Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CHOLECALCIFEROL”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

20-Cyclopropyl-cholecalciferol vitamin D3 analogs: a unique class of potent inhibitors of proliferation of human prostate, breast and myeloid leukemia cell lines.

We have synthesized and studied the ability of a series of nine novel 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] analogs to inhibit clonal growth of myeloid leukemic cells (HL,60), prostate (LNCaP, PC-3 and DU-145) and breast (MCF-7) cancers cells. DU-145 cells were actively resistant to compounds (cmpd) with all of these modifications, but when we removed C-19 (E, 1,25-Dihydroxy-23E-ene-26,27-hexafluoro-19-nor-20-cyclopropy l- cholecalciferol) an analog resulted that was inhibitory against all three prostate cell lines, breast and HL-60 cell lines. Further analysis showed that pulse exposure (3 days, 10(-7) M) to this analog was enough to inhibit clonal growth of PC-3 cell by 50%. Furthermore, cmpd E increased the number of PC-3 cells in G1 and decreased the number in S phase. 1,25(OH)2D3 mediates its biological activities through specific binding to the vitamin D3 receptor (VDR) and subsequent association with vitamin D3 response elements (VDRE) in genes modulated by 1,25(OH)2D3. Several novel vitamin D3 cmpds have recently been identified which have 5- to 1000-fold greater abilities to induce differentiation and to inhibit proliferation of prostate cancer, breast cancer and HL-60 leukemic blast cells as compared to the parental 1,25(OH)2D3. To clarify the mechanism by which nine of these vitamin D3 analogs mediate their remarkably potent biological activities, we have investigated their abilities in PC-3 prostate cancer cells to transactivate a chroramphenicol acetyl transferase (CAT) reporter gene containing a VDRE from the human osteocalcin gene attached to a thymidine kinase minimal promoter. Dose-response studies of Cmpd E showed that in serumless culture conditions, transactivation of the VDRE-CAT was stronger than cmpd J [1,25(OH)2D3]. Then, we investigated the effects of vitamin D3 cmpd J in mice. Our data showed the growth inhibitory action of the vitamin D3 cmpd E in prostate cancer cell line (PC-3) was stastically superior to the non-treatment group in terms of tumor size and tumor weight in mice. In summary, this is the first report of a potent series of 20-cyclopropyl-cholecalciferol vitamin D3 analogs with the ability to inhibit proliferation of LNCaP, PC-3, DU-145, MCF-7 and HL-60 cell lines. These cmpds may mediate their potent anti-proliferative activities through a cell cycle arrest pathway.

Animals↗
PubMedDate not supplied

Determination of cholecalciferol (vitamin D3) in selected foods by liquid chromatography: NMKL collaborative study.

Results are presented from an NMKL (Nordic Committee on Food Analysis) collaborative study of a method for the determination of cholecalciferol (vitamin D3) in foods. The method is based on the addition of an internal standard (vitamin D2), followed by saponification and extraction with n-heptane. The fraction that contains vitamin D2/D3 is separated by preparative normal-phase liquid chromatography (LC), and the analytes are determined by reversed-phase LC with UV detection at 265 nm. The method was tested by 8 participating laboratories. In this study 6 different matrixes were analyzed for cholecalciferol content: milk, liquid infant formula (gruel), cooking oil, margarine, infant formula, and fish oil. The contents varied from 0.4 to 12 microg/100 g. Three matrixes (milk, gruel, and margarine) were fortified with vitamin D3. In the other matrixes, vitamin D3 was added at 3 different levels at the Swedish National Food Administration. The milk was analyzed as a blind duplicate, whereas the other matrixes were analyzed as split-level pairs. The recoveries from the samples with vitamin D3 added varied from 93 to 102%. The repeatability relative standard deviation (RSDr) values for accepted results varied between 2.2% (fish oil) and 7.4% (cooking oil), whereas the reproducibility relative standard deviation (RSD(R)) values varied between 6.8% (margarine) and 24% (cooking oil).

Algorithms↗
PubMed1991

[Cholecalciferol Reference Standard (Control 901) of the National Institute of Hygienic Sciences].

