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Results for “Calcifediol”

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At least 109 records · Page 6Linked to original sources

PubMed1993

Hormonal alterations and osteoporotic syndromes.

Hormonal control of skeletal growth, modeling, and remodeling is characterized by a complex interaction between the calciotropic hormones (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, parathyroid hormone, and calcitonin), growth, and thyroid hormones in addition to the estrogenic and androgenic gonadal hormones. Although both growth and thyroid hormones are essential skeletal growth and modeling and also can produce detrimental skeletal effects in adults when circulating in excess concentrations, these hormones assume a minor role in the day-to-day bone remodeling of the mature skeleton. Following the attainment of the peak bone mass, bone mineral content begins to decline in the fourth and fifth decades of life, accelerating in females in the first 5-7 years after the menopause as a result of estrogen deficiency. Associated with this age-dependent loss in skeletal mass are decreases in calcitonin reserve primarily in the 5-7 years following the menopause, decreases in circulating 25-hydroxycholecalciferol, intestinal resistance to 1,25-dihydroxycholecalciferol, and a gradual progressive rise in blood parathyroid hormone. These changes in calciotropic hormone profiles, together with poor nutritional habits, anticonvulsant, glucocorticoid, and thyroid medications, diseases such as type I diabetes, immobilization, or decreased physical activity all serve to weaken the aging skeleton. The result is a gradual and subtle change in skeletal anatomy, which progresses to alterations in vertebral structure, such as kyphosis, scoliosis, and pseudospondylolisthesis, and a variety of sciatic and nerve entrapment syndromes. Vertebral, forearm, and hip fractures and edentulism ultimately comprise the syndrome of age-related bone loss, resulting in lifestyle disabilities, extensive morbidity, analgesic drug abuse, hospitalization, and escalating annual health care expenditures.

Aging↗

PubMed1994

Effects of 1,25-dihydroxyvitamin D3 on bone resorption and natural immunity in osteopetrotic (ia) rats.

Osteopetrois is an inherited bone disease characterized by an excessive accumulation of bone throughout the skeleton. The disease in the ia (incisors absent) rat is the result of reduced bone resorption caused by defective, although numerous osteoclasts. In addition to the bone defects, ia rats have suppressed natural immunity, even though these animals have excessive numbers of natural killer (NK) cells. The osteopetrotic condition also appears to have an associated abnormality in vitamin D metabolism. Because 1,25-dihydroxyvitamin D3[1,25-(OH)2D3] stimulates bone resorption and has a role in the immunoregulation of NK cells, mutant and normal rats were infused with 1,25-(OH)2D3 for 14 days in an attempt to correct the defects in this mutant. Serum levels of osteocalcin, 25-OHD3, and 1,25-(OH)2D3, as well as NK function and parameters of bone resorption, were evaluated after the infusion period. Serum levels of osteocalcin and 1,25-(OH)2D3 were elevated in both ia and normal rats treated with 1,25-(OH)2D3. Serum 25-OHD3 levels were significantly reduced in the treated animals. The elevated percentage of NK cells normally found in ia rats was reduced to normal in the treated mutants, and NK cell function was elevated to normal levels of lytic activity. The percentage of NK cells and NK function remained unchanged in the treated normal rats. The bone marrow cavity size was significantly increased in the 1,25-(OH)2D3-treated mutants, as was the percentage of osteoclasts exhibiting normal morphology. Radiographically, the mutant bones were less dense.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Prostatic 25-hydroxyvitamin D-1alpha-hydroxylase and its implication in prostate cancer.

Evidence suggests that vitamin D may have a protective role for prostate cancer. 1alpha,25-Dihydroxyvitamin D [1alpha,25(OH)(2)D] inhibits growth and induces differentiation of prostate cells. 25-Hydroxyvitamin D-1alpha-hydroxylase [1alpha-OHase], the enzyme that is responsible for the synthesis of 1alpha,25(OH)(2)D, is expressed in cultured prostate cells. We observed a marked decrease in 1alpha-OHase activity in prostate cancer cells, suggesting some defect of the 1alpha-OHase in these cells. To investigate whether the defect was due to dysregulation of the enzyme at the promoter level, a series of deletion constructs of the promoter was synthesized and incorporated upstream into the luciferase reporter gene. Two regions were identified with high basal activity in transfected normal prostate cell line (PZHPV-7), -1100 bp (AN2), and -394 bp (AN5) upstream of ATG start site of the 1alpha-OHase gene. When the reporter gene with either AN2 or AN5 was transfected into prostate cancer cell lines, we observed a lower basal promoter activity in PC-3 cells and DU145 cells than that found in PZHPV-7 cells for both constructs, and a loss of promoter activity in LNCaP cells. Thus, the results suggest that the defect in enzyme activity may result from the decreased promoter activity in prostate cancer cells.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed2003

Direct, rapid effects of 25-hydroxyvitamin D3 on isolated intestinal cells.

