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At least 109 records · Page 6Linked to original sources
PubMed1984

Relationship of dithiothreitol-dependent microsomal vitamin K quinone and vitamin K epoxide reductases inhibition of epoxide reduction by vitamin K quinone.

Vitamin K quinone was shown to be an effective inhibitor of vitamin K epoxide reduction by whole rat liver microsomes. Observation of inhibition was dependent upon the mode of addition of the substrate and inhibitor suggesting segregation of the compounds into different microsomal vesicles under certain conditions. The result is consistent with reduction of both vitamin K quinone and vitamin K epoxide by a single enzyme or a multisite enzyme complex.

Animals↗
PubMed2003

Microscopic aspects of autoschizic cell death in human ovarian carcinoma (2774) cells following vitamin C, vitamin K3 or vitamin C:K3 treatment.

Human ovarian carcinoma cells (MDAH 2774) were treated with sodium ascorbate (VC), menadione (VK3), or with a VC:VK3 combination for 1 h and then studied using light microscopy (LM) and scanning (SEM) and transmission electron (TEM) microscopy. Plasma membrane damage (blisters and blebs, hairy aspect) results from vitamin C (VC) treatment, while cytoskeletal damage and self-morsellation are caused by vitamin K3 (VK3) treatment. VC:VK3-treated cells exhibit exacerbated injuries characteristic of both VC and VK3 treatment as well as a significant decrease in cell diameters from 20-35 microm for control cells to 7-12 microm for VC:VK3 treatment. Moreover, after a 1-h exposure to the vitamin combination, autoschizis (43%), apoptosis (3%), and oncosis (1.9%) are observed at the percentages indicated. All cellular changes associated with autoschizis observed with SEM were confirmed by LM and TEM observations and are consistent with cell death by autoschizis: decrease in cell size, cytoplasmic self-excisions, degradation of the nucleus and nucleolus without formation of apoptotic bodies and, ultimately, karyorrhexis and karyolysis. These results also suggest that the vitamin combination may find clinical use in the treatment of ovarian cancer.

Ascorbic Acid↗
PubMed1996

Experimental studies on bovine Hyena disease induced by administration of excessive vitamin AD3E premix, vitamin A, or vitamin D3.

The effects of the excessive administration of the vitamin AD3E(V-AD3E) premix, vitamin A (V-A) or vitamin D3 (V-D3) on experimental development of Hyena disease in the calves were examined. Hyena disease was recognized in 4 calves, both of the 2 calves administered a high dose of V-AD3E premix (V-A 3,000,000, V-D3 300,000, and V-E 1,200 IU/day, V-AD3E group), 1 of the 2 calves administered a half dose of the V-AD3E premix, and 1 of the 2 calves administered only V-A (V-A 3,000,000 IU/day, V-A group) when each vitamin was administered orally for 10 days from 1 week after birth. Both of 2 calves administered only V-D3 (V-D3 300,000 IU/day) did not developed. In the 4 calves with Hyena disease (Hyena calves), the plasma retinylpalmitate showed high values which was suggesting the hypervitaminosis A, and the epiphysial growth plate was narrow and destroyed structure of column. Compared with the Hyena calf in the V-A group, the Hyena calves in the V-AD3E group showed earlier appearance time of Hyena disease, lower growth rate and shorter lengths of fore and hind limb bones. In conclusion, the present findings suggested that excessive V-A administration to suckling calves might cause Hyena disease by V-A effects to the epiphysial growth plate, moreover such effects may be promoted by the V-D3.

Aging↗
PubMed2000

[Antioxidant vitamins - importance for cardiopulmonary prophylaxis. Part II. Antioxidant food supplies - vitamin C and beta-carotene; current experience in antioxidant vitamin usage].

The faith that an oxidizing of LDL is necessary for he foam cell formation is basically for the so called oxidative hypothesis of atherosclerosis. The role of LDL-oxidation for the atherosclerotic plaque formation, as well as its association with inflammatory processes in the vascular wall, are well established. The important conclusion of this hypothesis is the possible role of the antioxidants attenuating atherosclerotic mechanisms. The advances in studying the principal antioxidant vitamins E, C and beta-carotene effects, revealed a great part of their molecular mechanisms, which are not necessarily antioxidative. The important aspects of the cooperative antioxidant action are revealed too, including the so called tocopherol-mediated peroxidation, suggesting the need for the co-antioxidants for effective antioxidant defense. In the recent years many vitamin antioxidant supplementations are used. The epidemiological results of such supplementation do not always reveal the same beneficial effects as expected theoretically or based on the observations made with a diet rich in fruits and vegetables. The present paper generalizes the thought concerning the impact of oxidized LDL in atherosclerosis, as well as mechanisms of action and pharmacokinetiks of the most widely used antioxidant vitamins--E, C and beta-carotene, and the perspectives of their usage in cardiovascular prophylaxy bazed upon the recent experience in antioxidant vitamin supplementation.

