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PubMed1979

Analysis of fat-soluble vitamins. XXI. High pressure liquid chromatographic assay methods for vitamin D in vitamin D concentrates.

Two high pressure liquid chromatographic methods, a straight and a reverse phase system, were developed and compared with the official (chemical) AOAC method for vitamin D concentrates. The effects of the systematic error and the reproducibility of using an internal or external standard were studied, as well as the effect of using peak height or peak height X retention time for calculating the potential vitamin D content. A method is given for determining the conversion factor to calculate previtamin D as vitamin D. Based on the results of the comparison, the following conditions were selected for collaborative study: straight phase, amyl alcohol-hexane mobile phase, external standard, and calculation of potency by peak height.

Cholecalciferol↗

PubMed2002

Signaling of monocytic differentiation by a non-hypercalcemic analog of vitamin D3, 1,25(OH)2-5,6 trans-16-ene-vitamin D3, involves nuclear vitamin D receptor (nVDR) and non-nVDR-mediated pathways.

Exposure of leukemia cells to the physiologically active form of vitamin D3, 1,25-dihydroxyvitamin D3 (1,25D3) normalizes their phenotype to cells that resemble mature monocytes. One of the earliest detectable events in this process is an upregulation of the nuclear receptor for 1,25D3, the vitamin D receptor (nVDR). In contrast, the novel analog of 1,25D3, 1,25-dihydroxy-5,6 trans-16-ene-vitamin D3 (5,6-16D3), which has recently been reported to have low calcium-mobilizing activity in vivo, rapidly induced the expression of CD14, CD11b, and monocyte-specific esterase (MSE), classical markers of the mature monocyte, but upregulated nVDR expression less than 1,25D3. This upregulation was shown to be the result of altered degradation of the nVDR protein, while the levels of nVDR mRNA were constant. Knock-out of nVDR transcriptional activity by a decoy VDRE double-stranded deoxyoligonucleotide, markedly abrogated 1,25D3-induced differentiation, but incompletely inhibited 5,6-16D3-induced differentiation. These findings suggest that the unique ability of 5,6-16D3 to induce cell differentiation but not systemic hypercalcemia, may be due to the activation of pathways which initiate differentiation independently of nVDR.

Antineoplastic Agents↗

PubMed1996

Induction of gap junctional intercellular communication by vitamin D in human skin fibroblasts is dependent on the nuclear Induction of gap junctional intercellular communication by vitamin D in human skin fibroblasts is dependent on the nuclear vitamin D receptor.

The physiologically active metabolite of vitamin D, 1alpha,25-dihydroxyvitamin D3 (calcitriol), induces gap junctional intercellular communication in human skin fibroblasts 161BR at a concentration of 10(-7) M. In human skin fibroblasts, FIB5, devoid of a functional nuclear vitamin D receptor (VDR), there is no effect on gap junctional intercellular communication. Parallel to the increase in cell-cell communication, we observed a VDR-dependent increase in connexin43 protein and connexin43 mRNA levels. These results suggest that 1alpha,25-dihydroxyvitamin D3 affects gap junctional intercellular communication at the level of transcription or of mRNA stability via the nuclear VDR.

Calcitriol↗

PubMed1994

1,25-Dihydroxy-24-OXO-16ene-vitamin D3, a renal metabolite of the vitamin D analog 1,25-dihydroxy-16ene-vitamin D3, exerts immunosuppressive activity equal to its parent without causing hypercalcemia in vivo.