Scattered reports in the literature have suggested that the metabolite 25-hydroxyvitamin D(3) [25(OH)D(3)] has biological activity. In the present work, perfusion of isolated duodenal loops of normal chickens with 100 nM 25(OH)D(3) resulted in enhanced transport of (45)Ca within 2 min relative to the vehicle controls. We then tested the effect of a range of 25(OH)D(3) concentrations on (45)Ca handling by isolated intestinal cells in time course studies. Following a basal uptake period, cell suspensions from 7-week old chicks were treated either with 25, 100, or 300 nM 25(OH)D(3), or the vehicle ethanol (0.01%, final concentration). Both 25 and 100 nM 25(OH)D(3) resulted in a significant (P < 0.05) reduction in (45)Ca levels, relative to controls, between 1-10 min after treatment, while 300 nM 25(OH)D(3) resulted in a significant increase in (45)Ca levels, relative to controls, after 10 min of incubation. The effect of 100 nM 25(OH)D(3) (a physiological level) on cell calcium was abolished by the presence of 6.5 nM 24,25-dihydroxyvitamin D(3). In cell preparations from 14- or 28-week old birds 100nM 25(OH)D(3) had no effect, relative to vehicle controls. Incubation of cells with 2 microM BAY K8644, a calcium channel activator, stimulated (45)Ca uptake within 3 min relative to vehicle controls (P < 0.05), while addition of either 20 microM forskolin or 100 nM phorbol ester (stimulators of the PKA and PKC pathways, respectively) resulted in enhanced radionuclide levels after 10 min of incubation (P < 0.05, relative to corresponding controls). Finally, cells were treated with 100 nM 25(OH)D(3) or vehicle and samples taken at various times for analyses of protein kinase C and A activities. No effect of 25(OH)D(3) on protein kinase C activity was observed, while protein kinase A activity was stimulated to nearly 200% of controls at 1 min after 25(OH)D(3) addition (P < 0.05, relative to corresponding controls) and began declining at 3 min, returning to control levels 5 min after additions. We conclude that 25(OH)D(3) has a direct effect on calcium handling in enterocytes of young animals that may in part be mediated by the protein kinase A signal transduction pathway.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1988

Hormonal effects of vitamin D3 on epidermal melanocytes.

The role of cholecalciferol, 25(OH) D3, and 1,25(OH)2 D3, as modulators of melanocyte function and proliferation has been examined. Topical application of 100 micrograms cholecalciferol to the pinnal epidermis of DBA/2J mice for 5 or 10 days increased the number of L-dihydroxyphenylalanine-positive (DOPA-positive) melanocytes and had a synergistic effect with a low dose of ultraviolet B light (UVB). Application of 1 microgram 1,25(OH)2 D3 had a transient effect on epidermal melanocytes. Addition of cholecalciferol to pure cultures of human melanocytes did not alter their tyrosinase activity (therefore, melanin synthesis) or growth rate even after 72 hours of treatment. However, treatment of similar cultures with 1,25(OH)2 D3 at a concentration equal to or greater than 10(-8) M suppressed tyrosinase activity but did not affect proliferation. The effect of 25(OH) D3 was similar to, but lower in magnitude than, that of 1,25(OH)2 D3. We attempted to demonstrate the presence of specific receptors for 1,25(OH)2 D3 in normal human melanocytes using the monoclonal antibody (Mo Ab) 9A7 gamma raised against the receptor for 1,25(OH)2 D3. Melanocytes were exposed to 9A7 gamma and to a secondary biotinylated Ab and analyzed by the fluorescence activated cell sorter (FACS). An increase in the specific fluorescent signal was constantly observed. By using the immunoblotting technique, we observed a major immunoreactive species that migrated in the 53-kD region in normal melanocytes. The size of this major immunoreactive species was smaller in melanoma cells than in normal melanocytes. This correlates with the finding that the former cells were unresponsive to cholecalciferol, 25(OH) D3, or 1,25(OH)2 D3 treatment. These results predict a direct role for 1,25(OH)2 D3 as an effector of normal melanocyte function.

