SEARCH · PubMed Health

Results for “CHOLECALCIFEROL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 379 records · Page 21Linked to original sources

PubMed2004

School-milk intervention trial enhances growth and bone mineral accretion in Chinese girls aged 10-12 years in Beijing.

A 2-year milk intervention trial was carried out with 757 girls, aged 10 years, from nine primary schools in Beijing (April 1999 - March 2001). Schools were randomised into three groups: group 1, 238 girls consumed a carton of 330 ml milk fortified with Ca on school days over the study period; group 2, 260 girls received the same quantity of milk additionally fortified with 5 or 8 microg cholecalciferol; group 3, 259 control girls. Anthropometric and bone mineralisation measurements, as well as dietary, health and physical-activity data, were collected at baseline and after 12 and 24 months of the trial. Over the 2-year period the consumption of this milk, with or without added cholecalciferol, led to significant increases in the changes in height (> or =0.6 %), sitting height (> or =0.8 %), body weight (> or 2.9 %), and (size-adjusted) total-body bone mineral content (> or =1.2 %) and bone mineral density (> or =3.2 %). Those subjects receiving additional cholecalciferol compared with those receiving the milk without added 25-hydoxycholecalciferol had significantly greater increases in the change in (size-adjusted) total-body bone mineral content (2.4 v. 1.2 %) and bone mineral density (5.5 v. 3.2 %). The milk fortified with cholecalciferol significantly improved vitamin D status at the end of the trial compared with the milk alone or control groups. It is concluded that an increase in milk consumption, e.g. by means of school milk programmes, would improve bone growth during adolescence, particularly when Ca intake and vitamin D status are low.

Analysis of Variance↗

PubMed1990

Relationship of membrane-bound sulfhydryl groups to vitamin D-stimulated uptake of [75Se]Selenite by the brush border membrane vesicles from chick duodenum.

The uptake of selenite by purified brush border membrane vesicles isolated from duodena of rachitic or vitamin D-treated chicks was studied by using radioactive selenite and a rapid filtration technique. Cholecalciferol treatment (500 IU at 72 h) significantly enhanced selenite uptake, a response that decreased when the vesicles were stored at room temperature for 2.5 h prior to the uptake measurement. Preincubation of the vesicles in 1.0 mmol/L H2O2 reduced [75Se]selenite uptake, indicating the involvement of oxidizable groups in the uptake reaction. Iodoacetic acid (IAA), a sulfhydryl-blocking reagent, at 1-2 mmol/L concentration eliminated the difference in selenite uptake due to cholecalciferol and had no effect on vesicles from rachitic animals. A higher concentration of IAA (10 mmol/L) enhanced selenite uptake manyfold and increased the absolute difference due to cholecalciferol treatment. Single intravenous doses of 100 IU cholecalciferol, 100 IU ergocalciferol, or 0.1 micrograms 1,25-dihydroxycholecalciferol also stimulated selenite uptake, suggesting a general response to vitamin D compounds. Normal animals given a single dose of 1,25-dihydroxycholecalciferol 12 h prior to killing also responded. Treatments that enhanced the uptake of [75Se]selenite also increased the amount of membrane-bound sulfhydryl groups, suggesting the involvement of membrane-bound sulfhydryl groups in the vitamin D response. A significant increase in selenite uptake by intravenous 1,25-dihydroxycholecalciferol occurred within 10 min. This rapid effect provides a new tool to probe early biochemical effects of vitamin D on intestinal epithelium.

Animals↗

PubMed1988

Improvement of dental development in osteopetrotic mice by maternal vitamin D3 sulfate administration.

Utilizing the microphthalamic mouse, (mi/mi) as a model of osteopetrosis, vitamin D3 (cholecalciferol) was administered prenatally and postnatally to study its effects on tooth development and subsequent eruption. It has previously been reported that vitamin D3 crosses the placental barrier and is absorbed into mammary gland milk. Fifteen heterozygotes (+/mi) were used as breeders. There were three study groups: A) 5.0 ng/gm cholecalciferol sulfate; B) 2.5 ng/gm cholecalciferol sulfate; and C) no therapy. Intraperitoneal injections were administered three times per week, beginning when pregnancy was evident, and continuing for 4 additional weeks during lactation. Approximately half of the 59 offspring were sacrificed at age 1 day and the other half at 4 weeks. The former group was studied for crown development, and the latter group was studied for root development and eruption. When the osteopetrotic offspring of group A were compared with osteopetrotic offspring of group C, crown development and tooth eruption were substantially more advanced. Parameters examined were maturity of the ameloblasts and odontoblasts, dentin and enamel formation, root sheath development, status of eruption, and degree of apex closure. It was concluded that cholecalciferol sulfate significantly improves tooth development and subsequent eruption in the osteopetrotic mouse. A genetic disease has had its phenotype modified by vitamin therapy during gestation.

