Effect of aluminum on bone and cell localization.
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Aluminum↗
Biomedical subjects
S Balsan
Publications and source records attributed to S Balsan.
Mitochondrial calcium and bone mineralization in the rat fetus.
The initial mineralization of the tibial bone collar of 17-day-old rat fetuses has been investigated. Images obtained after glutaraldehyde-paraformaldehyde-OsO4 fixation were compared to those obtained after K-pyroantimonate (PAO) fixation. Ca, P and Sb were identified and Ca/P intensity ratios evaluated by wavelength dispersive X-ray microanalysis. Alkaline phosphatase was detected on decalcified sections. Some osteoblasts showed degenerative changes and free mitochondria could be seen within the osteoid on the prolongation of their cytoplasmic processes. The mitochondria contained mineralized granules and clusters. Similar granules, numerous clusters and few matrix vesicles were observed within osteoid. The Ca/P intensity ratios (PAO fixed sections) of mitochondrial mineral (11.5 +/- 2.54) were different from the ratio of crystalline mineral in matrix vesicles (1.52 +/- 0.07). Alkaline phosphatase was present along plasmalemma of osteoblasts and around mineral deposits. These results show that in the rat fetus osteoblast mitochondria may be extruded from the cells, and that mitochondrial granules may represent the first mineral deposits in osteoid.
Animals↗
Elevated plasma 1,25-dihydroxyvitamin D concentrations in infants with hypercalcemia and an elfin facies.
We measured plasma concentrations of 1,25-dihydroxyvitamin D (1,25-(OH)2D) in the course of a 6-to-37-month survey of four children with hypercalcemia and an elfin facies (Williams syndrome). Levels of 1,25-(OH)2D were elevated (160 to 470 pg per milliliter) during the hypercalcemic phase of the disease, when the children were five to nine months old, and they decreased thereafter. Plasma 1,25 (OH)2D levels were higher than those found in three children (16 to 60 months old) with the elfin facies syndrome and no hypercalcemia (42 to 71 pg per milliliter) and eight children (1 to 36 months old) with hypercalcemia and no dysmorphy (12 to 140 pg per milliliter), including two children with vitamin D intoxication. Hypercalcemia in the three children with elfin facies was controlled by a low-calcium diet. Serum calcium levels fell to the normal range, and plasma 1,25-(OH)2D levels were normal for age (18 to 105 pg per milliliter) at 14 to 47 months of age, even after appropriate therapy had been discontinued. These observations suggest that hypercalcemia may be the consequence of abnormal synthesis or degradation of 1,25-(OH)2D in children with the elfin facies syndrome.
Calcitriol↗
1,25 Dihydroxyvitamin D3 is required for growth-independent expression of alkaline phosphatase in cultured rat osteoblasts.
Osteoblastic cells were isolated from periosteum-stripped parietal bones of neonatal rat calvaria, seeded at low density (5,000 cells/35 mm of Falcon dish), and cultured for 6 days in BGJ medium supplemented with 20% of vitamin D-depleted FCS or vitamin D and calcium-depleted FCS, with daily addition of 1,25 dihydroxyvitamin D3 (10(-9) M) or 24,25-dihydroxyvitamin D3 (10(-9) M). Plating efficiency, clonal growth (number and size distribution of the colonies formed), and the alkaline phosphatase phenotype were evaluated on days 2 and 6 of culture. (1) Culture for 6 days in media not supplemented with 1,25(OH)2D3 led to a significant (P less than 0.001) loss of the alkaline phosphatase phenotype of the osteoblastic cells; the loss was greater in proliferating cells than in nonproliferating ones and occurred in both 0.12 mM or 1.1 mM ionized calcium concentrations. (2) Daily addition of 1,25(OH)2D3 (10(-9) M) but not 24,25(OH)2D3 maintained the basal percentage of Alk Pase positive cell units in non-proliferating cells and significantly reduced the loss of this phenotype in proliferating colonies. (3) This effect did not stem from an action of the hormone on cell growth. 1,25(OH)2D3 was also found to enhance the adhesiveness of the seeded osteoblasts, irrespective of the medium calcium concentration.
