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At least 55 records · Page 3Linked to original sources
PubMed1981

Isolation and identification of 25-hydroxyvitamin D2 25-glucuronide: a biliary metabolite of vitamin D2 in the chick.

The biliary metabolites of vitamin D2 obtained from chickens dosed with 3H-labeled vitamin D2 were investigated. Most of the biliary radioactivity migrated as charged compounds on diethylaminoethyl-Sephadex chromatography, and the charged fraction could be resolved into several components by reversed-phase high pressure liquid chromatography. A major charged metabolite was further purified by reversed-phase high-pressure liquid chromatography. This compound was found to be beta-glucuronidase sensitive and to yield 25-hydroxyvitamin D2 upon mild acid hydrolysis. The metabolite was converted first to the methyl ester and then to silylated and acetylated derivatives, which were subjected to mass spectrometry. The structure of the original metabolite was established as 25-hydroxyvitamin D2 25-beta-D-glucuronic acid. This 25-hydroxyvitamin D2 25-beta-glucuronide is a major biliary metabolite of vitamin D2 in the chick and may play a role in the chick's discrimination against vitamin D2.

25-Hydroxyvitamin D 2↗
PubMed1983

Nonaqueous reverse phase liquid chromatographic determination of vitamin D2 in multivitamin tablets, using vitamin D3 as internal standard.

The technique of nonaqueous reverse phase chromatography has been successfully applied to the separation of lipophilic vitamins D2 and D3. Separation is achieved with a Zorbax-ODS column and a mobile phase of 10% methanol in acetonitrile. A predetermined amount of vitamin D3 internal standard is added to a portion of a powered tablet sample, which is then extracted and partitioned with a mixture of dimethyl sulfoxide, water, methanol, and hexane. A portion of the hexane extract is concentrated, and purified by passing it through a disposable silica cartridge to remove interfering materials. The method should also be applicable to formulations containing vitamin D3 where vitamin D2 can then be used as the internal standard. A system suitability test is included in the method.

Cholecalciferol↗
PubMed1992

Elevation of blood vitamin D2 levels does not impede the release of vitamin D3 from the skin.

The mechanism for the transfer of fat-soluble vitamin D3 from the avascular basal cellular layers of the epidermis to dermal capillaries and peripheral circulation is unknown, although vitamin D-binding protein (DBP) is thought to mediate this process. To evaluate the effect of increased occupancy of vitamin D carrier(s) on vitamin D3 removal from the skin, serial serum vitamin D2 and D3 concentrations were determined in three groups of six healthy volunteers given combinations of an oral dose of vitamin D2 (50,000 IU) and a fixed dose of UVB radiation (27 mJ/cm2). Serum vitamin D3 levels increased significantly following UVB (time effect, P < .01 by ANOVA), but the response remained unchanged after pretreatment with vitamin D2, increasing from 3 +/- 1 to 14 +/- 5 ng/mL (mean +/- SEM), versus UVB alone, 5 +/- 1 to 16 +/- 5 ng/mL. Elevation of serum vitamin D2 levels was also similar in the groups given vitamin D2 alone (< 1 to 64 +/- 8 ng/mL) and vitamin D2 + UVB (< 1 to 45 +/- 8 ng/mL). There was no time or treatment effect for changes in serum levels of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, or (DBP) levels (P > .1). We conclude that vitamin D3 egress from the skin is not affected by elevated circulating vitamin D concentrations; thus, the cutaneous release of vitamin D is probably mediated by a protein such as DBP with a high carrying capacity for the vitamin.

Administration, Oral↗
PubMed1983

Acute vitamin D3 toxicosis in horses: case reports and experimental studies of the comparative toxicity of vitamins D2 and D3.