Cholecalciferol Reference Standard for the Japanese Pharmacopoeia (JP RS) was prepared. The following analytical data were obtained: melting point 85.8 degrees C; UV and IR spectra were in agreement with both of the previous JP RS and USP RS of Cholecalciferol; absorptivity at 265 nm E1%lcm = 476; optical rotation [alpha]20D = + 110.1 degrees; no impurities were detected by TLC and HPLC analyses; assay 100.1% by HPLC against the USP RS. Based on the above results, the raw material was authorized as the Reference Standard of the National Institute of Hygienic Sciences.

Cholecalciferol↗
PubMed1991

Accidental ingestion of a cholecalciferol-containing rodent bait in a dog.

A diagnosis of cholecalciferol toxicity in a young dog was made on the basis of adequate history and the finding of extremely elevated serum calcium levels. The traditional treatment of fluid therapy, diuresis and corticosteroids resulted in lowering the serum calcium levels over a 5-d period. The dog displayed clinical signs of severe depression, anorexia and intermittent vomiting during this time interval. Serum calcium levels rose on day 6 and remained elevated up until the dog was euthanized on day 9. Gross and histopathological examinations revealed diffuse metastatic mineralization throughout the body, particularly involving the lung, kidney, atria and stomach. The amount of cholecalciferol ingested was determined well below the lethal dose reported in dogs. This report indicates that young dogs may be much more susceptible to the lethal effects of this compound than initially believed.

Animals↗
PubMed1991

Cholecalciferol rodenticide intoxication in a cat.

A 4-month-old 2.5-kg sexually intact female domestic shorthair cat was referred to the teaching hospital because of suspected cholecalciferol intoxication after ingestion of a cholecalciferol-containing rodenticide. At referral, the cat was hypercalcemic, hyperkalemic, and acidotic. Despite management of hypercalcemia and preservation of renal function with physiologic saline solution, furosemide, dopamine, and calcitonin, the cat died, apparently as a result of extensive pulmonary mineralization.

Animals↗
PubMed1975

[The requirements of vitamin D (cholecalciferol) and of 25-hydrocalciferol (25HCC) in premature children during their early life (author's transl)].

The necessary daily amount of vitamin D3 in premature infants was calculated by Hövels and his group as being 25 mcg (1000 I.U.). This was in agreement with our own investigations. Without vitamin D3, however, the incidence of rikkets in premature and small-for-dates newborns occurred usually at the beginning of the second month of life. Clinical signs of rickets are still absent at this time, while an increased activity of the serum alkaline phosphatase signals the beginning of the illness. Three groups of prematurely born infants received up to 50 days daily oral doses of 12.5 mcg vitamin D3 (=500 I.U.), 25 mcg vitamin D3 (=1000 I.U.) or 9 mcg 25-hydroxycholecalciferol (25-HCC), respectively, while one untreated group served as control. No differences were noted between the four groups in the serum values of calcium and phosphorus. The activity of the alkaline phosphatase tended to be higher in the untreated and the 500 I.U. groups. The differences were prouved by the chi2-test to be significant (see table 2 and 3). It appeared that 9 mcg of 25-HCC prevented the rise in alkaline phosphatase slightly better than 25 mcg of vitamin D3 (1000 I.U.). On a mcg base 25-HCC seems three times as effective as cholecalciferol. One could speculate about a delayed hydroxylation of cholecalciferol (vitamin D3) to 25-HCC.

Age Factors↗
PubMed1990

[Microencapsulization of cholecalciferol by coacervation].

Microcapsules with crystalline cholecalciferol were obtained by the use of gelatin (type A and B) as a main covering component by both simple and complex coacervation methods. The properties of the obtained microcapsules were determined by their size, release in gastric and intestinal juices, coat/core ratio, the content of cholecalciferol and its liberation. It was observed that both in the simple and complex coacervation, regardless of the type of gelatin used in the procedure, the effectiveness of the process and the properties of the microcapsules depend on coat/core ratio. In simple coacervation method optimal results were achieved when coat/core ratio was 0.25:1. In complex coacervation method optimal ratio was 0.5:1.