Alkaline Phosphatase↗
Vitamin D metabolite effects on membrane potential and potassium intracellular activity in rabbit cartilage.
In rabbit cartilage growth plates, the membrane potential, Vm, and potassium intracellular activities, alpha iK, were determined in order to study the effects of long-term (48 h) and short-term (1-2 min) exposures to vitamin D metabolites. Results are as follows: (i) in proliferative cells, Vm was -55.6 +/- 0.2 mV, n = 30, and alpha ik = 50.8 +/- 4.2 mM, n = 22; (ii) in hypertrophic cells, Vm was -35.5 +/- 0.8 mV, n = 88, and alpha iK = 85.1 +/- 5.4 mM, n = 20; (iii) Vm (-44.0 +/- 1.0 mV, n = 33) and alpha iK (114.7 +/- 8.7 mM, n = 14) were increased in metatarsal hypertrophic cells incubated with 10(-10)M of 1,25(OH)2D3 but were unaffected by the presence of 24,25(OH)2D3; (iv) an hyperpolarization of Vm was observed after short-term exposure of the hypertrophic cells to 10(-10)M of 1,25(OH)2D3 (-2.2 +/- 0.2 mV, n = 34) and 24,25(OH)2D3 (-2.2 +/- 0.7 mV, n = 17) but not to 25(OH)D3 (+0.3 +/- 0.8 mV, n = 10).
24,25-Dihydroxyvitamin D 3↗
[Circulating metabolites of vitamin D in 14 children with hypercalcemia].
Circulating vitamin D metabolite concentrations, i.e. 25-(OH)D, 24,25-(OH)2D, 1,25-(OH)2D have been assayed in 14 hypercalcemic children. Results are as follows: a) Children with vitamin D intoxication (n = 2) had elevated serum 25-(OH)D and 24,25-(OH)2D concentrations but their 1,25-(OH)2D concentrations were similar to those found in normocalcemic children (10-110 pg/ml); b) Children with familial idiopathic hypercalcemia and hypocalciuria (n = 5), children with hypercalcemia and either Bartter's syndrome (n = 1), hemangiomatosis (n = 1), osteopetrosis after medullary graft (n = 1), also had 1,25-(OH)2D concentrations in the normal range; c) In contrast, 1,25-(OH)2D were elevated (160-470 pg/ml) in the four children with severe idiopathic hypercalcemia and elfin facies.
24,25-Dihydroxyvitamin D 3↗
Skin calcium-binding protein: effect of vitamin D deficiency and vitamin D treatment.
The amount of skin calcium-binding protein, evaluated using a sensitive radioimmunoassay and indirect immunofluorescence, was decreased in vitamin-D deficient rats and increased after one week vitamin D3 or 1 alpha-hydroxyvitamin D3 treatment. In vitamin D replete and in vitamin D-deficient animals, skin calcium-binding protein was not sensitive to changes in dietary and/or serum calcium concentrations. These results indicate that this protein is different from other calcium-binding proteins such as parvalbumin and calmodulin which are not vitamin D-dependent, and also different from intestinal calcium-binding protein which, in D replete animals, is sensitive to changes in dietary and serum calcium concentrations. Skin calcium-binding protein may, therefore, represent a new class of vitamin D-dependent protein.
Animals↗
Hereditary resistance to 1,25-dihydroxyvitamin D.
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24,25-Dihydroxyvitamin D 3↗
Bone ultrastructure and x-ray microanalysis of aluminum-intoxicated hemodialyzed patients.