Animals↗

PubMed1983

Effect of u.v. rays on 7-dehydrocholesterol content in rat skin.

Long-term exposure of rat to ultraviolet irradiation affected the cholesterol metabolism in the skin. The 7-dehydrocholesterol content was increased to 1.6 times of non-irradiated rat. However, the cholesterol content was not altered. Ultraviolet-induced precholecalciferol and cholecalciferol bound with an activator protein of delta 5,7 sterol-delta 7-reductase. This observation suggested that precholecalciferol and cholecalciferol bound with an activator protein of delta 5,7 sterol-delta 7-reductase. This observation suggested that precholecalciferol and cholecalciferol inhibit the conversion of 7-dehydrocholesterol to cholesterol and accumulate 7-dehydrocholesterol. The action of ultraviolet rays on the cholesterol metabolism in the skin may be explained as the action of ultraviolet-induced precholecalciferol and cholecalciferol.

Animals↗

PubMed2005

Preventing bone loss during androgen deprivation therapy for prostate cancer: early experience with neridronate.

OBJECTIVE: Androgen-deprivation therapy (ADT) is the usual treatment for locally advanced or metastatic prostate cancer. Osteoporosis is a common complication of ADT. The aim of our study was to evaluate the efficacy of neridronate, a relatively new bisphosphonate to prevent bone loss during androgen ablation. METHODS: Sixty patients with prostate cancer and osteoporosis were enrolled and randomly assigned to 2 different treatment regimes: group A (30 patients) treated with maximum androgenic blockage (MAB), and group B (30 patients) treated with bicalutamide 150 mg. Each group was divided in 2 subgroups A1-A2 and B1-B2. All patients received calcium and cholecalciferol supplements (500 mg of elemental calcium and 400 IU cholecalciferol) daily. The A2 and B2 subgroups were also treated with neridronate (25 mg intramuscular monthly). Lumbar and femoral bone mineral density (BMD) was evaluated by dualenergy X-ray absorptiometry (DXA), both at baseline and after one year of treatment. Deoxypyridinoline (DPD) and bone-alkaline phosphatase (B-ALP) were determined at the beginning, midstudy and at the end. RESULTS: Patients treated only with calcium and cholecalciferol (A1, B1 subgroups) showed a marked bone loss after 6, and 12 months, with increased levels of DPD and BALP, compared to baseline values. Patients treated with neridronate (A2 et B2 subgroups) showed unchanged levels of these markers. After one year of treatment, lumbar and total hip BMD decreased significantly in patients treated only with calcium and cholecalciferol (A1 subgroup: -4.9% and -1.9% respectively). BMD did not change significantly at any site in patients treated also with neridronate (A2 subgroup: +1% and +0.8% respectively). Lumbar and total hip BMD did not change significantly (-1.5% and -1% respectively) in B1 subgroup. In B2 subgroup an important increase in lumbar spine and the total hip BMD was shown (+2.5% and 1.6% respectively). No relevant side effects were recorded during our study. CONCLUSION: In conclusion, neridronate is an effective and safe treatment in preventing bone loss in men receiving ADT for prostate cancer.

Absorptiometry, Photon↗

PubMed1978

Calcium-binding protein and kidney 25-hydroxycholecalciferol-1-hydroxylase activity in turkey poults.

A vitamin D-dependent calcium-binding protein (CaBP) has been found in the intestinal mucosa of turkeys (Meleagris gallopavo). This protein is similar, if not identical, to the corresponding one found in the intestine of the chicken (Gallus domesticus). The concentration of intestinal CaBP in the intestine of cholecalciferol-fed turkey poults was twice that found in the intestine of the domestic chicken of parallel age. Dietary calcium or phosphorus restriction resulted in a significant increase in intestinal CaBP. This increase was less pronounced than that obtained in chickens. The relationship between duodenal CaBP and dietary calcium appears to be linear. Cholecalciferol (vitamin D) deficiency or dietary calcium, but not phosphorus, restriction resulted in an increase of kidney 25 hydroxycholecalciferol-1-hydroxylase activity in vitro. The values of activity obtained in turkeys were higher than those obtained under the same experimental conditions in chicks. Bone ash was reduced by dietary calcium, phosphorus or cholecalciferol restriction. Plasma inorganic phosphorus was lower in either cholecalciferol- or phosphorus-restricted turkeys. Plasma calcium was significantly higher in the phosphorus-restricted turkeys than in the calcium-restricted or control turkeys.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1994

The dietary requirement of juvenile grass shrimp (Penaeus monodon) for vitamin D.

