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At least 19 recordsLinked to original sources
PubMed1977

Changes in plasma 25-hydroxycholecalciferol and selected blood parameters after injection of massive doses of cholecalciferol or 25-hydroxycholecalciferol in non-lactating dairy cows.

Plasma levels of 25-hydroxycholecalciferol, free hydroxyproline, calcium, phosphorus, and magnesium were determined in non-lactating, pregnant dairy cows injected intra-muscularly with 15 X 10(6) IU of cholecalciferol or 25 mg of 25-hydroxycholecalciferol. A lag in the conversion of cholecalciferol to 25-hydroxycholecalciferol was observed in the cows injected with cholecalciferol, while an immediate increase was observed when cows were injected with 25-hydroxycholecalciferol directly. The increased plasma levels of 25-hydroxycholecalciferol following injection of cholecalciferol were directly related to rises in plasma free hydroxy-proline, calcium, and phosphorus, while plasma magnesium was inversely related to plasma 25-hydroxycholecalciferol. Injection of 25-hydroxycholecalciferol caused an immediate increase in plasma calcium which persisted for the duration of the experiment. The biological half-life of 25-hydroxycholecalciferol in the injected cows was found to be 34 days. The data indicate the possibility of a feedback mechanism in which massive doses of cholecalciferol inhibit hydroxylation at the 25ths carbon preventing its conversion to 25-hydroxycholecalciferol until after 8 days post injection. The increase in plasma 25-hydroxycholecalciferol after 8 days resulted in increased bone resorption as indicated by plasma free hydroxyproline.

Animals↗
PubMed1976

[Activation of vitamin D 3 and the mode of action of 1,25-hydroxycholecalciferol and 24,25-hydroxycholecalciferol].

A survey is given on the present state of the animal-biochemical research concerning the effectivity of the D-vitamins. The vitamin D3 is transferred in 25-hydroxycholecalciferol in the microsome fraction of the liver. Then in the kidneys a transformation into the physiologically active forms - the 1,25- and the 24,25-hydroxycholecalciferol - takes place. The kind of transformation depends on the Ca- and P-supply as well as on the level of the parathormone secretion. In the mucous membrane of the small intestine the 1,25- and the 24,25-hydroxycholecalciferol stimulate the formation of the Ca-transport protein. The 1,25-hydroxycholecalciferol is above all formed in hypocalcaemia or hypophosphataemia and furthers the mobilisation of Ca- and phosphate-ions from the bones. In a liver damage disturbances of the formation of 25-hydroxycholecalciferol and in renal damage disturbances of the formation of 1,25- and 24,25-hydroxycholecalciferol may appear. A reduction of the formation of the active forms of the D-vitamins leads to a decrease of the Ca-utilisation as well as of the growth of bones.

Biological Availability↗
PubMed1986

Metabolism of 25-hydroxycholecalciferol in human promyelocytic leukemia cells (HL-60). Isolation and identification of (5Z)- and (5E)-19-nor-10-oxo-25-hydroxycholecalciferol.

Human promyelocytic leukemia cells incubated with 25-hydroxy[26,27-methyl-3H] cholecalciferol (1 microCi) or non-radioactive 25-hydroxycholecalciferol (550 micrograms) produced significant quantities of two vitamin D3 metabolites. The two metabolites were isolated and purified by methanol chloroform extraction and a series of chromatographic procedures. The metabolite purification and elution positions on these columns were followed by radioactivity and their ultraviolet absorption at 310 nm. The two metabolites have been unequivocally identified as (5Z)- and (5E)-19-nor-10-oxo-25-hydroxycholecalciferol by ultraviolet absorption spectrophotometry, mass spectrometry, Fourier-transform infrared spectrophotometry and co-chromatography with synthetic compounds on a high-performance liquid chromatograph. (5E)- but not (5Z)-19-nor-10-oxo-25-hydroxycholecalciferol was able to induce HL-60 cell phenotypic and functional differentiation. However, these two metabolites of 25-hydroxycholecalciferol did not bind specifically to the chick intestinal 3.7 S. receptor protein for 1 alpha,25-dihydroxycholecalciferol. The precise biological role of these metabolites is as yet unclear.