In hemodialyzed patients aluminum (Al) intoxication may induce osteomalacic lesions which are mainly observed when plasma immunoreactive parathyroid hormone (iPTH) concentrations are low, and osteitis fibrosa absent. In this study, the bone tissue of eight hemodialyzed patients with elevated plasma and bone Al concentrations was examined by histomorphometry, electron microscopy, and x-ray microanalysis. Five patients (group 1) had osteomalacia and minimal osteitis fibrosa, three patients (group 2) had severe osteitis fibrosa. In group 1, Al was concentrated at the mineralizing front, in hexagonal structures measuring 200 to 1,000 A which also contained phosphorus, but not calcium. Hydroxyapatite needles had a normal aspect. Osteoblasts appeared inactive. In group 2, Al was also present at the mineralizing layer of osteoid, but, in these cases, in small clusters next to abnormal calcium deposits. Osteoblasts appeared very active. Their mitochondria contained calcium and phosphorus granules, or amorphous material, measuring 1,500 to 2,000 A, emitting x-rays characteristic for Al and phosphorus. These results suggest that secondary hyperparathyroidism, by stimulating the cellular activity, may increase the uptake and release of Al by the osteoblasts. The presence of Al within the mitochondria of these cells may be one of the factors inducing the mineralization defect.
Adult↗
Alterations in rat epidermis provoked by chronic vitamin D deficiency.
Long-term effects of vitamin D deficiency on epidermis were studied using histometric techniques, [3H]thymidine incorporation into DNA (labeling index), estimation of epidermal acid phosphatase activity, and one-dimensional gel electrophoresis of keratin proteins. The decrease in epidermal thickness due to a reduced number of granular cell layers and a lower level of epidermal acid phosphatase activity were observed in vitamin D-deficient rats. The number of nuclei in the basal layer was increased. No changes in labeled index due to chronic vitamin D deficiency or to 'single injection of 1,25-dihydroxycholecalciferol to vitamin D-deficient rats were observed. A comparative study of the keratin composition revealed differences in the keratin polypeptide pattern: vitamin D-deficient epidermis specifically lacked two low-molecular-weight components and presented several quantitative differences among other keratin polypeptides. The changes in epidermal morphology and metabolism that took place with vitamin D deficiency were independent of plasma calcium levels because similar modifications were present in vitamin D-deficient but normocalcemic rats (fed a diet rich in calcium and supplemented with lactose). These findings suggest that vitamin D may be one of the important factors for maintaining normal epidermal structure and metabolism through an effect on cell differentiation and formation of granular cell layers. They offer the possibility of using epidermal modification as an additional marker of vitamin D deficiency.
Acid Phosphatase↗
Rat endometrial cells in primary culture: effects and interaction of sex hormones and vitamin D3 metabolite on alkaline phosphatase.
The present study was undertaken: 1) to investigate and compare the effects of two sex steroids, 17 beta-estradiol and progesterone, and two vitamin D3 metabolites, 24,25-dihydroxyvitamin D3 (24,25-(OH)2D3) and 1,25-dihydroxyvitamin D3 (1,25-OH)2D3) on the alkaline phosphatase activity (AP) of cultured endometrial cells of ovariectomized animals; 2) to see whether the in vitro or in vivo sex steroid pretreatment modifies the cellular AP responses to these vitamin D3 metabolites. Cells were cultured in Dulbecco's medium with 10% fetal calf serum until confluency and then for 18 h in a serum-free medium. All subsequent studies were performed in a fresh fetal calf serum-free medium. Results show that: 1) in endometrial cells from untreated ovariectomized rats, 17 beta-estradiol (10(-9) M) or progesterone (10(-9) M) induces increases in AP (40% or 30%) after 2- to 4-h incubation, respectively. A maximal increasing effect (20%) is observed with 24,25-(OH)2D3 (10(-9) M) after 4-h incubation contrasting with the total lack of action of 1,25-(OH)2D3 whatever the concentration (10(-13) to 10(-7) M) and the incubation time (1-18 h) tested. 2) After in vivo or in vitro pretreatment with each sex hormone taken separately, both 24,25-(OH)2D3 and 1,25-(OH)2D3 decrease AP whereas after pretreatment with sex steroids in association, these vitamin D3 metabolites induce an increase in AP. In conclusion, these data show that endometrial cell AP is sensitive to 24,25-(OH)2D3 and 1,25-(OH)2D3 and that the AP response of these cells is modulated by the presence of 17 beta-estradiol and/or progesterone.