Capsules↗
PubMed1989

[Cholecalciferol Reference Standard (Control 871) of National Institute of Hygienic Sciences].

Cholecalciferol Reference Standard (Control 871) for the Japanese Pharmacopoeia was prepared. The following analytical data were obtained: melting point, 86.3 degrees C; infrared spectrum, same as the Japanese Pharmacopoeia Standard "Cholecalciferol Standard (Control 851)"; absorbance, E1%1cm (265 nm) = 474.5; optical rotation, [alpha]20D = + 110.0 degrees; thinlayer chromatography, same as the Japanese Pharmacopoeia Standard; highperformance liquid chromatography, contaminants were not detected; assay, 100.7%. On the basis of those results, this material was authorized as the Japanese Pharmacopoeia Standard (control 871).

Chemical Phenomena↗
PubMedDate not supplied

Liquid chromatographic determination of cholecalciferol in rodent baits.

Cholecalciferol (vitamin D3) is extracted in acetonitrile on a Goldfisch apparatus, diluted to volume, and determined by reverse phase liquid chromatography (LC). The sum of the peak heights of pre-vitamin D3 and cis-vitamin D3 is used for quantitation. The method was tested for precision, linearity, and recovery. Quadruplicate analyses of 5 formulation samples gave relative standard deviations of 1.56-2.65%. Linearity was excellent with regression and correlation coefficients of 0.9997 and 0.9998, respectively. Recovery was 98.0 +/- 2.7%. The method is applicable to 0.075% cholecalciferol rodent baits.

Cholecalciferol↗
PubMed1993

A new role for vitamin D: cholecalciferol promotes dermal wound strength and re-epithelization.

Vitamin D endocrine system is a potent regulator of cell growth and maturation. Vitamin D3 modulates growth kinetics of many cells and produces divergent actions. Keeping this in view, cholecalciferol is evaluated for its actions on dermal wound healing in Wistar rats. Intraperitonial cholecalciferol at 5, 10, 15 IU/g body weight doses produces increases in wound breaking strength and promotes epithelization significantly. Results suggest that there is some biological role for vitamin D endocrine system, ir wound repair. A clear understanding of this role of vitamin D3 may define new avenues in wound medication.

Animals↗
PubMed1996

Calcium absorption in rats with distal intestinal resection: influence of type of dietary fat, cholecalciferol and nature of the adaptative response.

The effects of dietary fat and supplementation with cholecalciferol on calcium absorption at different luminal concentrations (2.07 mmol/l and 2.07 mmol/l with 0.5 mmol/l 2,4-dinitrophenol and 8.20 mmol/l) were studied in vivo in the perfused duodenum, residual jejunum and proximal colon of rats with resection of 50% of the distal small intestine, as well as the nature of the adaptative response (passive or active). Changing the source of dietary fat (diet B, containing 1/3 medium chain triglycerides, 1/3 olive oil, 1/3 sunflower oil) increased calcium absorption, preferentially via active transport, in both transected and resected rats. Supplementation of diet B with cholecalciferol further enhanced intestinal calcium absorption, especially in the colon. These results suggest the importance of diet in the adaptive processes and confirm that active mechanisms of transport adapt more readily to intestinal resection than do passive mechanisms.

Adaptation, Physiological↗
PubMed1995

1 alpha-Hydroxylated cholecalciferol compounds act additively with microbial phytase to improve phosphorus, zinc and manganese utilization in chicks fed soy-based diets.

