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PubMed2002

Cats discriminate between cholecalciferol and ergocalciferol.

A comparison was made of the ability of ergocalciferol and cholecalciferol to elevate plasma concentrations of vitamin D and 25-hydroxyvitamin D in cats. Cholecalciferol, given as an oral bolus in oil, resulted in a rapid elevation of plasma concentration of cholecalciferol followed by a rapid decline. In contrast, 25-hydroxyvitamin D concentration in plasma increased until day 3 after administration and remained elevated for a further 5 days. When 337 microg of both cholecalciferol and ergocalciferol in oil were given as an oral bolus to 10 cats, the peak plasma concentrations of cholecalciferol and ergocalciferol occurred at 8 or 12 h after administration. Peak concentrations of cholecalciferol were over twice those of ergocalciferol (570 +/- 80 vs. 264 +/- 42 nmol/l). The area under the curve 0-169 h for cholecalciferol was also more than twice that for ergocalciferol. When ergocalciferol and cholecalciferol were administered in a parenteral oil-based emulsion, higher concentrations of 25-hydroxyvitamin D3 than 25-hydroxyvitamin D2 were maintained in plasma. When both vitamins were included in the diet in the nutritional range, plasma concentrations of 25-hydroxyvitamin D2 were 0.68 of those of 25-hydroxyvitamin D3. Discrimination against ergocalciferol by cats appears to result from differences in affinity of the binding protein for the metabolites of the two forms of vitamin D. These results indicate that cats discriminate against ergocalciferol, and use it with an efficiency of 0.7 of that of cholecalciferol to maintain plasma 25-hydroxyvitamin D concentration.

Administration, Oral↗

PubMed1987

Growth retardation induced in rat fetuses by maternal fasting and massive doses of ergocalciferol.

The present study was conducted in Wistar rat fetuses to investigate the growth retardation induced by maternal fasting and/or massive doses of ergocalciferol during the third trimester of pregnancy. Growth indices examined in 21-d fetuses were body weight and ossification of sacrococcygeal vertebrae, supraoccipital bone, sternebrae and proximal phalanges in the forepaw stained by alizarin red S. Growth retardation was expressed in hours by comparison with the normal standard development, or in sigma by calculating the relative difference from the control, utilizing the standard variance in normal fetuses. Degrees of growth retardation expressed in the common scales were different among the indices and between fasting and massive doses of ergocalciferol; body weight and ossification of sacrococcygeal vertebrae were most severely retarded by fasting and least by ergocalciferol. Ossification of sternebrae was moderately retarded by fasting and by ergocalciferol, and ossification of supraoccipital bone was moderately retarded by fasting but not by ergocalciferol. Ossification of proximal phalanges in the forepaw was least retarded by fasting and most severely retarded by ergocalciferol. The observed retardations were progressions relatable to the duration of fasting. Combined treatments of fasting and ergocalciferol showed more deleterious effects on growth than fasting only or ergocalciferol only and induced face anomalies, "carnival fetuses." These findings show that growth retardations induced by different nutritional disturbances may vary among indices and that comparisons of various indices are important in the analysis of teratological experiments.

Animals↗

PubMed1985

Treatment of childhood renal osteodystrophy with calcitriol or ergocalciferol.

Quantitative bone histology, biochemistry and height velocities were studied in 18 children suffering from chronic renal failure. Eight received calcitriol, 7 ergocalciferol and 3, though alloted to a treatment group, failed to comply with therapy. A histochemical stain for aluminum showed heavy deposition at the calcification front in 3 patients; 2, in the calcitriol group had severe osteomalacia which worsened during treatment, and 1 in the ergocalciferol group had osteomalacia which did not improve. One had never undergone hemodialysis. Bone histology improved markedly in the remaining 12 patients, whichever vitamin D preparation was used; it was unchanged in 3 non-compliant children. Plasma calcium levels rose while parathyroid hormone and alkaline phosphatase levels fell following both treatments, and were unchanged in non-compliant children. Hypercalcemia occurred more frequently following calcitriol therapy (11 episodes) than following ergocalciferol therapy (3 episodes). Height velocities, studied in 11 children, increased in 5 (3 on ergocalciferol and 2 on calcitriol) and were unchanged in 6 (1 on ergocalciferol, 5 on calcitriol). Improved bone histology did not correlate with increase in height velocity. As ergocalciferol and calcitriol had similar therapeutic effects and as side-effects were more common with calcitriol, it is concluded that calcitriol provides no advantage over ergocalciferol in the treatment of renal bone disease in children.