Animals↗
PubMed1976

1 alpha hydroxycholecalciferol and 25 hydroxycholecalciferol in renal bone disease.

Four microgrammes of 1-alpha-hydroxycholecalciferol (1-alpha-OH D3) or 200 mug of 25-hydroxycholecalciferol (25-OH D3) were given orally every other day respectively to 10 uraemic patients (8 on chronic haemodialysis) for 1-12 weeks and to 3 patients on chronic haemodialysis for 4-8 weeks. A transilial bone biopsy and serial evaluation of serum immunoreactive PTH (iPTH) calcium phosphate and alkaline phosphatase were performed before and at the end of therapy. Both 1-alpha-OH D3 and 25-OH D3 (the latter at a 50 times higher dose) were able to depress hyperparathyroidism in two-thirds of the cases and to consistently improve the mineralisation defect. In no case did iPTH or the bone histomorphometric parameters return to normal, so that long term evaluation of these two drugs is warranted.

Absorption↗
PubMed1987

Specific 1,25-hydroxycholecalciferol receptors and stimulation of 25-hydroxycholecalciferol-24R hydroxylase in human amniotic cells.

We have analyzed the 1 alpha, 25-dihydroxycholecalciferol [1,25(OH)2D3] receptor content of cultured cells from human amniotic fluid. Six cell lines were grown to confluence in a minimum essential medium containing 20% fetal calf serum. All had a normal karyotype, five were male and one was female. Hypertonic cytosol extracts were prepared by sonication followed by centrifugation at 200,000 X g 30 min. Saturation analysis was performed by incubating the extracts with [3H]-1,25(OH)2D3 (20-500 pM, 160 Ci/mmol) with and without 100-fold molar excess of unlabeled 1,25(OH)2D3. Linear sucrose gradient (5-20% w/v) analysis was performed with 1.5 nM [3H]-1,25(OH)2D3 alone or in presence of 100-fold molar excess, 1,25(OH)2D3. Functional responsiveness was measured by induction of 25-hydroxycholecalciferol-24R-hydroxylase with 1 and 10 nM 1,25(OH)2D3. The six cell lines studied had receptors with dissociation constant of 44 +/- 6 pM (mean +/- SEM). The binding capacity was 10,200 +/- 1,750 sites/ng protein (mean +/- SEM) with extreme values of 4,700 and 15,500. A single peak for specific binding migrating at approximately 3S was observed by sucrose gradient centrifugation. 25-Hydroxycholecalciferol-24R-hydroxylase was induced by 1 and 10 nM 1,25(OH)2D3 in a dose-dependent fashion. The data show that receptors for 1,25(OH)2D3 are present in cultured amniotic fibroblast-like cells early in pregnancy. These cells may thus prove to be useful for further characterization of 1,25(OH)2D3 receptors in fetal tissue.

Amniotic Fluid↗
PubMed1991

The effects of intramuscularly administered vitamin D3, 25- and 1 alpha-hydroxycholecalciferol in cows on plasma mineral content, plasma 25-hydroxycholecalciferol and on mineral deposits in soft tissues.

The investigations were carried out to evaluate potential side effects of a prophylaxis with high doses of vitamin D3 and vitamin D metabolites in parturient paresis. For this reason, 10(7) IU vitamin D3 (= 250 mg), 4 mg 25-OHD3 or 420 micrograms 1 alpha-OHD3 were applied to non-gravid dairy cows at the end of lactation. The application was repeated 3 times at one week intervals and the changes of the mineral concentration and 25-OHD were measured in the plasma. The pathomorphological changes in the cardio-vascular system and other organs were examined macro- and microscopically. The application of vitamin D3 and 25-OHD3 led to an immediate and continuous increase of the 25-OHD concentration in the plasma. On the other hand, administration of 1 alpha-OHD3 resulted in a decrease of the 25-OHD level. After the application of vitamin D3 and 1 alpha-OHD3, the Ca and Pi concentration increased significantly. After 25-OHD3, the Ca concentration decreased below the initial level in the second week. The administration of all 3 compounds led to a significant decrease of the Mg concentration after the first injection. The administration of vitamin D3 and 1 alpha-OHD3 resulted in a significantly more pronounced calcinosis of inner organs while after the application of 25-OHD3 only occasionally calcium deposits were observed in the vascular system.