Alkaline Phosphatase↗
Genome-independent effects of 1,25-dihydroxy vitamin D-3 on membrane potential.
Cell membrane potential, Vm, was monitored in rabbit hypertrophic cartilage metatarsals, amphibian proximal tubule and muscle cells during application of 1,25-dihydroxy vitamin D-3, 25-hydroxy vitamin D-3 or cholesterol (10(-10) M). 1,25-Dihydroxy vitamin D-3 elicited quick variations of Vm (in less than 1 min) in proximal tubular cells (whether injected in the lumen or in peritubular capillaries) and in cartilage. The precursor 25-hydroxy vitamin D-3 and cholesterol produced a small shift of Vm in proximal tubule only when applied from the luminal side, but this change was significantly smaller than that observed with 1,25-dihydroxy vitamin D-3. Muscle cells were unresponsive to both metabolites and cholesterol. It is concluded that rapid effects of 1,25-dihydroxy vitamin D-3 on Vm, in target cells, are specific, most likely due to permeability changes and not related to nuclear protein synthesis; they may contribute to early modulation of cell function.
Animals↗
Circulating vitamin D metabolite concentrations in children with nutritional rickets.
Serum calcidiol, calcitriol, and 24,25-dihydroxyvitamin D concentrations were measured in 20 children with vitamin D-deficiency rickets. Vitamin D metabolite concentrations were measured in 17 of 20 patients before treatment and in 14 of 20 patients after vitamin D administration. Conclusions are as follows. (1) Before treatment, serum calcidiol seems to be the best criterion of D deficiency, as it was low (less than 8 ng/ml) in 15 of 17 studied children, whereas calcitriol and 24,25-dihydroxyvitamin D concentrations ranged from undetectable to high values (350 pg/ml and 5.9 ng/ml, respectively). (2) Low calcidiol concentrations may occur despite recent vitamin D intake: low serum values were found in children given vitamin D2 up to two months after the onset of therapy (50 micrograms/day). (3) Elevated calcitriol serum concentrations were observed in all children after initiation of vitamin D therapy; these high concentrations persisted for four weeks or more, even after normalization of serum calcium, phosphorus, and parathyroid hormone values. (4) Healing of biochemical abnormalities can occur even in children with low circulating concentrations of calcidiol and 24,25-dihydroxyvitamin D.
25-Hydroxyvitamin D 2↗
Skin calcium-binding protein: distribution in other tissues.
The distribution of epidermal calcium-binding protein was examined in rat tissues using immunodiffusion and immunofluorescence techniques to investigate its possible physiological role. Epidermal calcium-binding protein was demonstrated in the basal proliferative cell layer of all Malpighian epithelia and related tissues (epidermis, sebaceous glands, cornea, esophagus, and vagina) as well as in ependyma of brain and in the epithelia of the lens. No immunoreactivity for epidermal calcium-binding protein was found in other tissues including dermis, muscle, cartilage, blood vessels, nerve tissue, liver, endocrine glands, urogenital tract, and intestinal and respiratory epithelium. The presence of a protein immunologically indistinguishable from epidermal calcium-binding protein in proliferative cells suggests that it may be involved in the control of calcium-dependent processes perhaps related to mechanical damage and continued proliferation.
Animals↗
Changes in 25-hydroxyvitamin D3 alpha- and 24-hydroxylase activities of kidney cells isolated from rats with either unilateral kidney damage or acute renal insufficiency.