Animals↗

PubMed1982

Effects of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 on embryonic chick bone in organ culture.

The ability of embryonic chick bone to respond to 25 hydroxyvitamin D3 and 1,25 dihydroxyvitamin D3 was assessed in organ culture. These metabolites were added to prelabeled chick embryo long-bone explants, and the amount of calcium-45 released into the medium after 24 or 48 h of hormone exposure was measured. For each time period a significant release of calcium-45 from hormone-treated bones was observed. The response to 25 hydroxyvitamin D3 and 1,25 dihydroxyvitamin D3 was always greater at 48 h and a clear dose-dependency was established at this time as well. 1,25 dihydroxyvitamin D3 was the more potent resorbing agent at all concentrations tested. The results from this study suggest that vitamin D metabolites may be involved in bone regulation in the chick embryo.

Animals↗

PubMed1993

Vitamin D3 compounds regulate human immunodeficiency virus type 1 replication in U937 monoblastoid cells and in monocyte-derived macrophages.

We studied the effects of vitamin D3 compounds on the replication of human immunodeficiency virus type 1 (HIV-1) in the monoblastoid cell line U937 and in primary monocyte-derived macrophage cultures to understand how modulators of monocyte/macrophage effector function might affect the pathogenesis of HIV-1 infection. U937 cell cultures exposed to 1, alpha 25-dihydroxyvitamin D3 prior to HIV-1 infection showed enhanced virus replication that was apparently due to increased cellular resistance to viral cytopathic effects; a marked inhibition of virus replication was noted in cells exposed to 1 alpha,25-dihydroxyvitamin D3 subsequent to infection. Exposure of blood-derived monocyte/macrophages to vitamin D3 compounds prior to infection also affected virus growth; in most cases, substantial inhibition of HIV-1 replication was noted in vitamin D3-treated macrophage cultures. Our results demonstrate that vitamin D3 compounds with recognized abilities to induce cellular differentiation can modulate HIV-1 infection of human macrophages.

Calcifediol↗

PubMed1998

Effect of 25-OH-vitamin D on fracture healing in elderly rats.

To investigate the effect of 25-OH-vitamin D supplements (calcidiol) on fracture healing in the elderly, an experimental model with 15 18-month-old female Wistar rats was designed. An experimental fracture in the middle third of both femora of each rat was made. Then the rats were randomly assigned to two groups: one group was subcutaneously treated with 25-OH-vitamin D during all healing processes, and the other group (the control group) was not. After 5 weeks of healing, the animals were killed and both femora were extracted. Blood samples were collected before fracture and at death to determine the levels of 25-OH-vitamin D. All bones that were extracted were subjected to a torsion test to assess healing; a significantly greater maximum shear force before failure was supported in the treated group (p < 0.01). Moreover, a positive correlation (p < 0.01; r=0.55) was found between blood levels of 25-OH-vitamin D at death and the mechanical strength of the callus. Thus, the administration of 25-OH-vitamin D after the experimental fracture significantly improved the mechanical strength of the fractured bone. If similar results are found in the human, then treatment with 25-OH-vitamin D after the occurrence of a fracture would be a good way to improve fracture healing in the elderly.

Aging↗

PubMed1993

Bone turnover in asthmatic children treated with oral prednisolone or inhaled budesonide.

Biochemical markers of bone turnover were studied in prepubertal school children with asthma in two randomized double-blind crossover trials with run-in, treatment, and wash-out periods of 2 weeks. One group (n = 11) was treated with 2.5 and 5.0 mg prednisolone, the other (n = 14) with 200 and 800 micrograms inhaled budesonide per day. Serum osteocalcin, serum total alkaline phosphatase, fasting urinary excretion of hydroxyproline and calcium, serum 25-hydroxyvitamin D, and 1,25 dihydroxyvitamin D were assessed. A dose-related reduction of serum osteocalcin (Page's test for trend: P = 0.04; z = -2.3) and of the fasting urinary hydroxyproline:creatinine ratio (Page's test for trend: P = 0.05; z = -2.0) was found in the children who were treated with prednisolone. Inhaled budesonide was not associated with statistically significant effects on any of the biochemical markers. Short-term treatment with low daily doses of prednisolone may cause a suppression of bone turnover in children with asthma. To reduce the risk of adverse effects on bone turnover, doses of inhaled budesonide up to 800 micrograms daily may be preferable to low doses of prednisolone. Bone turnover remains to be evaluated during long-term treatment.