Animals↗
PubMed1978

Effect of 1alpha-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, 3 deoxy-1alpha-hydroxycholecalciferol, 24R, 25-dihydroxycholecalciferol and successful renal transplantation on calcium absorption in haemodialysis patients.

Using a 2-hour 47Ca absorption test, significant depression of active calcium absorption was demonstrated in 48 vitamin D untreated haemodialysis patients. This malabsorption of calcium could be corrected by the daily oral administration of 1--2 microgram of 1alphaOHD3 and 1--1.5 microgram of 1,25(OH)2D3. 5 microgram daily for 2 weeks of 3-deoxy-1alphaOHD3 AND 16 and 64 microgram daily for 1 week of 24R,25(OH)2D3 proved ineffective. In 32 successfully transplanted patients, restoration of normal or near normal renal function (serum creatinine less than 1.9 mg/100 ml) was not always followed by an immediate improvement in active calcium absorption. Calcium absorption, especially in female patients, was adversely affected by the required immunosuppressive prednisone therapy and improvement was slow.

Absorption↗
PubMed1977

[Effect of cortisone on calcium metabolism. Attempt at correction by 5,6 trans 25-hydroxycholecalciferol, 25-hydroxycholecalciferol and vitamin D2].

14 patients receiving small doses of predisolone and 7 high doses were divided at random into three groups. Each group received for four weeks, 100 microgram of vitamin D2 or 25 hydroxyvitamin D3 or 5,6 trans-25 hydroxyvitamin D3. The 25 hydroxy and 5,6 trans-25 hydroxyvitamine D3 were able to increase intestinal calcium absorption. 25 Hydroxyvitamin D3 had an osteolytic action, increasing urine calcium and hydroxyproline and, once, in a patient slight hypercalcemia was observed. By constrast, 5,6 trans-25 hydroxyvitamin D3 decreased PTH and caused a significant decrease in urine hydroxyproline.

Calcium↗
PubMedDate not supplied

[Long-term effects of a combination of 25-hydroxycholecalciferol and 1-alpha-hydroxycholecalciferol on osteodystrophy in chronic hemodialysis patients].

vitamin compounds to the basic dialytic treatment of renal osteodystrophy is of contestable interest. Because 1) optimum conditions of dialysis without D vitamin addition prevent efficiently the progress of severe gyperparathyroidism and osteomalacia 2) the D vitamin compunds could render the phosphatemia control more difficult thus contributing to aggravate the histologic lesions of hyperparathyroidism.

Adult↗
PubMed1993

[The effect of parenteral administration of 25-hydroxycholecalciferol and 1 alpha-hydroxycholecalciferol on the mineral concentrations in the blood of cows in late pregnancy].

The effect of 1 - 3 intramuscular injections of the vitamin D3 metabolite 25-OHD3, synthetic 1 alpha-OHD3, and a combination of both on the plasma concentrations of calcium (Ca), inorganic phosphate (P(i)) and magnesium (Mg) was tested in 67 older dry dairy cows. Administering 4,0 mg 25-OHD3 reduced Ca and P(i) for some time while Mg blood levels remained constant. Injecting 210 micrograms 1 alpha-OHD3 plus 2.0 mg 25-OHD3 only brought a marked increase in P(i) concentrations, whereas 420 micrograms 1 alpha-OHD3 plus 4.0 mg 25-OHD3, and 350 micrograms 1 alpha-OHD3 alone significantly raised Ca and P(i) levels beginning on the 2nd day after injection and lasting for at least 6 days. These higher levels can be maintained by repeated injections. Another effect of injecting 1 alpha-OHD3 was to depress Mg blood levels, and a negative effect on the Ca and vitamin D3 metabolism is suggested which may cause hypocalcaemia when the effect of 1 alpha-OHD3 subsides. Metastatic calcifications of soft tissues were observed in some 1 alpha-OHD3-treated cows.

Animals↗
PubMed1976

Acute administration of 25-hydroxycholecalciferol in man.