Two 8-wk experiments were conducted to determine the adequate level of dietary vitamin D for juvenile grass shrimp (Penaeus monodon). In Experiment 1, purified diets with six levels (0, 0.1, 0.5, 2.5, 12.5 and 62.5 mg/kg diet) of supplemental ergocalciferol and cholecalciferol were fed to P. monodon (mean weight 0.19 +/- 0.02 g). In Experiment 2, we used 0, 0.05, 0.1, 0.2, 0.3, 0.6 and 1.0 mg/kg of supplemental cholecalciferol in basal diet fed to the shrimp (mean weight 0.25 +/- 0.03 g). In both experiments, shrimp fed vitamin D-deficient diets grew poorly. In Experiment 1, poorer growth performance was observed in shrimp fed diets containing ergocalciferol compared with those fed the diets containing cholecalciferol. In Experiment 2, weight gain was highest in shrimp fed the diet supplemented with 0.2 mg cholecalciferol/kg diet, followed by the groups fed 0.1 mg/kg, then 0.3 mg/kg, 0.05 and 0.6 mg/kg, 1.0 mg/kg, and finally the unsupplemented control group. The differences among these groups were significant (P < 0.05). The feed efficiency ratio and alkaline phosphatase activity generally followed the same pattern as the weight gain. Analysis by brokenline regression of weight gain and alkaline phosphatase activity of the shrimp in Experiment 2 indicated that the adequate dietary cholecalciferol concentration for growing P. monodon is approximately 0.1 mg/kg.

Alkaline Phosphatase↗

PubMed2005

All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats.

An antagonistic interaction between retinol and calciferol has been established. However, the mechanism by which this antagonism occurs is unclear. One possibility is that retinol affects the metabolism of calciferol. To investigate this hypothesis, retinol- and calciferol-depleted rats were given various amounts of ergocalciferol, cholecalciferol, 1alpha,25-dihydroxycholecalciferol [1,25(OH)2D3], or 24,24-difluoro-1alpha,25-dihydroxycholecalciferol [24-F2-1,25(OH)2D3] in combination with various amounts of retinyl acetate or all-trans retinoic acid (ATRA) in a series of studies. Rats administered 1720 or 3440 microg retinyl acetate once every 3 d for 33 d in combination with 25.8 ng ergocalciferol or 25 ng cholecalciferol every 3 d had lower serum calcium and greater serum phosphorus concentrations than rats fed 0 or 11.4 mug retinyl acetate every 3 d. In addition, rats fed 400 microg ATRA/d in combination with 25.8 ng ergocalciferol every 3 d, 25 ng cholecalciferol every 3 d, 2-5 ng 1,25(OH)2D3/d, or 0.5-1 ng 24-F2-1,25(OH)2D3/d had significantly lower serum calcium and higher serum phosphorus concentrations than rats not given ATRA in the diet. Therefore, both retinyl acetate and ATRA are able to antagonize the action of ergocalciferol and cholecalciferol in vivo. Additionally, ATRA antagonizes the in vivo action of 1,25(OH)2D3 and an analog, 24-F2-1,25(OH)2D3, that cannot be 24-hydroxylated. Together, these results suggest that retinol does not antagonize the action of calciferol by altering the metabolism of calciferol or 1,25(OH)2D3, but does so by another mechanism.

Animals↗

PubMed2003

Effectiveness of twenty-five-hydroxycholecalciferol in the prevention of tibial dyschondroplasia in Ross cockerels depends on dietary calcium level.