The hormone, 1,25-(OH)2D3, is metabolized into 1,25-(OH)2-24-OXO-D3, in kidney prior to conversion to its final inactive product, calcitroic acid. Similarly, 1,25-(OH)2-24OXO-16eneD3, is produced in the kidney from the Vitamin D analog, 1,25-(OH)2-16eneD3, but resists further hydroxylation. The analog's metabolite was synthesized and its biologic activity compared to the parent compound. Naive SJL/J mice, 4 weeks old, were immunized with neuroantigen in adjuvant to induce experimental autoimmune encephalomyelitis [EAE]. Treatment with 1,25-(OH)2-24OXO-16eneD3 was given at 0.05, 0.15 and 0.3 microgram I.P., on alternate days, starting 3 days prior and for up to 5 days post immunization and compared to a similar treatment with 0.1 microgram 1,25-(OH)2D3 or 1,25-(OH)2-16eneD3. Suppression of EAE was observed with 0.15 microgram 1,25-(OH)2-24OXO-16eneD3, comparable to the suppression induced with the parent compound and more potent than 1,25-(OH)2D3. However, no hypercalcemia was seen in mice treated with 0.15 microgram of OXO-metabolite (9.7 +/- 0.6 vs 9.3 +/- 1.1 mg/dl, treated vs controls), in contrast to 1,25-(OH)2D3 and 1,25-(OH)2-16eneD3 (11.2 +/- 1.0 and 11.0 +/- 0.9 mg/dl respectively; p < 0.001). In summary, our results suggest that 1,25-(OH)2-24OXO-16eneD3, a stable intermediary metabolite of the vitamin D analog, 1,25-(OH)2-16eneD3 exerts immunosuppressive activity equal to its parent without causing hypercalcemia in vivo.

Animals↗

PubMedDate not supplied

[Use of the magnitude of vitamin and vitamin metabolite excretion as indicators of availability of vitamins B2, B6, and niacin].

Alimentary deficiency of riboflavin in rats caused a decrease in excretion of vitamin B2 with urine simultaneously with lowering in daily excretion of 4-pyridoxylic acid (4-PA) and N1-methyl nicotinamide (N1-MNA); these patterns are usually used as indicators of pyridoxine and niacin availability. The similar decrease in excretion of 4-PA and N1-MNA with urine but without alterations in NAD+NADP concentrations in erythrocytes was detected in women deficient in vitamin B2. Content of nicotinamide coenzymes in erythrocytes correlated with excretion of N1-MNA with urine only under normal conditions of riboflavin availability. Use of the criteria involving rates of 4-PA and N1-MNA excretion for evaluation of pyridoxine and niacin deficiency is discussed.

Adult↗

PubMed1985

Vitamin E and vitamin C plasma levels in premature infants following supplementation of vitamin C.

Our preliminary data suggest that supplementation of premature neonates with vitamin C is required to maintain adequate ascorbate plasma levels and may have a sparing effect on vitamin E metabolism. Further studies are required to validate our findings and evaluate the possible antioxidant advantage of ascorbic acid administration.

Ascorbic Acid↗

PubMed1992

Normal 24-hydroxylation of vitamin D metabolites in patients with vitamin D-dependency rickets type I. Structural implications for the vitamin D hydroxylases.

The steady state serum concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2D] is determined by the relative rates of its biosynthesis via the renal mitochondrial 1-hydroxylase and catabolism via renal and target cell 24-hydroxylases. It is not yet known whether the two catalytic activities are mediated by the product of a single gene or products of distinct genes. To address this question, we undertook to assess 24-hydroxylase function in patients with vitamin D-dependency rickets type I (VDDR-I), a Mendelian disorder of 1,25-(OH)2D synthesis attributable to a defect in renal 1-hydroxylase activity. To assess renal 24-hydroxylase activity, we measured the serum concentration of 24,25-dihydroxyvitamin D [24,25-(OH)2D] and its 25-hydroxyvitamin D (25OHD) precursor. We also measured target cell, 1,25-(OH)2D3-inducible 24-hydroxylase activity and calcitroic acid production in skin fibroblasts from VDDR-I patients and age- and sex-matched controls. Serum levels of 24,25-(OH)2D and 25OHD were similar in VDDR-I patients and controls [ratio of product to substrate, 0.062 +/- 0.013 (n = 5) vs. 0.067 +/- 0.005 (n = 10), mean +/- SEM, for patients and controls, respectively]. Circulating levels of 1,25-(OH)2D were also comparable in both groups [80.6 +/- 15.5 (n = 5) vs. 86.1 +/- 5.2 (n = 10) pmol/L, for patients and controls, respectively], presumably indicative of compliance with calcitriol therapy. Skin fibroblasts from VDDR-I patients exhibited 24-hydroxylase activity which was indistinguishable from that observed in control fibroblasts [108 +/- 14 (n = 5) vs. 96 +/- 25 fmol/10(6) cells.min (n = 6), for patients and controls, respectively]. Similarly, calcitroic acid production was comparable in fibroblast cultures derived from the two groups of subjects [31 +/- 6 vs. 33 +/- 3 fmol/10(6) cells.min (n = 3), for patients and controls, respectively]. Our data demonstrate that renal and target cell 24-hydroxylase activities are normal in patients with VDDR-I and suggest that the renal 1- and 24-hydroxylases likely represent, or contain, distinct polypeptides encoded by different genes.