25-Hydroxyvitamin D 2↗

PubMed2001

Growth of heterotopic LNCaP prostate cancer tumor in nude mice is not affected by dietary calcium.

BACKGROUND: We attempted to provide experimental evidence linking increased dietary calcium to progression of prostate cancer, as suggested by some epidemiological studies, using a heterotopic prostate cancer nude mice model. METHODS: Twenty heterotopic LNCaP prostate cancer tumor bearing nude mice were randomly assigned to one of the four groups: (I) high fat/low calcium diet, (II) high fat and high calcium diet, (III) high fat diet fortified with Vitamin D3, and (IV) high fat and high calcium diet fortified with Vitamin D3. In addition to weekly animal weights and tumor size measurements, the serum prostate specific antigen (PSA), 25-hydroxy Vitamin D3, calcium, phosphorus, total protein, albumin (to account for bound calcium) [1], and serum alkaline phosphatase (a measure of bone loss) [2] were determined at the termination of experiments. RESULTS: Although the serum calcium and 25-hydroxy Vitamin D3 were significantly higher in groups III and IV compared to groups I and II (P < 0.05), there was no significant difference between the tumor growth rates, final tumor weights (P = 0.9), and the serum PSA levels (P = 0.94) between the four groups. CONCLUSIONS: The results suggest that dietary calcium does not significantly affect the growth of heterotopic LNCaP prostate cancer in nude mice.

Adenocarcinoma↗

PubMed1984

The effect of vitamin D3 metabolites on normal and leukemic bone marrow cells in vitro.

We studied the effects of 1,25-dihydroxyvitamin D3 and other metabolites of vitamin D3 on the maturation in liquid culture and on colony formation in semisolid media of marrow and buffy coat cells from patients with myeloid leukemias and from normal individuals. After incubation with 1,25-dihydroxy-vitamin D3, a proportion of both normal and leukemic myeloid cells resembled cells of the monocyte-macrophage lineage; these cells expressed alpha-naphthylacetate esterase and were able to phagocytize and kill candida organisms. When granulocyte-macrophage progenitor cells (CFU-GM) were incubated with 1,25-dihydroxyvitamin D3, the number of monocyte-macrophage colonies was increased and the number of granulocyte colonies was reduced; megakaryocyte colony formation (CFU-Mk) was inhibited substantially; and there was no effect on erythroid (BFU-E) or multilineage (CFU-GEMM) progenitor cell colony formation. We propose that 1,25-dihydroxyvitamin D3 may induce cells that are normally committed to differentiate along the granulocytic pathways to differentiate instead along the monocyte-macrophage pathway. If these in vitro observations reflect the in vivo activity of 1,25-dihydroxyvitamin D3, it may be involved in the modulation of collagen deposits in the bone marrow.

24,25-Dihydroxyvitamin D 3↗

PubMed1993

Vitamin D deficiency suppresses cell-mediated immunity in vivo.

Severe vitamin D deficiency has been produced in mice as evidenced by severe hypocalcemia and an absence of 25-hydroxyvitamin D in blood. Vitamin D deficiency was accompanied by a slight decrease in body weight and food consumption. Vitamin D-deficient and vitamin D-sufficient mice were sensitized with dinitrofluorobenzene (DNFB). Sensitivity to DNFB was determined by treatment of one ear with DNFB. The ratio of thickness of the treated ear to that of nontreated ear was used as an index of cell-mediated immune reaction. The incorporation of [3H]thymidine into the DNA of the ear was also used as an index of cell-mediated immunity as was the response of thymus lymphocytes to concanavalin A. Vitamin D deficiency markedly decreased the ear thickness ratio and the [3H]thymidine incorporation ratio in DNFB-sensitized mice. Similarly, the incorporation of [3H]thymidine into the DNA of concanavalin A-treated thymus lymphocytes from DNFB-sensitive mice was significantly reduced in vitamin D deficiency. These results show that in vivo vitamin D deficiency impairs cell-mediated immunity. The provision of a vitamin D-sufficient diet for 8 weeks corrected the impaired response of the immune system, while vitamin D administration for 3 weeks did not.