Five experiments were conducted to evaluate the efficacy of 25-hydroxycholecalciferol [25-(OH)D3] to minimize the development of tibial dyschondroplasia (TD) and improve phytate phosphorus retention in Ross cockerels during the starter period. In experiment 1, chicks were fed a TD-inducing (0.67% calcium) diet with or without exposure to ultraviolet light and no supplemental cholecalciferol. Dietary 25-(OH)D3 was added at 0, 10, or 70 microg/kg for both light treatments. In experiment 2, 25-(OH)D3 was added at 0, 10, 40, or 70 microg/kg to a TD-inducing diet containing 27.5 microg/kg added cholecalciferol. Experiment 3 was similar to experiment 2 except a diet marginal (0.85%) in calcium was fed, and cholecalciferol was added at 55 microg/kg. In experiments 4 and 5, 25-(OH)D3 was added at 0, 18, 36, 54, 72, or 90 microg/kg to a diet marginal in calcium. Dietary 25-(OH)D3 decreased the incidence of TD similarly at 40 and 70 microg/kg 25-(OH)D3 and improved phytate phosphorus retention when the TD-inducing diet was fed. The incidence of TD was decreased when 70 microg/kg 25-(OH)D3 was added to a diet marginal in calcium in experiment 3 only. Phytate phosphorus retention was generally not affected by dietary 25-(OH)D3 when a diet containing marginal calcium, adequate phosphorus, and high cholecalciferol was fed. The effectiveness of 25-(OH)D3 to reduce the incidence of TD in young broilers was higher when the dietary calcium level was below 0.85%. The incidence of TD in Ross cockerels was low (< 25%) when dietary calcium was greater than 0.85%.

Animals↗

PubMed1978

A field trial of 1alpha-hydroxycholecalciferol (1alpha-OH D3) in the prevention of milk fever.

The efficacy of 1alpha-OH cholecalciferol for the prevention of milk fever has been tested in a controlled field trial using 597 cows on 19 farms all of which had previously had a high incidence of milk fever. Of 293 cows receiving 1alpha-OH cholecalciferol 34 had milk fever and of 304 control cows 51 had milk fever. Although there was an apparent efficacy of 31 per cent the difference in incidence was not statistically significant. There was no effect if 1alpha-OH cholecalciferol was administered less than 24 hours before the cows succumbed to milk fever. However, if 1alpha-OH cholecalciferol was administered more than 24 hours and less than one week before the occurrence of milk fever the efficacy increased to 61 per cent and the effect was highly significant.

Animals↗

PubMed2005

Vitamin D insufficiency does not affect bone mineral density response to raloxifene.

CONTEXT: Vitamin D insufficiency and osteoporosis are common and often coexist in postmenopausal women. OBJECTIVE: The objective of this study was to test whether the presence of vitamin D insufficiency at the initiation of raloxifene therapy affected the subsequent response of bone mineral density (BMD). DESIGN, SETTING, AND PARTICIPANTS: We studied 7522 postmenopausal participants of the Multiple Outcomes of Raloxifene Evaluation, a placebo-controlled trial of the effects of raloxifene on BMD and fracture. INTERVENTION: After enrollment, all participants began daily supplements of 500 mg calcium and 400-600 IU cholecalciferol; 1 month later, women were randomly assigned to placebo or raloxifene. MAIN OUTCOME MEASURE: Serum levels of vitamin D [25-hydroxy vitamin D (25OHD)] were measured at enrollment, randomization, and 6 months later. We categorized participants' vitamin D status (deficient, insufficient, or sufficient) based on their randomization 25OHD level. We estimated the effects of treatment on BMD within these subgroups using linear regression models. RESULTS: At enrollment, 3.2% of participants were vitamin D deficient, and 51.8% were insufficient; after 7 months of cholecalciferol supplementation, 0.2% of all participants remained D deficient, and 23.6% remained insufficient. The effects of raloxifene on hip and spine BMD did not vary by vitamin D status at randomization (P = 0.08 and P = 0.7, respectively). CONCLUSION: We conclude that vitamin D status at initiation of raloxifene therapy does not affect the subsequent BMD response when coadministered with cholecalciferol and calcium. After 7 months of cholecalciferol therapy, very few women continued to have 25OHD levels in the deficient range; however, 25OHD levels remained suboptimal in nearly one fourth of the cohort. Additional research is needed to determine whether these observations can be generalized to other antiresorptive agents.

Aged↗

PubMed2005

Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials.