Antioxidants↗
PubMed1984

Vitamin D, 25-hydroxy-vitamin D and 1,25-dihydroxy-vitamin D in cow's milk, infant formulas and breast milk during different stages of lactation.

Vitamin D and its metabolites were determined in cow's milk, infant formulas, and colostrum, transitional and mature breast milk by specific protein-binding assays following HPLC (high-pressure liquid chromatography). Cow's milk contains (mean +/- SEM) 50.4 +/- 4.1 pg/ml vitamin D (n = 10), 499 +/- 47 pg/ml 25-OH D (n = 10) and 9.7 +/- 1.0 pg/ml 1,25 (OH)2D (n = 3). 86.6% of the added vitamin D3 was recovered from infant formulas. The mean content (mean +/- SEM) of 25-OH D and 1,25(OH)2D of infant formulas are 299 +/- 35 pg/ml and 5.4 +/- 0.9 pg/ml (n = 9), respectively. Vitamin D concentration of colostrum and mature breast milk is 122 +/- 3.4 pg/ml (n = 7, mean +/- SEM) and 38 +/- 3.3 pg/ml (n = 9) respectively; the 25-OH D content increases from 294 +/- 50.6 pg/ml (n = 10) to 845 +/- 190 pg/ml (n = 14) during lactation. The increase of 1,25-(OH)2D from early to mature breast milk (3.2 +/- 0.6 pg/ml, n = 8 versus 5.3 +/- 0.7 pg/ml, n = 20) is still statistically significant.

Animals↗
PubMed1980

Metabolites of vitamin D in human vitamin-D deficiency: effect of vitamin D3 or 1,25-dihydroxycholecalciferol.

Circulating concentrations of hydroxylated metabolites of vitamin D were measured in seven Asian patients with histologically proven osteomalacia before and during treatment with either cholecalciferol (vitamin D3) or 1,25-dihydroxycholecalciferol. All patients showed an excellent clinical and biochemical response to treatment irrespective of type of vitamin D administered. Circulating concentrations of 25-hydroxycholecalciferol and 24,25, 25,26, and 1,25 dihydroxycholecalciferols were abnormally low in the untreated patients. In five patients treated with small doses of cholecalciferol (3000 units, 75 micrograms daily) the concentration of 1,25-dihydroxycholecalciferol rose rapidly to normal and reached supra-normal levels within 72 h. Raised concentrations (up to 200 pg/ml) were sustained for several months and then started falling to normal. Serum 24,25 and 25,26 dihydroxycholecalciferols rose only gradually, after circulating 25-hydroxycholecalciferol concentration had increased to normal. In contrast, in the two patients who received 1,25-dihydroxycholecalciferol (1 microgram daily) serum concentrations of this metabolite rose to normal and only occasionally exceeded the upper limit of normal. The highest concentration observed was 80 pg/ml. Healing of osteomalacia occurred, however, in these two patients in the absence of any measurable increases in 25-hydroxycholecalciferol and 24,25 or 25,26 dihydroxycholecalciferols which all remained abnormally low. Thus, it seems that 1,25-dihydroxycholecalciferol is the most important factor for the healing of vitamin D-deficient osteomalacia and that other hydroxy metabolites are unimportant.

Adolescent↗
PubMed1977

Analysis of fat-soluble vitamins. XVI. Antirachitic activity of 5,6-trans-vitamin D3 alone and in the presence of 5,6-cis-vitamin D3 resin, using chick bioassays.

Two biological assays were conducted in which the antirachitic activity in chicks of 5,6-trans-vitamin D3 added to feed is compared with that of 5,6-cis-vitamin D3. On the basis of the results obtained it is concluded that the relative potency of the trans isomer is, at the most, 5% and that the antirachitic activity of the trans isomer is not markedly enhanced (an increase to a relative potency of 16%, at the most) if the cis isomer is also included in the diet. The results are not conclusive on the inhibition or lack of inhibition of the antirachitic activity of 5,6-cis-vitamin D3 by the presence of 5,6-trans-vitamin D3 in the feed.

Animal Feed↗
PubMed1983

Isolation and identification of 1,25-dihydroxy-24-oxo-vitamin D3 and 1,23,25-trihydroxy-24-oxo-vitamin D3. New metabolites of vitamin D3 produced by a C-24 oxidation pathway of metabolism for 1,25-dihydroxyvitamin D3 present in intestine and kidney.