Animals↗

PubMed1996

Affinity labeling of rat serum vitamin D binding protein.

Vitamin D binding protein (DBP) plays an essential role in the vitamin D hormone endocrine system in sequestering vitamin D3 and its metabolites with high affinity, and transporting them to various target organs and tissues. In the present investigation, 25-hydroxyvitamin D3-3 beta-(1,2-epoxypropyl)ether (25-OH-D3-epoxide) and 25-hydroxyvitamin D3-3 beta-bromoacetate (25-OH-D3-BE), synthetic analogs of 25-hydroxyvitamin D3 (25-OH-D3), were developed as affinity alkylating reagents for the covalent modification of the 25-OH-D3-binding site in rat vitamin D binding protein (rDBP). Competitive radioligand binding assays of 25-OH-D3-BE and 25-OH-D3-epoxide with affinity-purified rDBP demonstrated that these analogs displaced 25-hydroxy[26(27)-3H]vitamin D3 (3H-25-OH-D3), specifically bound to rDBP, in a dose-dependent fashion. Incubation of rDBP samples with radiolabeled versions of these analogs, i.e., 3H-25-OH-D3-epoxide and 3H-25-OH-D3-BE, resulted in the covalent labeling of rDBP. This labeling was largely prevented when incubations were carried out in the presence of an excess of 25-OH-D3, the natural ligand for rDBP. Labeling-specificity by these analogs was further demonstrated by the covalent labeling, inhibited by coincubation with a large excess of 25-OH-D3, of a single protein band, upon incubating rat serum Cohn IV fraction with 3H-25-OH-D3-epoxide and 3H-25-OH-D3-BE. Collectively, these results strongly suggested that 3H-25-OH-D3-epoxide and 3H-25-OH-D3-BE covalently modified the 25-OH-D3-binding site in rDBP. The reagents described in this report could be important in mapping the 25-OH-D3-binding pocket in rDBP.

Affinity Labels↗

PubMed1998

Inhibition of 25-hydroxyvitamin D3 production by 1, 25-dihydroxyvitamin D3 in rats.

The regulation of the hepatic vitamin D3 25-hydroxylase enzyme system by 1,25-dihydroxyvitamin D3 was examined using male rats. Circulating 25-hydroxyvitamin D3 levels decreased in response to increasing doses of 1,25-dihydroxyvitamin D3 as determined by HPLC and serum protein binding assay. A maximum reduction in serum 25-hydroxyvitamin D3 of 57.7% was achieved by the administration of 1,25-dihydroxyvitamin D3 and higher doses produced no further reduction. The in vitro rate of vitamin D 25-hydroxylation by liver homogenates from rats given 1,25-dihydroxyvitamin D3 was also reduced by 60.4%. Whole rat extracts from animals given [3H]vitamin D3 contained 50.4% less 25-[3H]hydroxyvitamin D3 in treated rats given 1,25-dihydroxyvitamin D3 than in those given only the vehicle. Further, 1,25-dihydroxyvitamin D3 treatment had no effect on in vivo disappearance of 25-[3H]hydroxyvitamin D3. Taken together, these results demonstrate that the decrease in 25-hydroxyvitamin D3 levels observed in 1,25-dihydroxyvitamin D3-treated rats results from a decrease in production and not an increase in the metabolic clearance of 25-[3H]hydroxyvitamin D3.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed2000

Probing the vitamin D sterol-binding pocket of human vitamin D-binding protein with bromoacetate affinity labeling reagents containing the affinity probe at C-3, C-6, C-11, and C-19 positions of parent vitamin D sterols.