25-Hydroxyvitamin D3 1 alpha- and 24-hydroxylase, NADPH-cytochrome c reductase, heme oxygenase, and ATPase activities were studied in viable kidney cells isolated from rats submitted to unilateral kidney damage (cortical electrocoagulation) and during the development of acute renal failure subsequent to excision of the contralateral undamaged kidney. Measurements of blood pH, plasma total and ionized calcium, phosphorus, creatinine, kidney histology, and phosphorus nuclear magnetic resonance spectroscopy determinations of phosphorus-containing compounds in kidney tissue were also performed. Seventy-two hours after unilateral kidney damage, no significant changes were observed in blood pH or in the plasma parameters studied. During this period, a significant increase in the activity of the 25-hydroxyvitamin D3 hydroxylases could be demonstrated in the cells of the contralateral undamaged kidney. A similar pattern of compensatory rise in the activity of the other enzymes studied was not detected. However, in the damaged kidney viable cells, the hydroxylase activities remained unchanged relative to those in sham-operated controls, despite a 5-fold increase in the inorganic phosphate content and a marked decrease in the organophosphorus and ATP content of this tissue. During the development of acute renal failure, a significant decrease in the activity of the hydroxylases occurred only when the rise in plasma creatinine concentration suggested severe renal insufficiency.
25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
Rickets and alopecia with resistance to 1,25-dihydroxyvitamin D: two different clinical courses with two different cellular defects.
UNLABELLED: Two unrelated patients, aged 22 months and 31 months, with alopecia and rickets resistant to 1,25-dihydroxyvitamin D (1,25-(OH)2D] (vitamin D-dependency type II) presented with similar biochemical and radiologic features. They were treated with large doses of vitamin D3 derivatives [25-hydroxyvitamin D3 (25-(OH)D3), 1,25-(OH)2D3, and 1 alpha-hydroxyvitamin D3] for 28 months and 6 yr, respectively. In both patients, serum 1,25-(OH)2D levels remained high (approximately 10- to 100-fold normal) during the different therapeutic regimens. Circulating 1,25-(OH)2D and 24,25-dihydroxyvitamin D levels at various stages of the disease suggested in these children disturbances in the regulation of 25-hydroxyvitamin D (25(OH)D) 1 alpha- and 24-hydroxylase systems. In one child, all therapeutic trials were unsuccessful. Studies of her cultured skin fibroblasts showed low capacity (10% normal) for saturable (presumably receptor mediated) nuclear uptake of tritiated 1,25-(OH)2D3; the uptake process of nucleus associated 1,25-(OH)2D3 was normal in apparent affinity for 1,25-(OH)2D3 and in sedimentation velocity of nucleus-associated hormone. In the second child, correction of biochemical abnormalities, healing of rickets, and catch-up growth were obtained during similar therapeutic trials up to the age of 6 yr when a relapse occurred. This relapse has persisted for 2 yr in spite of similar or higher circulating concentrations of 25-(OH)D and 1,25-(OH)2D than those obtained previously when she was responsive to therapy. In her cultured skin fibroblasts, saturable high affinity nuclear uptake of 1,25(OH)2D was unmeasurable. IN CONCLUSION: 1) distinct patterns of clinical response can occur in patients with the syndrome of vitamin D-dependency type II, and can be associated with differing abnormalities in interaction of 1,25-(OH)2D3 with cultured skin fibroblasts; 2) aggravation of the resistance to 1,25-(OH)2D3 may occur during long term therapy in some patients.
24,25-Dihydroxyvitamin D 3↗
Evaluation of 25-hydroxyvitamin D and vitamin D binding protein losses in thirteen children on continuous ambulatory peritoneal dialysis.
Thirteen children, 6 females, 7 males, aged 2 to 13 years were studied. At the time of study they were on continuous ambulatory peritoneal dialysis (CAPD) for 1 to 22 months. 25-(OH)D loss in daily dialysate fluids represented 2 to 22 micrograms/day. A significant correlation was found between 25-(OH)D plasma concentration and 25-(OH)D dialysate concentration. 25-(OH)D clearance was correlated to 25-(OH)D binding protein clearance (p less than 0.001). These findings of important 25-(OH)D losses in the dialysate fluid of children on CAPD demonstrate the necessity of carefully adapted vitamin D intakes with such a treatment.
Adolescent↗
Metabolites of vitamin D3 in pituitary dwarfs.
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Calcifediol↗