Two new vitamin D metabolites were isolated in pure form from separate incubations of homogenates of chick small intestinal mucosa or rat kidney employing either 1 alpha,25-dihydroxyvitamin D3 (28 microM) or 1 alpha,24R,25-trihydroxyvitamin D3 as substrate (0.17-1.3 microM). The newly characterized compounds and the amounts isolated in pure form from separate isolations are, respectively: 1 alpha,25-dihydroxy-24-oxo-vitamin D3 (1,25(OH)2-24-oxo-D3), 147 micrograms from kidney and 4.2 and 40 micrograms from intestine; 1 alpha,23,25-trihydroxy-24-oxo-vitamin D3 (1,23,25(OH)3-24-oxo-D3), 155 micrograms from kidney and 5.9 and 34 micrograms from intestine. Their structures were identified after extensive high pressure liquid chromatography by means of ultraviolet absorption spectrometry, mass spectrometry of the free compounds and their trimethylsilylated derivatives, proton nuclear magnetic resonance spectrometry, specific chemical reduction of the 24-oxo functionality with sodium borohydride, as well as direct comparison with synthetic 1,25(OH)2-24-oxo-D3. These structural assignments for both compounds correct previous determinations which had been proposed (Ohnuma, N., Kruse, J. R., Popjak, G., and Norman, A. W. (1982) J. Biol. Chem. 257, 5097-5102). The activity of the C-24 oxidation pathway used for the production of the 1,25(OH)2-24-oxo-D3 and 1,23,25(OH)3-24-oxo-D3 can be enhanced 10-fold by prior priming of the chicks or rats with a single intravenous dose of 1,25(OH)2D3 (1-12 nmol/100 g body weight); the induction of the enzyme activity is maximal by 3-6 h and returns to basal levels within 12 h. Further, 1,25(OH)2D3, 1,24,25(OH)3D3, and 1,25(OH)2-24-oxo-D3 all were found to be capable of serving as a precursor with chick intestine and rat kidney homogenates of 1,23,25(OH)3-24-oxo-D3. Collectively these results suggest the existence of a C-24 oxidation pathway for metabolism of 1,25(OH)2D3 by the target intestinal mucosa and kidney to 1,23,25(OH)3-24-oxo-D3. The pathway may play an important role in controlling the tissue levels of this hormonally active form of vitamin D3.

Animals↗
PubMed1982

Isolation and chemical characterization of two new vitamin D metabolites produced by the intestine. 1,25-Dihydroxy-23-oxo-vitamin D3 and 1,25,26-trihydroxy-23-oxo-vitamin D3.

Two new vitamin D metabolites were isolated in pure form from incubations of 53 nM 1,25-dihydroxyvitamin D3 with homogenates of small intestinal mucosa of vitamin D-replete chicks. The birds were injected intravenously with 8 to 9 nmol of 1,25-dihydroxyvitamin D3/100 g body weight 5 to 8 h before death. The isolation involved methanol-chloroform extraction and four successive chromatographic procedures (Sephadex LH-20 and high performance liquid chromatography). Chemical structures of the metabolites are proposed on the basis of (a) their chromatographic behavior, (b) their mass spectra, and (c) ultraviolet absorption spectra. They are identified as 1 alpha,25-dihydroxy-23-oxo-vitamin D3 and 1 alpha,25,26-trihydroxy-23-oxo-vitamin D3. Neither of the two new metabolites is produced by the intestinal mucosa when 1,25S,26-trihydroxyvitamin D3 is used as a substrate.

Animals↗
PubMed1978

[Methods for the determination of vitamins by means of HPLC. IV. Determination of vitamin K3 in vitamin premixes and mineral supplements (author's transl)].

A method is described for rapid determination of vitamin K3 (menadione) in vitamin premixes and mineral supplements. The menadione is extracted in the form of the bisulphite compound. After conversion into menadione the vitamin is taken up in n-hexane and is determined by HPLC without further clean-up.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Injection of vitamin A acid, vitamin E, and vitamin C for treatment of tissue necrosis.

Experimental studies concerning All-Trans Retinoic acid 0.1% with the antioxidant action of the Vitamin E (tocopherol acetate 0.20%) and Vitamin C (coated ascorbic acid 0.20%) efficacy in both the vascular neoformation induction and cellular membrane stabilization have been conducted by us to improve skin necrosis regression after routine plastic surgeries. Patients after rhytidectomy, breast reduction, and abdominoplasty with localized skin flap necrosis, were submitted to daily intradermic injections for a period of 15 days and had their skin healed by the effects of these vitamins.

