oxide reductase activity was 118-fold enriched over the activity in intact rat liver microsomes. A major component of the multi-protein mixture was identified as a 50 kDa protein that strongly cross-reacts with antiserum prepared against homogeneous rat liver microsomal epoxide hydrolase. The reductase preparation also had a high level or epoxide hydrolase activity against two xenobiotic epoxide substrates. The K(m) values for hydrolysis by the reductase preparation were similar to those for homogeneous microsomal epoxide hydrolase itself, and the specific hydrolase activities of the reductase preparation were 25-35% of the specific activities measured for the homogeneous hydrolase preparation. Antibodies prepared against homogeneous microsomal epoxide hydrolase inhibited up to 80% of reductase activity of the reductase preparation. Homogeneous microsomal epoxide hydrolase had no vitamin K1 oxide reductase activity. This evidence suggests that microsomal epoxide hydrolase, or a protein that is very similar to it, is a major functional component of a multi-protein complex that is responsible for vitamin K1 oxide reduction in rat liver microsomes.

Animals↗