Alkaline Phosphatase↗

PubMed2005

Failure of high-dose ergocalciferol to correct vitamin D deficiency in adults with cystic fibrosis.

RATIONALE: Treatment guidelines for vitamin D monitoring and supplementation in cystic fibrosis (CF) have recently been developed and published by a consensus committee, but have not been prospectively tested. OBJECTIVES: To use these guidelines to determine the percentage of adults with CF requiring vitamin D repletion therapy and to evaluate the effectiveness of the currently recommended high-dose oral ergocalciferol repletion protocol. METHODS: Prospective study of clinical outcomes after therapy with the recommended vitamin D repletion algorithm. RESULTS: Of 134 adults with CF, 109 (81.3%) were found to have 25-hydroxyvitamin D (25-OHD) levels below the recommended 30 ng/ml. Sixty-six of these adults completed the recommended course of 400,000 IU of oral ergocalciferol over 2 months, and only five (8%) responded with correction of their serum 25-OHD to the goal of 30 ng/ml or greater (mean change, +0.3 ng/ml; from 18.8 to 19.1 ng/ml). In the 33 adults with CF who also completed the recommended second course of 800,000 IU of ergocalciferol over 2 months, none demonstrated correction of their deficiency (mean change, -1.2 ng/ml). CONCLUSION: The results of this study demonstrate that a majority of adults with CF have serum 25-OHD levels below 30 ng/ml, and the currently recommended ergocalciferol repletion regimen often does not fully correct vitamin D deficiency and may need to be revised to include even higher dosing of ergocalciferol. Further work is needed to establish the ideal 25-OHD level for maximizing calcium absorption and bone health in CF.

Adult↗

PubMed1975

Microdetermination of ergocalciferol (vitamin D2) in pharmaceutical preparations by differential spectroscopy using trifluoroacetic acid in the absence of vitamin A.

A differential spectroscopy method for the determination of microgram quantities of ergocalciferol, using trifluoroacetic acid and hydrogen peroxide, was applied to commercially available pharmaceutical preparations. Tablets were powdered and extracted with methanol after being made basic with diethylamine. The methanol was concentrated, chloroform was added, and the mixture was chromatographed on neutral alumina using chloroform as the eluent. Ergocalciferol was determined in an aliquot of the eluate by differential spectroscopy and was compared with a reference ergocalciferol standard treated similarly. The method applied to low potency formulations (2.5-6 mug/tablet) is simple and quantitative, needs less than 5 hr for completion, and has a precision of less than +/- 2%. A simple and accurate chromatographic method for the determination of ergocalciferol in stabilized powders and high potency tablets, which precludes the necessity of solvent-solvent extraction, was also developed. The results are comparable with those obtained by the rat bioassay and the USP XVIII chemical assay.

Animals↗

PubMed1997

Chicken parathyroid hormone gene expression in response to gastrin, omeprazole, ergocalciferol, and restricted food intake.