Seven experiments were conducted to determine the efficacy of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and microbial phytase in improving P, Zn and Mn utilization of chicks fed P, Zn- and Mn-deficient soy protein diets containing surfeit levels of cholecalciferol. Efficacy of 1 alpha-hydroxycholecalciferol (1 alpha-OH D3) was also studied. A dose titration study indicated that supplemental phytase at 1200 units/kg diet would increase bone ash by at least 65% when added to a corn-soybean meal diet containing 0.43 g P/100 g (0.1 g nonphytate P/100 g). These responses were similar to those obtained from supplemental P (0.1 g/100 g) as KH2PO4 or from added 1,25-(OH)2D3 (10 micrograms/kg). Dietary addition of both 1200 units phytase and 10 micrograms/kg 1,25-(OH)2D3 elicited bone ash responses that were near 100%. When chicks were fed a Zn-deficient soy-concentrate diet (13 mg Zn/kg), diet supplementation with 1,25-(OH)2D3 or phytase increased growth rate by 40% and tibia Zn content by > 100%; adding 1,25-(OH)2D3 together with phytase increased tibia Zn content by 160%. Utilization of both Zn and Mn contained in the corn-soybean meal diet also was markedly enhanced by supplemental phytase, 1,25-(OH)2D3, or the combination. The cholecalciferol analog 1 alpha-OH D3 was found to improve dietary P utilization maximally (70% bone ash response) at a dose of 20 micrograms/kg diet, and effects were additive when 1 alpha-OH D3 was fed in the presence of phytase.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Phytase↗
PubMed1997

1alpha-hydroxycholecalciferol does not increase the specific activity of intestinal phytase but does improve phosphorus utilization in both cecectomized and sham-operated chicks fed cholecalciferol-adequate diets.

Two chick assays were conducted in an attempt to understand how 1alpha-hydroxylated cholecalciferol compounds [1,25-(OH)2 D3 and 1alpha-OH D3] function in chicks to improve utilization of phytate-bound phosphorus (P) and trace minerals. Mucosal tissue from chicks fed a P-deficient corn-soybean meal diet, with or without supplemental 1alpha-OH D3, was incubated with sodium phytate. Inorganic P (Pi) release from sodium phytate, a measure of mucosal phytase activity, was not influenced by 1alpha-OH D3 presence in the diet. Increasing doses of mucosal protein in tubes containing sodium phytate resulted in marked increases (P < 0.01) in Pi release, but 1alpha-OH D3 in the diet from which the duodenal mucosal tissue was obtained had no effect on Pi release. Similarly, addition of either 1alpha-OH D3 or 1,25-(OH)2 D3 directly to the incubation tubes had no effect on Pi production. Efficacy of supplemental 1alpha-OH D3 and phytase was also tested in cecectomized vs. sham-operated chicks that were fed P-deficient and cholecalciferol-adequate corn-soybean meal diets. Removal of the twin ceca was done in an attempt to remove much of the intestinal microbial activity, and in turn, much of the gut microbial phytase activity. Marked increases (P < 0.01) in bone ash occurred in response to phytase or 1alpha-OH D3 supplementation, and cecectomized birds responded to either addition in the same manner as sham-operated controls. The data suggest that the marked phytate-P releasing capacity of dietary 1alpha-OH D3 or 1, 25-(OH)2 D3 is not caused by an increased specific activity of intestinal phytase.

6-Phytase↗
PubMed1987

Presence in human serum, associated with cancer, of an abnormal cholecalciferol derivative, the 1-ceto-24-methyl-25-hydroxycholecalciferol. Preliminary results of a prospective study.

Using new techniques for micro-determinations of blood fat soluble vitamin concentrations, this study from a large population of cancer patients compared to healthy controls led to the finding, extraction and isolation of an abnormal cholecalciferol derivative the 1-ceto-24-methyl-25-hydroxycholecalciferol. This factor was shown to be present in serum from cancer patients and absent in most normal controls. A double blind study has confirmed the diagnostic value of this new marker of cancer. In the same time, an animal study was performed. The abnormal cholecalciferol derivative, absent in intact rats, was found in the blood of rats transplanted by the Ehrlich carcinoma. The compound, extracted from serum of human cancer patients, injected to transplanted rats significantly decreased their survival time. Injected to untransplanted rats it induced hypocalcemia. The genesis and the possible role of this factor in cancer development are discussed.

Adult↗
PubMed2003

Metabolic responses to dietary cholecalciferol and phosphorus in abalone Haliotis discus hannai ino.