CONTEXT: The role and dose of oral vitamin D supplementation in nonvertebral fracture prevention have not been well established. OBJECTIVE: To estimate the effectiveness of vitamin D supplementation in preventing hip and nonvertebral fractures in older persons. DATA SOURCES: A systematic review of English and non-English articles using MEDLINE and the Cochrane Controlled Trials Register (1960-2005), and EMBASE (1991-2005). Additional studies were identified by contacting clinical experts and searching bibliographies and abstracts presented at the American Society for Bone and Mineral Research (1995-2004). Search terms included randomized controlled trial (RCT), controlled clinical trial, random allocation, double-blind method, cholecalciferol, ergocalciferol, 25-hydroxyvitamin D, fractures, humans, elderly, falls, and bone density. STUDY SELECTION: Only double-blind RCTs of oral vitamin D supplementation (cholecalciferol, ergocalciferol) with or without calcium supplementation vs calcium supplementation or placebo in older persons (> or =60 years) that examined hip or nonvertebral fractures were included. DATA EXTRACTION: Independent extraction of articles by 2 authors using predefined data fields, including study quality indicators. DATA SYNTHESIS: All pooled analyses were based on random-effects models. Five RCTs for hip fracture (n = 9294) and 7 RCTs for nonvertebral fracture risk (n = 9820) met our inclusion criteria. All trials used cholecalciferol. Heterogeneity among studies for both hip and nonvertebral fracture prevention was observed, which disappeared after pooling RCTs with low-dose (400 IU/d) and higher-dose vitamin D (700-800 IU/d), separately. A vitamin D dose of 700 to 800 IU/d reduced the relative risk (RR) of hip fracture by 26% (3 RCTs with 5572 persons; pooled RR, 0.74; 95% confidence interval [CI], 0.61-0.88) and any nonvertebral fracture by 23% (5 RCTs with 6098 persons; pooled RR, 0.77; 95% CI, 0.68-0.87) vs calcium or placebo. No significant benefit was observed for RCTs with 400 IU/d vitamin D (2 RCTs with 3722 persons; pooled RR for hip fracture, 1.15; 95% CI, 0.88-1.50; and pooled RR for any nonvertebral fracture, 1.03; 95% CI, 0.86-1.24). CONCLUSIONS: Oral vitamin D supplementation between 700 to 800 IU/d appears to reduce the risk of hip and any nonvertebral fractures in ambulatory or institutionalized elderly persons. An oral vitamin D dose of 400 IU/d is not sufficient for fracture prevention.

Aged↗

PubMed1988

Aluminum intoxication in vitamin D-deficient rats: studies of bone aluminum localization and histomorphometry before and after vitamin D repletion.

Aluminum accumulation by both dialysis patients and nonuremic patients, requiring chronic total parenteral nutrition, may be an etiological factor in the development of severe osteomalacia. To study the role of aluminum toxicity in bone, further experiments have been conducted in the nonuremic, vitamin D-deficient rat. Weanling rats were raised on vitamin D-deficient diets, and half received parenteral aluminum (5 mg/wk), for 30 days. In the first experiment low doses of 25-OH cholecalciferol (500 ng/week) were given subcutaneously for a further 30 days. Control rats were maintained on a similar protocol, but were supplemented with cholecalciferol (5 micrograms/week) from the outset until sacrifice at 60 days. In the second experiment a single bolus of cholecalciferol (5 micrograms) was given to study short-term changes in serum biochemistry and bone histology at 96 hr. Quantitative bone histomorphometric analyses of the proximal tibial metaphysis were made in all experimental groups. In the experimental vitamin D-deficient group, with the highest bone aluminum content (as assessed by extraction of whole bone aluminum), X-ray microanalysis was performed to determine the distribution of aluminum in bone tissue and bone cell organelles. The results showed that control rats treated with prolonged aluminum therapy (30 mg over 60 days) had evidence of both reduced osteoid matrix synthesis and mineralization. However, in vitamin D-deficient rats, there was no evidence that aluminum exacerbated the osteomalacic lesion, even though there was histochemical evidence of aluminum deposition at the bone-osteoid interface.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗

PubMed1975

The functional metabolism of vitamin D in chicks fed low-calcium and low-phosphorus diets.

Radioactively labelled cholecalciferol was administered continuously to chicks that were fed normal, low-calcium and low-phosphorus diets. It has been possible to show that under such steady state conditions with regard to cholecalciferol, and mineral restriction, the animal reacts by increased accumulation of 1, 25-dihydroxycholecalciferol in the intestinal and the kidney cell, which was associated in the intestine with an increased calcium-binding activity. A similar accumulation of 1, 25-dihydroxycholecalciferol in bone was not noticed. It is proposed that the intestine and the kidney, but not bone, are the main target organs for cholecalciferol in the maintenance of calcium homeostasis, and that both calcium and phosphorus play a role in the regulation of the formation and subsequent function of 1, 25-dihydroxycholecalciferol.

Animals↗

PubMed1978

The parotid gland: a new target organ for vitamin D action.