The multiple physiological properties of vitamin D-binding protein (DBP) include organ-specific transportation of vitamin D(3) and its metabolites, manifested by its ability to bind vitamin D sterols with high affinity. In the present investigation we probed the vitamin D sterol-binding pocket of human DBP with affinity labeling analogs of 25-hydroxyvitamin D(3) ¿25-OH-D(3) and 1, 25-dihydroxyvitamin D(3) ¿1,25(OH)(2)D(3) containing bromoacetate alkylating probe at C-3 (A-ring), C-6 (triene), C-11 (C-ring), and C-19 (exocyclic methylene) of the parent sterol. Competitive binding assays with DBP showed approximately 22-, 68-, and 2000-fold decrease in the binding of 1,25(OH)(2)-D(3)-11-BE, 25-OH-D(3)-3-BE, and 25-OH-D(3)-6-BE, respectively, compared to that seen with 25-OH-D(3), while there was no significant difference in the DBP-binding affinity of 25-OH-D(3)-19-BE and 25-OH-D(3). Surprisingly, ¿(14)C25-OH-D(3)-11-BE and ¿(14)C1, 25(OH)(2)-D(3)-19-BE failed to label DBP despite high-affinity DBP-binding, indicating the absence of any nucleophilic amino acid in the vicinity of their bromoacetate moiety to form a covalent bond, while these analogs are inside the binding pocket. In contrast, ¿(14)C25-OH-D(3)-6-BE and ¿(14)C25-OH-D(3)-3-BE specifically labeled DBP. BNPS-skatole digestion of DBP labeled with ¿(14)C25-OH-D(3)-3-BE or ¿(14)C25-OH-D(3)-6-BE produced two peptides (M(r) 17,400 and 33,840), with radioactivity associated with the N- and C-terminal peptides, respectively, raising the possibility that either different areas of the same vitamin D sterol-binding pocket, or different domains of DBP might be labeled by these analogs. Successful affinity labeling of recombinant domain I (1-203) of DBP with both reagents indicated that different areas of the same vitamin D-binding pocket (domain I) were labeled. These affinity analogs are potentially useful for "mapping" the vitamin D sterol-binding pocket and developing a functional model.

Acetates↗

PubMed1994

Vitamin D metabolites and extracellular calcium regulate calcium currents in hemocytes of land snails.

Intracellular exchangeable calcium and calcium efflux were investigated in cultured amoebocytes of land snails. Low extracellular calcium concentration (0.32 mM) initiated a rapid increase of outward calcium currents and decrease of intracellular exchangeable calcium. On the other hand, high extracellular calcium concentration (32 mM) increased intracellular exchangeable calcium. Actions of vitamin D metabolites were most prominent under non-physiological concentrations of extracellular calcium. Metabolite E activated a calcium pump while 25-hydroxy-vitamin D3 deactivated the pump. Both metabolites increased calcium transfer into stored pools.

Animals↗

PubMed1994

On the induction of 5-lipoxygenase expression and activity in HL-60 cells: effects of vitamin D3, retinoic acid, DMSO and TGF beta.

Induction of 5-LO activity in DMSO differentiated HL-60 cells, by the serum protein TGF beta, was partially dependent on the presence of serum lipids (Steinhilber, D., Hoshiko, S., Grunewald, J., Rådmark, O., and Samuelsson, B. (1993) Biochim. Biophys. Acta 1178, 1-8). Here we demonstrate that the serum lipid fraction can be substituted by picomolar concentrations of 1,25-dihydroxyvitamin D3 (VD3). A high concentration of VD3 (24 nM) gave a 4-fold induction of 5-LO mRNA, a 14-fold increase in 5-LO protein, and a 38-fold upregulation of the 5-LO activity of intact HL-60 cells after differentiation in the presence of DMSO and serum proteins for 4 days. Also VD3 alone gave a substantial upregulation of 5-LO protein expression and activity. On the other hand, TGF beta alone was a poor inducer of the 5-LO pathway, the presence of a differentiation inducer (retinoic acid, DMSO or VD3) was required. The most prominent induction of 5-LO protein expression and activity in cell homogenates and intact cells was observed when VD3 and TGF beta were combined.

Arachidonate 5-Lipoxygenase↗

PubMed1995

Binding of vitamin D to low-density-lipoprotein (LDL) and LDL receptor-mediated pathway into cells.

The present study was undertaken to identify serum components other than vitamin D-binding proteins that bind to 1,25(OH)2 D3, and its analog. The binding rate of 1,25(OH)2 D3, 22-oxa-1,25(OH)2D3 (OCT) or 25(OH) D3 to total lipoprotein(TLP) represented 16.7%, 4.65%, and 3.11% of total counts added, respectively. Polyacrylamide gel electrophoresis of the TLP revealed that 1,25(OH)2 D3 and OCT were associated with LDL. The binding studies of OCT-bound LDL to the fibroblasts showed specific pathway to the cells mediated by LDL-receptor. These findings may have important implications in understanding the mechanisms of the diverse biological actions of 1,25(OH)2 D3 and in designing a novel delivery system for vitamin D analogs.

Apolipoprotein B-100↗