Metabolic responses of cholecalciferol (VD(3)) and minerals (Ca, P and Mg) in abalone Haliotis discus hannai Ino to dietary VD(3) and phosphorus (P) were investigated. Based on a 2 x 2 factorial design, four casein-gelatin-based diets were formulated. The basal diet was supplemented with either 0 or 2000 IU VD(3)/kg diet and 0 or 10 g P/kg diet. The abalone was reared in P-free artificial seawater for 55 days. Results showed that dietary VD(3) was hydroxylated to 25-hydroxyvitamin D(3) [25(OH)D(3)] and 1 alpha,25-dihydroxyvitamin D(3) [1 alpha,25(OH)(2)D(3)] in abalone, and subsequently raised the serum levels of these two VD(3) metabolites. Dietary P deficiency elevated serum 1 alpha,25(OH)(2)D(3) level only when the dietary VD(3) supplementation was sufficient. The supplementations of either dietary VD(3) or P significantly increased the levels of P in serum, mantle and hepatopancreas, and only the addition of VD(3) significantly raised the concentrations of Ca in serum and mantle (P<0.05). Interaction between dietary VD(3) and P was only found significant on the concentrations of P and Mg in mantle (P<0.05). The concentrations of Ca, P and Mg in muscle were not significantly influenced by these dietary treatments. Hence, the metabolic responses in serum, muscle, mantle and hepatopancreas of abalone to dietary VD(3) and P were in different manners.

Analysis of Variance↗
PubMed1982

Effect of cholecalciferol derivatives on the mechanical properties of chick bones.

Chicks were depleted of vitamin D, divided into groups, and treated daily with (a) cholecalciferol, (b) 1 alpha-hydroxycholecalciferol [1 alpha (OH)-D3], (c) 24R, 25-dihydroxycholecalciferol [24R,25-(OH)2D3], or (d) 1 alpha (OH)D3 and 24R,25(OH)2D3. Two additional groups of chicks were studied, one that was continuously depleted of vitamin D, and another that was continuously supplemented with the vitamin, since day 1. After killing, the tibiae were removed and tested for their mechanical properties. Bending load was applied to the midshaft, and the intrinsic properties of this site, its quantity and geometry were analyzed. From a mechanical point of view, the weakest bones found were of birds depleted of vitamin D, whereas the strongest were of those treated with 1 alpha (OH)D3. Only the bones of the 24R,25(OH)2D3-treated or the 1 alpha (OH)D3 and 24R,25(OH)2D3-treated groups of birds showed mechanical properties comparable to those obtained with vitamin D-replete chicks.

24,25-Dihydroxyvitamin D 3↗
PubMed1988

Suppression of rat hepatic vitamin D-25-hydroxylase by cholecalciferol, but not by 25-hydroxy- or 1,25-dihydroxymetabolites.

Hepatic vitamin D-25-hydroxylase activity is greater in vitamin D-depleted than replete animals. We investigated whether vitamin D itself or a metabolite of vitamin D was responsible for modulating the activity of vitamin D-25-hydroxylase. Accordingly, we repleted vitamin D-depleted rats with subcutaneous injections of 2600, 520, and 130 pmoles of cholecalciferol (D3), 25-hydroxycholecalciferol (25(OH)D3), and 1,25-dihydroxycholecalciferol (1,25(OH)2D3), respectively, for up to 3 weeks. Repletion resulted in accelerated weight gain and in increased activity of gut mucosal alkaline phosphatase. Using an improved assay to measure vitamin D-25-hydroxylase activity in liver homogenates, we found 78% reduction (P less than 0.001) in the D3-repleted group, maximal by 1 week, in contrast to no change in those groups treated with D3 metabolites. D3, 25(OH)D3, and D3-esters remaining in livers at the time of assay were estimated in a parallel experiment using [3H]D3-repleted rats. Residual D3 accounted for only a 9% dilution of substrate in the assay. 25(OH)D3 was present in the liver at concentrations two orders of magnitude lower than the amount required to inhibit vitamin D-25-hydroxylase activity in vitro. D3 esters had no inhibitory effect in vitro at 250-fold excess of that found in the repleted rat liver. Vitamin D appears to modulate its D-25-hydroxylase activity in biological systems by a mechanism other than feedback inhibition by 25(OH)D3, 1,25(OH)2D3, or D3-esters.

Animals↗