Treatment with omeprazole, a long-acting proton pump inhibitor of acid secretion, induces hypergastrinemia. In chickens, omeprazole induces growth not only of the acid-producing mucosa (probably reflecting the trophic action of gastrin), but also of the parathyroid glands (hypertrophy + hyperplasia), while suppressing bone density and body weight gain without affecting blood calcium. The first part of the present study was concerned with the effect of omeprazole, ergocalciferol (vitamin D2), and restricted food intake on the gene expression of parathyroid hormone (PTH) in the parathyroid glands of the chicken. Chickens were treated with omeprazole (400 micromol/kg/day, I.M.), food restriction, omeprazole + food restriction, ergocalciferol (250 000 IU/kg/day, S.C.), or ergocalciferol + omeprazole for 5 weeks. The weight gain of the chickens was monitored, and the weights of the parathyroid glands and femurs were determined at sacrifice. PTH mRNA in the parathyroid glands was analyzed by Northern blot. The second part of the study examined the effect of 3 weeks of continuous gastrin infusion (chicken gastrin 20-36, 5 nmol/kg/hour, S.C.) on the expression of PTH mRNA in the parathyroid glands. Omeprazole reduced the body weight and femur density (ash weight per volume) while greatly increasing the weight of the parathyroid glands and the PTH gene expression. Food restriction alone and ergocalciferol alone (at a dose that raised blood Ca2+) were without effect, but food restriction greatly enhanced the omeprazole-evoked increase in parathyroid gland weight and PTH gene expression. Gastrin increased the weight of the parathyroid glands and reproduced the effect of omeprazole on PTH gene expression. Hence, it seems likely that the effect of omeprazole reflects the ensuing hypergastrinemia.

Animals↗

PubMed1996

Ergocalciferol and cycloheximide in vivo stimulate protein kinase C of intestinal crypt cells.

Previous reports have suggested that 1,25-dihydroxychole-calciferol regulated cellular differentiation via its effects on protein kinase C activity. This study examined the in vivo effects of ergocalciferol on the activity of protein kinase C, and whether the differentiation of crypt intestinal cells is dependent on the activation of this enzyme. Ergocalciferol in saline was injected intramuscularly into rats and the animals sacrificed 24 hr after fasting. Protein kinase C specific activity was determined from the rate of incorporation of 32p-ATP into protamine. Injections of 60 micrograms ergocalciferol/200 g of body wt, raised protein kinase C specific activity to 59818 +/- 4010 (SEM, n = 5) cpm 32p-protamine/min/mg cell protein, compared with a control of 46173 +/- 4612 (P < 0.0005). Optimal specific activities were seen within 72 hr of injection. Administration of 120 micrograms ergocalciferol/200 g of body wt, raised the concentrations of serum calcium to 9.8 and 10.4 mg/dl following the intramuscular injection by 24 and 72 hr, respectively, compared with a control of 7.7 mg/dl. Actinomycin D (intramuscular, 100 micrograms/200 g of body wt) together with ergocalciferol (120 micrograms/200 g of body wt) reduced protein kinase C activity by 51% 24 hr after injection. Cycloheximide blocked the activation, but when injected alone stimulated endogenous protein kinase C activity by 34% 24 hr injection. The study shows activation of crypt protein kinase C by ergocalciferol. The inhibition of activation by actinomycin D and cycloheximide suggests the involvement of both transcriptional and translational processes in this activation.

Animals↗

PubMed1983

The stability of ergocalciferol in rodenticidal baits.

Concentrations of the rodenticide ergocalciferol (vitamin D2) in samples of rodent baits laid in foodstores and in the laboratory were monitored over several months. Bait samples were solvent extracted and ergocalciferol concentration determined by high pressure liquid chromatography (HPLC). Ergocalciferol levels were constant for more than 21 days in dry samples and did not fall by more than 30% in 100 days. When water (10% w/w) was added to the baits in the laboratory the ergocalciferol concentration fell by approximately 30% in 30 days. In these wet laboratory samples there was a rapid visible growth of fungus and in normal rodent control use baits should have been replaced when such deterioration became evident.

Drug Stability↗

PubMed1982

Discrimination in the metabolism of orally dosed ergocalciferol and cholecalciferol by the pig, rat and chick.