24,25-Dihydroxyvitamin D 3↗

PubMed1983

Biological activity assessment of the vitamin D metabolites 1,25-dihydroxy-24-oxo-vitamin D3 and 1,23,25-trihydroxy-24-oxo-vitamin D3.

Two new metabolites of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], namely 1,25(OH)2-24-oxo-vitamin D3 and 1,23,25(OH)3-24-oxo-vitamin D3, have been prepared in vitro using chick intestinal mucosal homogenates. To investigate the binding of 1,25(OH)2-[23-3H]-24-oxo-D3 and 1,23,25(OH)3-[23-3H]-24-oxo-D3 to the chick intestinal receptor we have isolated both metabolites in radioactive form using an incubation system containing 1,25(OH)2-[23,24-3H))-D3 with a specific radioactivity of 5.6 Ci/mmol. Both metabolites were highly purified by using Sephadex LH-20 chromatography followed by high-pressure liquid chromatography (HPLC). Sucrose density gradient sedimentation analysis showed specific binding of both tritium-labeled metabolites to the chick intestinal cytosol receptor. Experiments were carried out to determine the relative effectiveness of binding to the chick intestinal mucosa receptor for 1,25(OH)2D3. The results are expressed as relative competitive index (RCI), where the RCI is defined as 100 for 1,25(OH)2D3. Whereas the RCI obtained for 1,25(OH)2-24-oxo-D3 was 98 +/- 2 (SE), the RCI for 1,23,25(OH)3-24-oxo-D3 was only 28 +/- 6 (SE). Also, the biological activity of both new metabolites was assessed in vivo in the chick. In our assay for intestinal calcium absorption, 1,25(OH)2-24-oxo-D3 was active at a dose level of 1.63 and 4.88 nmol/bird (at 14 h), whereas 1,23,25(OH)3-24-oxo-D3 showed only weak biological activity in this system. In our assay for bone calcium mobilization, administration of both new metabolites showed modest activity at the 4.88-nmol dose level, which was reduced at the 1.63-nmol dose level. The results indicate that biological activity declines as 1,25(OH)2D3 is metabolized to 1,24R,25(OH)3D3, 1,25(OH)2-24-oxo-D3, and then 1,23,25(OH)3-24-oxo-D3.

Animals↗

PubMed1996

1alpha,25-dihydroxy-24-oxo-16-ene vitamin D3, a metabolite of a synthetic vitamin D3 analog, 1alpha,25-dihydroxy-16-ene vitamin D3, is equipotent to its parent in modulating growth and differentiation of human leukemic cells.