Serum 25-hydroxyvitamin D responses to oral doses of 25-hydroxycholecalciferol were measured in healthy volunteers. Peak serum 25-hydroxyvitamin D levels occurred 4 to 8 hours after doses of 1.5, 5, and 10 mug per kg of body weight. The mean increments above baseline serum 25-hydroxyvitamin D concentrations at 4 hours were linear over this dose range. Following a single oral dose, serum 25-hydroxyvitamin D levels fell to 33% of their peak values after one week. The serum 25-hydroxyvitamin D responses measured by competitive protein-binding radioassay were similar to the serum 3H responses exhibited by three volunteers who received simultaneous oral doses of 3H 25-hydroxycholecalciferol and 14C-cholecalciferol. The appearance of 14C in plasma was slower and less marked compared with 3H, probably reflecting a more rapid plasma clearance of the 14C-cholecalciferol. The disappearance of 25-hydroxycholecalciferol from the circulation of two volunteers following acute intravenous delivery of 1.0 mg of 25-hydroxycholecalciferol was multiphasic over 10 days. 60% of the dose administered remained in the circulation 24 hours after the dose. When analyzed several days after single 10 mug/kg oral doses of 25-hydroxycholecalciferol to 4 volunteers, the mean rate of decline to total serum 25-hydroxycholecalciferol was slow (t 1/2 = 22 days). When baseline serum 25-hydroxyvitamin D levels were subtracted, however, the apparent serum half-life of administered 25-hydroxycholecalciferol was 12 days, similar to that reported after tracer doses of 3H-25-hydroxycholecalciferol. The rapid and predictable serum 25-hydroxyvitamin D increases following the oral administration of 25-hydroxycholecalciferol suggest its possible therapeutic advantages compared with vitamin D administration.

Administration, Oral↗
PubMed1978

Vitamin D and cartilage. I. In vitro metabolism of 25-hydroxycholecalciferol by cartilage.

In the present work, the capacity of cartilage to metabolize 25-hydroxycholecalciferol was investigated. Cartilage preparations from growth plate, articular surface, rib, scapula, and ear were isolated from 3-week-old normal rabbits and chickens. Each tissue was separately incubated with tritiated 25-hydroxycholecalciferol (, x 10(-9) M) for 1-24 h. Incubations of kidney and muscle were performed simultaneously for comparison. Similarly, cultured chondrocytes isolated from rabbit growth plate and articular cartilage were incubated for 1 or 20 h in medium free of fetal calf serum. After methanol-chloroform extraction of tissues, cells, and their respective media, chloroform phases were chromatographed on Sephadex LH-20 columns. The results show that kidney and cartilage are able to convert 25-hydroxycholecalciferol into a derivative which migrates in the 24,25-dihydroxycholecalciferol region. Cartilage tissue previously boiled is unable to metabolize 25-hydroxycholecalciferol. The conversion of 25-hydroxycholecalciferol occurs with all types of cartilage and is also observed in incubations of cultured chondrocytes. In the latter, the polar 25-hydroxycholecalciferol derivative is detected as early as 1 h after addition of 25-hydroxycholecalciferol. Two findings suggest that the polar derivative of 25-hydroxycholecalciferol produced by cartilage is 24,25-dihydroxycholecalciferol: 1) the cartilage derivative and 24,25-dihydroxycholecalciferol (synthetic and biosynthetic) comigrate during Sephadex LH-20 and high liquid pressure chromatography; and 2) both the cartilage derivative and 24,25-dihydroxycholecalciferol are sensitive to periodate treatment.

Animals↗
PubMed1978

[Biological activity of 1alpha-hydroxycholecalciferol (1). Effect on intestine and bone in rats (author's transl)].