Vitamin D-deficient pigs, rats and chicks were repleted with four daily oral doses of crystalline ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) containing equal concentrations of each. At 24 h after the last dose, the plasma of each species was analysed for vitamin D and 25-hydroxyvitamin D by standard methods. The mean (+/- S.D.) ratios of plasma cholecalciferol to ergocalciferol concentration were 1.5 +/- 0.1 (pig). 1.7 +/- 0.1 (rat) and 6.3 +/- 1.2 (chick). The mean ratios of plasma 25-hydroxycholecalciferol to 25-hydroxyergocalciferol concentration were 4.0 +/- 0.1 (pig), 0.4 +/- 0.02 (rat) and 10.7 +/- 3.4 (chick). The mean plasma cholecalciferol/ergocalciferol ratios for the 24,25-dihydroxy-, 25,26-dihydroxy- and 1,25-dihydroxy-derivatives in the pig were 2.6 +/- 0.6, 5.8 +/- 1.3 and 5.8 +/- 0.8 respectively. This is the first evidence that mammals other than the New World monkey, like birds, discriminate between ergocalciferol and cholecalciferol. These data, therefore, suggest that species discrimination between the different forms of vitamin D is probably a general phenomenon in mammals. Moreover, this is the first indication of a species (rat) that discriminates against a cholecalciferol metabolite in favour of an ergocalciferol metabolite. Species discrimination against particular forms of vitamin D may be important to the choice of experimental animal models for studying the regulation of vitamin D metabolism and may also be an important consideration in dietary vitamin supplementation.

25-Hydroxyvitamin D 2↗

PubMed1983

Metabolism of orally administered [3H]ergocalciferol and [3H]cholecalciferol by dairy calves.

Concentrations of ergocalciferol, cholecalciferol, and their metabolites in plasma were determined after a single oral dose of [3H]ergocalciferol or [3H]cholecalciferol was given to 95- to 105-kg Jersey bull calves. One group (three calves) was given 365 muCi of [3H]ergocalciferol (1.2 Ci/mmol) per calf, and the other group (three calves) was given 365 muCi of [3H]cholecalciferol (1.2 Ci/mmol) per calf. Fourteen blood samples were taken from each calf during the 3 weeks after administration. Total plasma radioactivity was highest at 80 hours in both groups (8400 dpm/ml and 4600 dpm/ml in the [3H]cholecalciferol- and [3H]ergocalciferol-treated calves, respectively). For determination of the time-dependent appearance and disappearance of plasma vitamin D and vitamin D metabolites, the plasma 3H-labeled steroids were extracted and separated by high-performance liquid chromatography. In both groups, [3H]vitamin D peaked at 24-48 hours and was the predominant radioactive form in plasma 10-15 hours after dosing. After 15 hours, 25-[3H]hydroxyvitamin D became the predominant labeled metabolite, reaching its maximal concentration between 48 and 96 hours. Concentrations of 25-[3H]hydroxycholecalciferol were about twice those of 25-[3H]hydroxyergocalciferol. The appearance/disappearance profile of 25,26-[3H]dihydroxycholecalciferol and 1,25[3H]hydroxycholecalciferol resembled that of 25-[3H]hydroxycholecalciferol.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed2001

[Ergocalciferol Reference Standard (Control 001) of National Institute of Health Sciences].

The raw material of ergocalciferol was examined for the preparation of "Ergocalciferol Reference Standard (Control 001)". Analytical data obtained were: melting point, 114.8 degrees C; UV and infrared spectra, the same as those of JP Ergocalciferol Reference Standard (Control 971); specific absorbance, E1ca1% = 471(265 nm); optical rotation, [alpha]D20 = +102.4 degrees; thin-layer chromatography, no impurities were detected until 100 micrograms; high-performance liquid chromatography (HPLC), total amount of impurities estimated to be less than 0.1%. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Ergocalciferol Reference Standard (Control 001).

Chemical Phenomena↗

PubMedDate not supplied

The prevention of hip fracture with risedronate and ergocalciferol plus calcium supplementation in elderly women with Alzheimer disease: a randomized controlled trial.

