The Use of Radioactive Phosphorus in the Assay of Vitamin D

Numerof, Paul; Sassaman, H. L.; Rodgers, Allegra; Schaefer, Arnold E.

doi:10.1093/jn/55.1.13

Cited by 30 publications

(10 citation statements)

References 2 publications

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“…Rachitic group (R): Vitamin D-deficient, low phosphate diet [8], consisting of the following: yellow corn 75.6%, wheat gluten 19.9%, CaCQ 3.0%, NaC 1 1%, lycine monhydrochloride 0.5%, thiamine hydrochloride 0.0002%, riboflavin 0.0004%; niacin 0.001%; Ca pantothenate 0.0004%.…”

Section: Methodsmentioning

confidence: 99%

Changes in bone mineral in experimentally induced rickets in the rat: Electron microprobe and chemical studies

et al. 1980

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Summary. The elemental composition of trabecular bone was compared for: (a) rats made rachitic on a low phosphorus, vitamin D-deficient diet; (b) rats fed the same diet but supplemented with vitamin D; (c) normal rats fed a standard laboratory diet with normal phosphorus and vitamin D levels.Quantitative energy dispersive X-ray microanalysis was performed on mineralized bone matrix at four sites: (1) clusters of mineral crystals in osteoid; (2) bone matrix adjacent to osteoid containing mineralization clusters: (3) peri-lacunar bone matrix; and (4) deep bone matrix distant from osteocytes. Estimations were also made of serum calcium, phosphorus, and 25-hydroxy-vitamin D, and of calcium, phosphorus, and hydroxyproline in whole bone.At bone sites 2, 3, and 4, the mineral content was greater in the normal group than in the other two groups.At each site, the mineral content of the rachitic bone matrix was greater than that from the vitamin D-treated group.A normal pattern of increasing mineral content with distance into the bone from a recently mineralized border was found in the normal and vitamin Dtreated groups but was notably absent in the rachitic bones.Microprobe measurements of Ca:P molar ratios in hydroxyapatite standards and in normal rat bone were approximately 1.7. In both rachitic and vitamin D-treated bones, the Ca:P molar ratio was significantly higher than that in normal bones and correlated with serum Ca:P ratios.It is suggested that the increased Ca:P ratios in the rachitic and vitamin D-treated bones may be explained by an increased carbonate deposition.Senti ofl~n'int rcquc~t.s to D.W. Dempster at the above address.

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Section: Methodsmentioning

confidence: 99%

Changes in bone mineral in experimentally induced rickets in the rat: Electron microprobe and chemical studies

et al. 1980

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“…Weanling black-hooded rats, housed in overhanging wire cages, were made rachitic as diagnosed radiologically by feeding a vitamin D-deficient low P diet (0.25%) [14] for a 21-25 day period. Plasma 25OHD~ levels were measured by competitive protein binding assay [15] in a sample of five rats.…”

Section: Animalsmentioning

confidence: 99%

Histological observations on the failure of rachitic rat bones to respond to 1,25/OH)2D3

Gallagher

Lawson

1980

Calcif Tissue Int

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Rachitic rats, maintained on diets with low or normal P contents, were given daily intraperitoneal doses of 1,25(OH)2D3 or 25OHD3 at levels of 100 or 200 ng. Plasma chemistry was measured and the ash content and histological appearance of the bones investigated. Using labeled material it was shown that the dosing levels of 1,25(OH)2D3 employed ensured a higher than normal plasma concentration of that metabolite over the period between doses. 1,25(OH)2D3 was not effective as 25OHD3 in raising bone ash or reducing the amount of osteoid. The difference between the effects of the metabolites was evident at both dietary P levels, but more marked at the higher P level. In contrast, the metabolites reduced the width of the epiphyseal plate to an approximately similar degree, and this is possibly the reason why there are discrepancies between previous reports of the effectiveness of 1,25(OH)2D3 compared with 25OHD3 or vitamin D3. Dosing with 1,25(OH)2D3 failed to maintain a constant plasma Pi value over the period between doses in animals fed the low P diet.

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“…Piebald weanling rats were raised on a vitamin D-deficient diet as described by Numerof, Sassaman, Rodgers & Schaefer (1955). After 2-3 weeks, blood was collected by intracardial puncture, and serum prepared.…”

Section: Preparation Of Binding Proteinmentioning

confidence: 99%

Competitive Protein-Binding Assay for 25-Hydroxycholecalciferol

et al. 1974

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911 Comment Increases in osteoid volume with sodium fluoride, calcium, and vitamin D treatment are well documented. Small decreases in mineralisation rate have also been reported.2 But osteomalacia in the presence of high plasma 25-OHD concentrations has not been described in patients treated with this regimen. The plasma 1,25-(OH)2D3 concentration in our patient was just below the lower limit of normal, but the total plasma 1,25-(OH)2D (1,25-(OH)2D2-+1,25-(OH)2D3) concentration was probably normal since she was taking vitamin D2 and the radioimmunoassay did not measure plasma 1,25-(OH)2D2. The mechanisms by which fluoride may produce osteomalacia despite high plasma 25-OHD concentrations require further investigation. Possibilities include fluoride-induced end-organ resistance in bone to active vitamin D metabolites or an effect of fluoride on processes of bone mineralisation that are unaffected by vitamin D metabolites. Alternatively, fluoride might affect the metabolism of 25-OHD to other metabolites. Although lack of calcium supplements was probably unimportant in our patient, since the plasma calcium concentration remained above 2 40 mmol,l throughout treatment and dietary calcium intake was adequate, we cannot exclude it as a factor in the development of osteomalacia. Our results indicate that vitamin D in doses that produce high plasma 25-OHD concentrations does not protect against fluoride-induced mineralisation defects and that patients treated with this regimen require careful supervision. Trans-iliac biopsy provides a sensitive method for diagnosing generalised bone disease such as osteomalacia and may be necessary to detect its development when, as in our patient, plasma biochemical changes are not diagnostic. We thank J Sainsbury Ltd and the Special Trustees, St Thomas's Hospital, for generous financial support, and Dr T L Clemens, the Middlesex Hospital, London, WI, for 1,25-(OH)2D3 assays. Jowsey J, Riggs BL, Kelly PJ, Hoffman DL. Effect of combined therapy with sodium fluoride, vitamin D and calcium in osteoporosis. AmJ Med 1972 ;53 :43-9. 2 Meunier PJ, Bressot C, Vignon E, et al. Radiological and histological evolution of post-menopausal osteoporosis treated with sodium fluoride, vitamin D, and calcium. Preliminary results. In: Courvoisier B, Donath A, Baud CA, eds. Fluoride and bone. Berne: Hans Huber, 1978:263-76. 3Cass RM, Croft JD, Perkins P, Nye W, Waterhouse C, Terry R. New bone formation in osteoporosis following treatment with sodium fluoride.

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The Use of Radioactive Phosphorus in the Assay of Vitamin D

Cited by 30 publications

References 2 publications

Changes in bone mineral in experimentally induced rickets in the rat: Electron microprobe and chemical studies

Changes in bone mineral in experimentally induced rickets in the rat: Electron microprobe and chemical studies

Histological observations on the failure of rachitic rat bones to respond to 1,25/OH)2D3

Competitive Protein-Binding Assay for 25-Hydroxycholecalciferol

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