Biological activity of 1alpha-hydroxycholecalciferol was studied in rats. 1alpha-Hydroxycholecalciferol was found to be more potent and rapidly active than vitamin D in stimulating intestinal calcium transport and calcium mobilization from bone both in normal and vitamin D deficient rats. 1alpha-Hydroxycholecalciferol was also active in nephrectomized and/or thyroparathyroidectomized rats both in intestine and bone. Although it is well known that 1alpha-hydroxycholecalciferol is metabolized to 1alpha, 25-dihydroxycholecalciferol in the liver, there is the possibility that the former is active without further metabolism. In rats in which hepatitis was induced by CCl4, 1alpha-hydroxycholecalciferol was active both in the intestine and in the bone, while it was inactive in hepatectomized rats. These data clearly demonstrate that 1alpha-hydroxycholecalciferol is not active by itself and must be metabolized in the liver. This idea also shows the lag time in response of rats to 1alpha-hydroxycholecalciferol has more potent antirachitic activity than vitamin D and does not lose its activity with chronic oral administration. In view of these findings, 1alpha-hydroxycholecalciferol appears to have a good potential for clinical application in cases of renal failure and metabolic bone diseases.

Animals↗
PubMed1998

Exogenous 25-hydroxycholecalciferol does not attenuate salt-induced hypertension.

We have reported that an inverse relationship exists between blood pressure and plasma concentration of 25-hydroxyvitamin D, the precursor of the hormonal form of vitamin D, for Dahl salt-sensitive rats fed a high salt diet. Plasma 25-hydroxyvitamin D concentrations decreased with time on the diet, as blood pressure increased. Experiments were conducted to determine whether the blood pressure increase of salt-sensitive rats fed a high salt diet could be attenuated by exogenous 25-hydroxycholecalciferol. Dahl salt-sensitive rats were fed a high salt diet and administered exogenous 25-hydroxycholecalciferol via subcutaneously implanted Alzet pumps. Exogenous 25-hydroxycholecalciferol (various doses from 28 to 80 microg/kg body weight-day) had no significant effect on the blood pressure of vitamin D-replete rats fed a high salt diet for 15 days. When exogenous 25-hydroxycholecalciferol (28 and 60 microg/day-kg body weight) was administered to vitamin D-depleted salt-sensitive rats, plasma 25-hydroxyvitamin D concentrations of the rats fed a low salt diet (26 +/- 2 and 59 +/- 6 nM) were proportional to the 25-hydroxycholecalciferol concentration in the pumps. Plasma 25-hydroxyvitamin D concentrations of the rats fed a high salt diet (18 +/- 1 and 23 +/- 3 nM) were not proportional to the 25-hydroxycholecalciferol concentration in the pumps, but were inversely proportional to the blood pressure of the rats. These data indicate no ameliorating effect of exogenous 25-hydroxycholecalciferol on salt-induced hypertension, but accelerated metabolism and/or clearance of 25-hydroxycholecalciferol in salt-induced hypertension.

Animals↗
PubMed1984

Hydroxylation of carbon-24 of 25-hydroxycholecalciferol is not necessary for normal embryonic development in chickens.

Laying hens fed 25-hydroxycholecalciferol, 24,24-difluoro-25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol or 24,25-dihydroxycholecalciferol were used to investigate whether hydroxylation of C-24 of cholecalciferol is necessary for normal embryonic development in chickens. Laying hens were fed a rachitogenic diet and 25-hydroxycholecalciferol from hatching until normal egg production, fertility and hatchability were achieved. When the hens were 40 weeks old, 25-hydroxycholecalciferol was withdrawn and egg production ceased in 4 weeks. The hens were divided into 6 groups of 5 and dosed daily for 19 weeks with either 2.0 micrograms of 25-hydroxycholecalciferol, 2.0 micrograms of 24,24-difluoro-25-hydroxycholecalciferol, 0.4 microgram of 1,25-dihydroxycholecalciferol, 2.0 micrograms of 24,25-dihydroxycholecalciferol, both 1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol or vehicle only. Egg production during this period was high for all hens fed the cholecalciferol compounds. Egg production of 3% occurred in hens given vehicle only. Fertility was over 90% for all groups of cholecalciferol compound-fed hens. Hatchability of over 90% was achieved with the eggs from hens given 25-hydroxycholecalciferol or 24,24-difluoro-25-hydroxycholecalciferol and 6% with eggs from hens fed both 1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol. No eggs from hens fed 1,25-dihydroxycholecalciferol or 24,25-dihydroxycholecalciferol alone hatched (over 140 eggs in each group.

24,25-Dihydroxyvitamin D 3↗