BACKGROUND: A high incidence of fractures, particularly of the hip, represents an important problem in patients with Alzheimer disease (AD), who are prone to falls and have osteoporosis. We previously found that deficiency of 25-hydroxyvitamin D and compensatory hyperparathyroidism cause reduced bone mineral density in female patients with AD. We address the possibility that treatment with risedronate sodium and ergocalciferol plus calcium supplementation may reduce the incidence of nonvertebral fractures in elderly women with AD. METHODS: A total of 500 elderly women with AD were randomly assigned to daily treatment with 2.5 mg of risedronate sodium or a placebo, combined with 1000 IU of ergocalciferol and 1200 mg of elementary calcium, and followed up for 18 months. RESULTS: At baseline, patients of both groups showed 25-hydroxyvitamin D deficiency with compensatory hyperparathyroidism. During the study period, bone mineral density in the risedronate group increased by 4.1% and decreased by 0.9% in the control group. Vertebral fractures occurred in 29 patients (24 hip fractures) in the control group and 8 patients (5 hip fractures) in the risedronate group. The relative risk in the risedronate group compared with the control group was 0.28 (95% confidence interval, 0.13-0.59). CONCLUSIONS: Elderly patients with AD hypovitaminosis D are at increased risk for hip fracture. Treatment with risedronate and ergocalciferol may be safe and effective in reducing the risk of a fracture in elderly patients with AD.

Accidental Falls↗

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↗

PubMed1984

Comparison of equilibrium and disequilibrium assay conditions for ergocalciferol, cholecalciferol and their major metabolites.

The comparison of equilibrium and disequilibrium assay conditions for ergocalciferol, cholecalciferol and their major metabolites were investigated to evaluate: (1) optimization of sensitivity (2) crossreactivity of these compounds in their respective assays and (3) side chain steric requirements of the vitamin D molecule for optimum binding to the calciferol binding protein or bovine thymus receptor. Disequilibrium assay conditions improved assay sensitivity 30-fold for the calciferol assay and approx 3-fold for metabolites in the 25-hydroxycalciferol and 1,25-dihydroxycalciferol assays. Ergocalciferol compounds were uniformly less efficient in their association with the proteins tested than were their cholecalciferol counterparts, with one exception. In the calciferol assay, cholecalciferol had greater affinity for the the calciferol binding protein than did ergocalciferol. In the 25-hydroxycalciferol assay affinity for the calciferol binding protein was 25-hydroxycholecalciferol = 24,25-dihydroxycholecalciferol greater than 25-hydroxyergocalciferol greater than 25S,26-dihydroxycholecalciferol greater than 24,25-dihydroxyergocalciferol greater than 25,26-dihydroxyergocalciferol. In the assay for 1,25-dihydroxycalciferol, bovine thymus receptor recognized 1,25-dihydroxyergocalciferol and 1,25-dihydroxycholecalciferol equally. From the forthcoming data it appears that hydroxyl and/or methyl groups on the calciferol side chain alter the ability of these physiological compounds to associate with the calciferol binding protein.

Binding, Competitive↗

PubMed1995

Cyclical etidronate plus ergocalciferol prevents glucocorticoid-induced bone loss in postmenopausal women.

OBJECTIVE: To assess the benefit of cyclical etidronate plus ergocalciferol for the prevention of glucocorticoid-induced bone loss in a 2-year, prospective, open study based in an osteoporosis clinic. PATIENTS AND METHODS: Group 1 consisted of 15 postmenopausal women (mean age 62.6 +/- 3.3 years) who commenced glucocorticoid therapy and were treated with cyclical etidronate (400 mg/d for the first month; thereafter, 400 mg/d for 2 weeks of every 3-month period), elemental calcium (1 g/d), and ergocalciferol (0.5 mg/wk). Group 2 consisted of 11 postmenopausal women (mean age 60.2 +/- 4.7 years) with glucocorticoid-induced osteoporosis, who were attending the clinic at the same time and were treated with calcium supplements only (1 g/d). MEASUREMENTS: Lumbar spine and femoral neck bone mineral densities (BMD) were measured at baseline and after 12 and 24 months of glucocorticoid therapy using a dual energy x-ray absorptiometer. RESULTS: The two groups did not differ with respect to age, years since the menopause, mean daily glucocorticoid dose, and baseline BMD values. During the first year of therapy, mean lumbar spine BMD increased from an initial value of 0.88 g/cm2 to 0.94 g/cm2, an increase of 7% per year (95% confidence interval [CI] 3.7% to 10.2%; P < 0.001 compared with controls). Significant increases in BMD of 2.5% per year were also observed in the femoral neck (95% CI -1% to 6%; P < 0.01 compared with controls). After the second year of cyclical etidronate therapy, femoral neck BMD continued to increase (P < 0.05 compared with value at 12 months), while lumbar spine BMD remained stable. CONCLUSION: Chronic glucocorticoid therapy may result in bone loss at most skeletal sites. Therapy with cyclical etidronate plus ergocalciferol not only prevented glucocorticoid-induced bone loss, but even increased lumbar spine and femoral neck BMD in postmenopausal women commencing glucocorticoid therapy.