1alpha,25(OH)2-16-ene-D3, a synthetic analog of the steroid hormone, 1alpha,25(OH)2D3, has great potential to become a drug in the treatment of leukemia and other proliferative disorders, because of its minimal in vivo calcemic activity associated with a potent inhibitory effect on cell growth. However, at present, the mechanisms through which 1alpha,25(OH)2-16-ene-D3 expresses its biological activities are still not completely understood. Our previous in vitro study in a perfused rat kidney indicated for the first time that 1alpha,25(OH)2-16-ene-D3 and 1alpha,25(OH)2D3 are metabolized differently. 1alpha,25(OH)2-24-oxo-16-ene-D3, an intermediary metabolite of 1alpha,25(OH)2-16-ene-D3 formed through the C-24 oxidation pathway, accumulated significantly in the perfusate when compared to 1alpha,25(OH)2-24-oxo-D3, the corresponding intermediary metabolite of 1alpha,25(OH)2D3. In a subsequent in vivo study, we also reported that 1alpha,25(OH)2-24-oxo-16-ene-D3 exerted immunosuppressive activity equal to its parent, without causing significant hypercalcemia. In order to establish further the critical role of 1alpha,25(OH)2-24-oxo-16-ene-D3, in generating some of the key biological activities ascribed to its parent, we performed the present in vitro study using a human myeloid leukemic cell line (RWLeu-4) as a model. Comparative target tissue metabolism studies indicated that 1alpha,25(OH)2-16-ene-D3 and 1alpha,25(OH)2D3 are metabolized differently in RWLeu-4 cells, and the differences were similar to the ones we previously observed in the rat kidney. The significant finding was the accumulation of 1alpha,25(OH)2-24-oxo-16-ene-D3 in RWLeu-4 cells because of its resistance to further metabolism. Biological activity studies indicated that both 1alpha,25(OH)2-16-ene-D3 and its 24-oxo metabolite produced growth inhibition and promoted differentiation of RWLeu-4 cells to the same extent, and these activities were several fold higher than those exerted by 1alpha,25(OH)2D3. In addition, the genomic action of each vitamin D compound was assessed in a rat osteosarcoma cell line (ROS 17/2.8) by measuring its ability to transactivate a gene construct containing the vitamin D response element of the osteocalcin gene linked to the growth hormone reporter gene. In these studies, both 1alpha,25(OH)2-16-ene-D3 and its 24-oxo metabolite exerted similar but potent transactivation activity which was several fold greater than that exerted by 1alpha,25(OH)2D3 itself. In summary, our results indicate that the production and slow clearance of the bioactive intermediary metabolite, 1alpha,25(OH)2-24-oxo-16-ene-D3, in RWLeu-4 cells contributes significantly to the final expression of the enhanced biological activities ascribed to its parent analog, 1alpha,25(OH)2-16-ene-D3.

Calcitriol↗

PubMed1998

Total synthesis of 25-hydroxy-16,23E-diene vitamin D3 and 1 alpha,25-dihydroxy-16,23E-diene vitamin D3: separation of genomic and nongenomic vitamin D activities.

Separation of genomic and nongenomic vitamin D activities was achieved by structural modification of 1,25-dihydroxy vitamin D3 by introduction of 16 and 23E double bonds. The modified compound 3, lacking a 1 alpha-hydroxy group, exhibits only nongenomic activity. Its 1 alpha-hydroxy relative 4 expresses fully both genomic and non-genomic activities. A total synthesis of analogues 3 and 4 is described.

Animals↗

PubMed1996

Antagonistic effects of transforming growth factor-beta on vitamin D3 enhancement of osteocalcin and osteopontin transcription: reduced interactions of vitamin D receptor/retinoid X receptor complexes with vitamin E response elements.

Osteocalcin and osteopontin are noncollagenous proteins secreted by osteoblasts and regulated by a complex interplay of systemic and locally produced factors, including growth factors and steroid hormones. We investigated the mechanism by which transforming growth factor-beta (TGF beta) inhibits 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3)-enhanced expression of the osteocalcin (OC) and osteopontin (OP) genes. ROS 17/2.8 cells, in which both genes are expressed, were transfected with reporter constructs driven by native (i.e. wild-type) rat OC and mouse OP promoters. TGF beta abrogated the 1,25-(OH)2D3 enhanced transcription of both the OC and OP genes. The inhibitory TGF beta response for each requires vitamin D response element (VDRE) sequences, although there are additional contributions from proximal basal regulatory elements. These transcriptional effects were further investigated for contribution of the trans-activating factors, which interact with OC and OP VDREs, involving the vitamin D receptor (VDR) and retinoid X receptor (RXR). Gel mobility shift assays show that TGF beta significantly reduces induction of the heterodimers VDR/RXR complexes in 1,25-(OH)2D3-treated ROS 17/2.8 cells. However, Western blot and ligand binding analysis reveal that TGF beta does not affect nuclear availability of the VDR. We also show that activator protein-1 activity is up-regulated by TGF beta; thus, activator protein-1 binding sites in the OC promoter may potentially contribute to inhibitory effects of TGF beta on basal transcription. Our studies demonstrate that the inhibitory action of TGF beta on the 1,25-(OH)2D3 enhancement of OC and OP transcription in osteoblastic cells results from modulations of protein-DNA interactions at the OC and OP VDRE, which cannot be accounted for by changes in VDR protein levels. As OC and OP participate in bone turnover, our results provide insight into the contributions of TGF beta and 1,25-(OH)2D3 to VDR-mediated gene regulatory mechanism operative in bone formation and/or resorption events.

Animals↗

PubMed1961