Acute vitamin D toxicosis was diagnosed in 2 horses fed a grain ration containing 1,102,311 IU of cholecalciferol (vitamin D3)/kg (500,000 IU/lb) for about 30 days. Horse 1 died acutely with extensive mineralization of cardiovascular and other soft tissues. Horse 2, which had severe clinical signs and clinicopathologic changes of toxicosis, was treated with nonsteroidal antiinflammatory drugs and recovered in about 6 months. In an experimental study, the toxicity of ergocalciferol (vitamin D2) and cholecalciferol was compared in 2 horses (No. 3 and 4) given the respective vitamins at a daily dosage of 33,000 IU/kg of initial (day 0) body weight for 30 days. Except for slight loss in body weight (8%) during the 1st few days of treatment, horse 3 remained clinically normal. Horse 4 developed limb stiffness and tachycardia, became anorectic, weak, and recumbent, lost 29% of body weight, and had polydipsia and polyuria. Horses 2, 3, and 4 developed persistent hyperphosphatemia. Horse 2 remained normocalcemic whereas horses 3 and 4 became hypercalcemic by day 28. In horse 3, serum vitamin D2 metabolite concentrations on days 0, 1, 14, and 26 were: vitamin D2 (ng/ml) = less than 5.0, 5.7, 71.4, and 188.0; 25-hydroxy-vitamin D2 (ng/ml) = less than 5.0, less than 5.0, 43.1, and 117.5; and 1,25-dihydroxy-vitamin D (pg/ml) = 19.7, 23.2, 25.0, and 45.7, respectively. In horse 4, serum vitamin D3 metabolite concentrations on the same days were: vitamin D3 (ng/ml) = less than 5.0, 110.0, 1,049.0, and 887.0; 25-hydroxy-vitamin D3 (ng/ml) = less than 5.0, 18.9, 201.0 and 182.0; and 1,25-dihydroxy-vitamin D (pg/ml) = 21.5, 18.9, 25.2, and 21.6, respectively. Urine of horses 2 and 4 became acidic (pH 6). Horses 2, 3, and 4 became hyposthenuric, but the decrease in urine specific gravity (sp gr) in horse 3 occurred only after 3 weeks of treatment and was only moderate (sp gr, 1.018 to 1.021) and nonprogressive. Hyposthenuria was evident in horse 4 on day 4 (sp gr, 1.028), and was progressive and marked (sp gr, days 28 to 32: 1.006 to 1.009). Urine sp gr of horse 2 ranged from 1.002 to 1.007. Fractures were demonstrated radiographically and histologically in the costochondral junctions of horses 3 and 4. Mineralization of cardiovascular and other soft tissues developed in horses 3 and 4, with lesions being more severe and having a wider tissue distribution in horse 4.

Acute Disease↗
PubMed1980

Determination of potential content of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) in gelatin-coated beadlets, oil-based mixtures, and multivitamin tablet and capsule formulations.

A high-performance liquid chromatographic procedure was used to determine routinely the potential vitamin D content in raw materials and multivitamin formulations. The method employs a microparticulate silica column to separate vitamin D from its degradation products as well as other fat-soluble vitamins. Sample preparation is simple, and the chromatographic time is less than 20 min when progesterone is added to the injection mixture as an internal standard. Replicate analyses of complex multivitamin formulations demonstrate precision with a relative standard deviation of less than 4%. Spiked placebos typically show 98--100% recovery and a linear chromatographic response. The use of bulk drug as a working reference standard is recommended for the determination of the potential vitamin D concentration in pharmaceutical multivitamin preparations.

Capsules↗
PubMed1980

Stability of solid drugs: degradation of ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) at high humidities and elevated temperatures.

Ergocalciferol and cholecalciferol powders were studied at 25 and 40 degrees and at different humidities. Ergocalciferol decomposed rapidly at 25 and 40 degrees when stored in dry air. Decomposition of ergocalciferol led to the formation of products of higher polarity. Cholecalciferol was not as labile under dry conditions, but decomposed rapidly at high temperature.

Cholecalciferol↗
PubMed1978

High-performance liquid chromatography determination of potential content of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) in resins, oils, dry concentrates and multivitamin formulations.

The determination of potential vitamin D concentrations in raw materials and in multivitamin formulations by high-performance liquid chromatography is reported. Simple experimental conditions allow the rapid separation of the vitamins from their respective pro- and pre-vitamins, from their irradiation side-products and from some of their overirradiation products. Vitamin extraction is performed directly from dry concentrates, tablets and capsules, without saponification; all procedures are carried out at room temperature so as to preserve the ratio of vitamin D and pre-vitamin D present in the prepatation. The relative standard deviation is less than 1.5%.

Cholecalciferol↗
PubMed1980

Vitamin D metabolites in serum from hypoparathyroid patients treated with vitamin D2 and 1 alpha-hydroxyvitamin D3.

Vitamin D and its metabolites 25-hydroxyvitamin D (25OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], 25,26-(OH)2D, and 1,25-(OH)2D were measured after separation on high pressure liquid chromatography in sera from two hypoparathyroid patients treated with high doses of vitamin D2. Fractions with displacement activities in the competitive protein-binding assays were found which were not detectable in sera from controls not supplemented with vitamin D2. These fractions, presumably representing vitamin D2 metabolites, were quantitated separately from the vitamin D3 metabolites. After a change of treatment from milligram doses of vitamin D2 to microgram doses of 1 alpha OHD3, the serum metabolites of vitamin D2 and vitamin D3 were followed from 8-13 months. During the first 2-3 months, there was an initial relatively rapid fall in serum vitamin D2 levels and metabolites, followed by a slower decline. High levels of vitamin D2 metabolites were still present after 13 months. Taking into account the marked preponderance of 25OHD2 to 25OHD3, the relative concentration of (OH)2D3 metabolites were higher than expected, which might indicate a preferential 25OHD3 hydroxylation or alternatively, a more rapid degradation of vitamin D2 metabolites in these patients. The high and sustained release of vitamin D2, presumably from fat stores, more than a year after vitamin D2 ingestion was stopped has obvious clinical implications and should be considered in the long term follow-up of patients shifted from the traditional high doses of vitamin D to the newly synthesized 1 alpha OHD3 or 1,25(OH)2D3.