Absorptiometry, Photon↗

PubMed1998

[Ergocalciferol Reference Standard (Control 971) of National Institute of Health Sciences].

The raw material for ergocalciferol was examined for preparation of the "Ergocalciferol Reference Standard (Control 971)". Analytical data obtained were as follows: melting point, 116.7 degrees C; UV and infrared spectra, the same as those for JP Cholecalciferol Reference Standard; specific absorbance, E1 cm 1% = 461(265 nm); optical rotation, [alpha]D20 = +102.5 degrees; thin-layer chromatography and high-performance liquid chromatography (HPLC), no impurity was detected; assay, 102.4% by HPLC. Based on the above results, the raw material was authorized as the Ergocalciferol Reference Standard (Control 971) of National Institute of Health Sciences.

Chemical Phenomena↗

PubMed2003

[Ergocalciferol Reference Standard (Control 031) of National Institute of Health Sciences].

The raw material of ergocalciferol was examined for the preparation of the "Ergocalsiferol Reference Standard (Control 031)", The analytical data obtained were: melting point, 114.5 degrees C; UV spectrum, lambda max of 264.8 nm and specific absorbance in ethanol at 265 nm = 474.7; IR spectrum, same as that of the Ergocalciferol Reference Standard (Control 003); optical rotation, [alpha]20(D) = +104.6 degrees ; thin-layer chromatography, two impurities were detected at 50 micrograms; high-performance liquid chromatography, total amount of impurities estimated to be less than 0.04%. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Ergocalciferol Reference Standard (Control 031) of the National Institute of Health Sciences.

Chemical Phenomena↗

PubMedDate not supplied

[Comparative study of the biological activity and toxic effect of 1alpha-hydroxycholecalciferol and ergocalciferol in rats].

Single administration of 0.25 microgram of sunthetic Ialpha-hydroxycholecalciferol (IalphaOHD3) into nephrectomized rats, maintained at D-avitaminous diet, improved the active transport of calcium ions against the concentration gradient in small intestine of these animals, whereas ergocalciferol was biologically inactive under the same conditions. Administration of IalphaOHD3 during 5 days at a dose 0.025 microgram normalized calcium content in blood serum of rats with D-avitaminosis, Increased doses of IalphaOHD3, administered into intact animals, caused transient hyperphosphatemia, hypercalcemia, calcinosis of internal tissues (kidney heart, aorta) as well as death of some animals. IalphaOHD3 exceeded 400-fold the hypercalcemic and calcinose effects of ergocalciferol. LD50 for IalphaOHD3 was equal to 100 microgram/kg, if it was administered during 5 days per os. Tissue calcinosis was developed after administration of a daily dose 10 microgram/kg, moderate hypercalcemia was caused by a daily dose 1 microgram/kg or 0.25 microgram per an animal; this amount is only 10-fold higher as compared with the physiologic requirement. Ergocalciferol caused hypercalcemia and metastatic calcification only at a dose 4000 microgram/kg. Clinical use of IalphaOHD3 at doses, exceeding the physiologic requirements, has to be prohibited due to high activity of the preparation and to toxicity of its increased doses.

Animals↗