Adolescent↗
PubMed2004

Vitamins in human arteriosclerosis with emphasis on vitamin C and vitamin E.

INTRODUCTION: This review focuses on the process of arteriosclerosis arising from oxidative stress on lipoproteins and the general failure of randomized human trials using vitamins to retard this process. REVIEW: As well as clinical trials, the paper reviews the mechanisms by which a variety of oxidants act. Antioxidants are discussed, emphasizing interactions of vitamins C and E with transition metals that can lead to prooxidation. There is a focus on interactions between supplemental or co-antioxidants that counterbalance prooxidant effects of one another. CONCLUSIONS: It is concluded that normal cellular supplementation mechanisms are poorly accessible in the arteriosclerotic plaque leading to a prooxidant environment in which the haphazard introduction of vitamins could potentially be hazardous. Continued investigations into basic and clinical redox interactions of the kind discussed in this review using new measuring techniques may lead to approaches whereby antioxidants can be introduced into tissue in controlled ways for reducing arteriosclerosis.

Animals↗
PubMed1983

High-performance liquid chromatography of fat-soluble vitamins. Simultaneous quantitative analysis of vitamins D2, D3 and E. Study of percentage recoveries of vitamins from cod liver oil.

Vitamins D2, D3 and E were resolved and quantified by applying reversed-phase high-performance liquid chromatography to extracts of cod liver oil. The method, using two reversed-phase C18 columns and a ternary mixture of acetonitrile, methanol and water as the eluent resolved all fat-soluble vitamins well, including the pair D2-D3. The extraction procedure was studied; the recoveries, using two different solvents (hexane and diethyl ether) for extractions were 60.6 +/- 1.0 and 77.1 +/- 1.1, 56.9 +/- 1.2 and 74.8 +/- 0.8, and 14.1 +/- 0.7 and 89.8 +/- 1.4% for vitamins D2, D3 and E, respectively.

Cholecalciferol↗
PubMed1995

Healing of rickets during vitamin D therapy despite defective vitamin D receptors in two siblings with vitamin D-dependent rickets type II.

We report the healing of severe rickets despite hypocalcemia in two siblings with absent vitamin D receptors; long periods of treatment with excessive doses of vitamin D led to relative hypoparathyroidism and a return to normal of calcium metabolism during calcitriol treatment. This finding suggests that some other regulating factor may substitute for the defective vitamin D receptor.

Dose-Response Relationship, Drug↗
PubMed1999

Vitamin D analogs, 20-Epi-22-oxa-24a,26a,27a,-trihomo-1alpha,25(OH)2-vitamin D3, 1,24(OH)2-22-ene-24-cyclopropyl-vitamin D3 and 1alpha,25(OH)2-lumisterol3 prime NB4 leukemia cells for monocytic differentiation via nongenomic signaling pathways, involving calcium and calpain.

Side-chain modified vitamin D analogs including 20-Epi-22-oxa-24a,26a,27a-trihomo-1alpha,2 5-dihydroxyvitamin D3 (KH1060), and 1,24-dihydroxy-22-ene-24-cyclopropyl-vitamin D3 (MC903) were originally designed to aid in the treatment of hyperproliferative disorders including psoriasis and cancer. Here we demonstrate that these analogs, as well as the 6-cis-locked conformer, 1alpha,25-dihydroxy-lumisterol3 (JN) prime NB4 cells for monocytic differentiation. Previously, the action of MC903 and KH1060 was presumed to be mediated by the nuclear vitamin D receptor (VDRnuc). Differentiation in response to all analogs was shown to be inhibited by 1beta,25-dihydroxyvitamin D3 (HL), the antagonist to the nongenomic activities of 1,25D3. These data suggest that although MC903 and KH1060 may bind the VDRnuc, that the differentiative activities of these agents requires nongenomic signaling pathways. Here we show that 1alpha,25(OH)2-d5-previtamin D3 (HF), JN, KH1060, and MC903 induce expression of PKC alpha and PKC delta and translocation of both isoforms to the particulate fraction, and PKC alpha to the nuclear fraction. The full differentiation response with combinations of analogs and TPA was inhibited 50% by the membrane permeable Ca2+ chelator, 1,2-bis(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM) or calpain inhibitor I. These data demonstrate that intracellular free calcium and the calcium-dependent protease, calpain play critical roles in monocytic differentiation. Intracellular calcium appears to be most critical in the 1,25D3-priming stage of differentiation, while calpain is essential in the TPA maturation response.

Biological Transport↗