Radioactively labelled cholecalciferol was administered continuously to rats which were fed a vitamin D-deficient diet. It has been possible to show that all the metabolites of the cholecalciferol which normally occur in known target tissues of vitamin D are present in the parotid gland, and the pattern resembled that obtained for the kidney, a known target tissue for vitamin D action. The accumulation of cholecalciferol metabolites in the parotid gland was shown to be functional, as a calcium-binding protein was found to be present in the gland, possessing similar properties to the renal vitamin D-dependent calcium-binding protein.

Animals↗

PubMed1969

Isolation of chick intestinal nuclei. Effect of vitamin D3 on nuclear metabolism.

1. Chick intestinal nuclei were isolated, with practically no contamination from other organelles and whole cells, by centrifugation through 2.4m-sucrose. 2. The proportions of RNA, DNA and protein of the isolated nuclei were unaffected by the vitamin D status of the birds. The RNA/DNA ratio was 0.15. 3. The incorporation of [5-(3)H]orotic acid into the rapidly labelled intestinal nuclear RNA, after a 10min. pulse of the orotic acid, was increased in vitamin D-deficient chicks only 10min. after a 125mug. dose of cholecalciferol. 4. There was no stimulation of the DNA-dependent RNA polymerase activity of the isolated nuclei from birds treated with cholecalciferol. 5. The results are discussed in relation to the changes occurring during the lag period, after administration of cholecalciferol and before Ca(2+) transport is detected, and the function of the vitamin.

Animals↗

PubMed1969

Investigations on metabolites of vitamin D in rat bile. Separation and partial identification of a major metabolite.

1. Young rats with cannulated bile ducts were given 0.34mg. of [1alpha-(3)H]cholecalciferol or 0.54mg. of [(14)C]ergocalciferol by intravenous infusion. Of the radioactivity in the dose of [1alpha-(3)H]cholecalciferol 31% was recovered in bile within 24hr. 2. The metabolites in bile were separated by gradient-elution column chromatography on silicic acid into five components, all more polar than cholecalciferol or 25-hydroxycholecalciferol. [(14)C]Ergocalciferol gave a similar pattern of metabolites in bile. 3. The three most polar metabolites were shown to be ionic. The major component has been identified as a glucuronide conjugate, which was not identical with synthetic cholecalciferyl glucuronide.

Animals↗

PubMed1971

The localization of 1,25-dihydroxycholecalciferol in bone cell nuclei of rachitic chicks.

1. A simple technique has been developed to obtain subcellular fractions of chick bone. The method yielded 60-70% of total DNA in the nuclear debris fraction and 80-90% of total (14)C recovered in bone after a dose of radioactive vitamin D. 2. After a dose of [4-(14)C,1,2-(3)H(2)]cholecalciferol (0.5mug) was given to vitamin D-deficient chicks, the time-course of total (14)C radioactivity in the epiphysis, metaphysis and diaphysis of proximal tibiae was measured. The maximum concentrations were reached at 6h, corresponding to a similar peak of radioactivity in blood, decreasing until 24h and indicating the dependence on the circulating (14)C and on the blood supply of the three bone components. 3. The (14)C radioactivity of cholecalciferol and 25-hydroxycholecalciferol (expressed per mg of DNA) followed the pattern of incorporation of total (14)C radioactivity in all three bone components. The more polar metabolite fraction reached a peak of radioactivity at 6-9h and maintained its concentration over the 24h period studied in all anatomical bone components. 4. After a dose of [4-(14)C,1-(3)H]cholecalciferol (0.5mug) was given to vitamin D-deficient chicks, the subcellular distribution was studied. At 24h after dosing, the nuclear fraction contained 27% and the supernatant fraction had 67% of total (14)C recovered in the bone filtrate. When the (14)C in the residual bone fragments was included, the nuclear fraction contained up to 35% of the total radioactivity in the bone. 5. The subcellular distribution pattern of individual vitamin D metabolites indicated that the purified nuclear fraction concentrated the polar metabolite, which lost (3)H at C-1, so that 77% of the radioactivity could be accounted for by 1,25-dihydroxycholecalciferol. The supernatant fraction contained smaller amounts of 1,25-dihydroxycholecalciferol (9%), with 66% of 25-hydroxycholecalciferol forming the major metabolite, corresponding to its concentration found in blood at 24h. 6. The preferential accumulation of 1,25-dihydroxycholecalciferol in the nuclear fraction and the overall pattern of other metabolites, found previously in intestinal tissue, suggests a similar mechanism of action in bone to that postulated for the intestinal cell in calcium translocation.

Animals↗