Adult↗
PubMed1983

Vitamin D nutritional status of premature infants supplemented with 500 IU vitamin D2 per day.

The vitamin D nutritional status of premature infants was assessed by determining plasma 25-hydroxyvitamin D concentrations before and during supplementation with 500 IU vitamin D2 per day. Fifty-one samples were collected from 25 healthy infants fed breast milk and a vitamin D3 fortified formula. Gestational age was 32.2 +/- 2.4 weeks (mean +/- 1 SD). 25-hydroxyvitamin D levels before supplementation correlated well with maternal values (r = 0.81). The infants' mean plasma concentration increased from 30.6 +/- 13.7 nmol/l (mean +/- 1 SD) after birth to 46.3 +/- 10.5 nmol/l after 9 +/- 1 days (p less than 0.0025), and to 65.3 +/- 16.6 nmol/l after 37 +/- 10 days of vitamin D2 treatment (p less than 0.0005). 25-hydroxyvitamin D2 and 25-hydroxyvitamin D3 were determined separately, and it appeared that the rise was accounted for by the D2 fraction while 25-hydroxyvitamin D3 concentrations were unchanged. The results demonstrate that vitamin D2 is well absorbed and hydroxylated in the 25 position by premature infants free of associated disease, and that a supplementation of 500 IU per day in addition to breast milk and a regular vitamin D fortified formula is adequate to rapidly establish 25-hydroxyvitamin D levels within the normal adult range.

25-Hydroxyvitamin D 2↗
PubMed2004

Effect of vitamin D2- and D3-enriched diets on egg vitamin D content, production, and bird condition during an entire production period.

Vitamin D insufficiency during winter is a common problem for humans in Europe. One way to ease this problem is through the production of vitamin D-fortified eggs. To evaluate such a production process, the effects of vitamin D supplementation during an entire production period were assessed. Transfer of vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol) from the diet to egg yolks was measured using 2 different levels of both vitamins (6,000 and 15,000 IU/kg feed) relative to a control treatment (2,500 IU vitamin D3/kg feed). During the experiment, production parameters, egg quality (egg weight, Haugh unit, specific gravity, eggshell fracture force, and Ca content of eggshell), and the condition of hens were monitored. At the end of the experiment histopathological tests were performed. Supplementing diets with vitamin D3 increased egg yolk vitamin D content more effectively than did supplementation with vitamin D2. For groups of hens receiving 6,000 or 15,000 IU of vitamin D3/kg feed, egg yolk vitamin D3 content ranged from 9.1 to 13.6 and from 25.3 to 33.7 microg/100 g, respectively. Corresponding values for birds fed vitamin D2 were 4.7 to 7.0 and 13.3 to 21.0 microg/100 g. Both supplements enhanced vitamin D3 content of egg yolks relative to the control diet (2.5 to 5.0 microg/100 g of egg yolk). Vitamin D supplements had no effects on production parameters compared with the control diet. However, especially vitamin D3 improved bone strength (P < 0.05). Autopsy at the end of the experiment indicated no detrimental accumulation of calcium in the kidneys, liver, heart, muscles, or lungs.

Animals↗
PubMed1986

25-Hydroxylase activity in subcellular fractions from human liver. Evidence for different rates of mitochondrial hydroxylation of vitamin D2 and D3.

25-Hydroxylation of vitamin D2 and D3 was studied in subcellular fractions from human liver, using a technique based on isotope dilution-mass spectrometry. The mitochondrial fraction fortified with isocitrate catalysed 25-hydroxylation of vitamin D3 at a rate of about 10 pmol/mg protein X min. Under the same conditions, the rate of 25-hydroxylation of vitamin D2 was less than 2 pmol/mg protein X min. Crude microsomes fortified with NADPH catalysed 25-hydroxylation of vitamin D3 to a very low extent, and this activity was not linear with the amount of microsomal protein. A higher rate of conversion was obtained with a partially purified cytochrome P-450 fraction in the presence of NADPH-cytochrome P-450 reductase and NADPH. This fraction also catalysed 25-hydroxylation of 1 alpha-hydroxyvitamin D3 and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha-triol. 25-Hydroxylation of vitamin D2 could not be detected, neither with crude microsomes, nor with the microsomal cytochrome P-450 fraction. Since the assay for 25-hydroxyvitamin D2 was less sensitive than that for 25-hydroxyvitamin D3, these experiments do not rule out the presence of some 25-hydroxylase activity towards vitamin D2 in the microsomes. The results are discussed in relation to previous work in which a lower toxicity has been reported for vitamin D2 than for vitamin D3 in some mammalian species.

Cholecalciferol↗