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Biomedical subjects

S Balsan

Publications and source records attributed to S Balsan.

At least 73 records · Page 4Linked to original sources
PubMed1980

Lack of effect on ovariectomy on the metabolism of vitamin D and intestinal calcium-binding protein in female rats.

The metabolism of 25-hydroxycholecalciferol (25-(OH)D3), plasma concentration of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and the amount of calcium-binding protein (CaBP) in duodenal mucosa were determined in ovariectomized rats and were compared with data observed in normal age-matched cyclic rats. Sephadex LH-20 and high-pressure liquid chromatography were used for the study of the metabolism of 25-(OH)D3. The concentration of 1,25-(OH)2D3 in plasma and prolactin in serum were measured by radioimmunoassay. Calcium-binding protein in duodenal mucosa was determined immunologically using electroimmunodiffusion. The results showed that the lack of ovarian hormones and low prolactin levels observed in ovariectomized rats did not promote a significant change in the metabolism of 25-(OH)D3, in the levels of 1,25-(OH)2D3 in the circulation or in the amount of CaBP in duodenal mucosa. It is possible that the regulation of 25-(OH)D3 by sex hormones is restricted to the state of calcium stress such as during egg-laying in birds or pregnancy and lactation in mammals.

Animals↗
PubMed1979

Interaction of 24,25-dihydroxyvitamin D3 and parathyroid hormone on bone enzymes in vitro.

The in vitro effects of vitamin D3 metabolites, parathyroid extract (PTE), purified parathyroid hormone (bPTH), vitamin A, and heparin on acid and alkaline phosphatases in rat or mouse calvaria in culture were investigated. Results show that: (a) when compared to values found in half calvaria incubated for 24 h in control medium, the bone acid and alkaline phosphatase content is significantly higher in paired halves incubated with PTE (L USP/ml), bPTH (4 x 10(-8)M), heparin (5 USP/ml), vitamin A (23 USP/ml), 25-(OH)D3 (2.5 x 10(-11) to 2.5 x 10(-8)M), 24,25-(OH)2D3, and 1,25-(OH)2D3 (2.5 x 10(-12) to 2.5 x 10(-7M); (b) the presence of 24,25-(OH)2D3 at low concentrations in the incubation medium decreases significantly the PTE, bPTH, vitamin A, or heparin induced stimulation of the phosphatase activities. This interaction is also observed when measuring beta glucuronidase and glucose-6-phosphatase activities and 45Ca release from previously labeled mouse calvaria; (c) a similar activity could not be found with 1,25-(OH)2D3 suggesting that 24,25-(OH)2D3 may have a specific role in bone metabolism.

Acid Phosphatase↗
PubMed1978

Vitamin D and cartilage. I. In vitro metabolism of 25-hydroxycholecalciferol by cartilage.

In the present work, the capacity of cartilage to metabolize 25-hydroxycholecalciferol was investigated. Cartilage preparations from growth plate, articular surface, rib, scapula, and ear were isolated from 3-week-old normal rabbits and chickens. Each tissue was separately incubated with tritiated 25-hydroxycholecalciferol (, x 10(-9) M) for 1-24 h. Incubations of kidney and muscle were performed simultaneously for comparison. Similarly, cultured chondrocytes isolated from rabbit growth plate and articular cartilage were incubated for 1 or 20 h in medium free of fetal calf serum. After methanol-chloroform extraction of tissues, cells, and their respective media, chloroform phases were chromatographed on Sephadex LH-20 columns. The results show that kidney and cartilage are able to convert 25-hydroxycholecalciferol into a derivative which migrates in the 24,25-dihydroxycholecalciferol region. Cartilage tissue previously boiled is unable to metabolize 25-hydroxycholecalciferol. The conversion of 25-hydroxycholecalciferol occurs with all types of cartilage and is also observed in incubations of cultured chondrocytes. In the latter, the polar 25-hydroxycholecalciferol derivative is detected as early as 1 h after addition of 25-hydroxycholecalciferol. Two findings suggest that the polar derivative of 25-hydroxycholecalciferol produced by cartilage is 24,25-dihydroxycholecalciferol: 1) the cartilage derivative and 24,25-dihydroxycholecalciferol (synthetic and biosynthetic) comigrate during Sephadex LH-20 and high liquid pressure chromatography; and 2) both the cartilage derivative and 24,25-dihydroxycholecalciferol are sensitive to periodate treatment.

Animals↗
PubMed1978

Effect of growth hormone on the metabolism of 25-hydroxycholecalciferol in hypophysectomized rats on a diet without vitamin D and low in calcium.

The metabolism of 25-hydroxycholecalciferol (25-(OH)D3) was investigated in rats fed a diet low in calcium and without vitamin D for 4 weeks after hypophysectomy. Compared with intact rats on the same diet these animals had a low serum phosphorus concentration, a less marked degree of hypocalcaemia and their parathyroid gland was not hypertrophied. Eighteen hours after i.p. injection of a single dose of tritiated 25-(OH)D3, chromatography of serum extracts on Sephadex LH-20 showed that the percentage of radioactivity corresponding to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was lower in hypophysectomized rats than in control rats. High-pressure liquid chromatography demonstrated that 81% of this material had the same elution profile as 1,25-(OH)2D3. The percentage of 1,25-(OH)2D3 in the serum of hypophysectomized rats could be increased to the level seen in the controls by chronic treatment with bovine growth hormone. This action of growth hormone was most probably independent of the parathyroid glands since the injection of parathyroid extract did not alter 25-(OH)D3 metabolism in hyophysectomized animals. These results suggest that the decrease in the conversion of 25-(OH)D3 to 1,25-(OH)2D3 after hypophysectomy may be related to the lack of growth hormone.

Animals↗
PubMed1978

[Effects of the main derivatives of vitmain D in 3 siblings with "pseudo-deficiency" rickets].

Three siblings, respectively 20, 16 and 12 years old, presented with hypocalcemic vitamin D resistant rickets (Prader's type). Their clinical history included several periods of spontaneous cessation of therapy, with severe relapses. Since 1973, treatment was strictly observed, allowing to test the therapeutic effects of 25 OH D3, 1-25 (OH) 2 D3 and 1-alpha (OH) D3. The clinical effects are reported as well as biochemical data. Among them, an inactive form of hyperparathyroidism is emphasized, which may resemble some cases of pseudohypoparathyroidism. Simultaneous resistance to exogenous PTE was also demonstraded.

Adolescent↗
PubMed1978

[Biological effects and activity threshold of a long-acting purified porcine calcitonin in the child].

The biologic effects of a purified long-acting porcine calcitonin (pTCT) were investigated in 45 children without any known renal, skeletal, endocrine, or metabolic disorder. pTCT was given as a single im injection at dose levels varying from 1 to 150 MRC u/1.73 m2. Administration of the highest dose was followed by a decrease in serum calcium and phosphorus concentrations and in tubular reabsorption of phosphorus, serum calcium and phosphorus concentrations and in tubular reabsorption of phosphorus. Mean maximal variation of serum calcium was -- 13.8 +/- 2.1 mg/l in children less than 3 years old, versus -- 8.2 +/- 0.9 mg/l (p less than 0.01) in older ones. Such an age-related differences was not observed for the hypophosphatemic action of pTCT. In 40 subjects aged 3 to 14 years the threshold for pTCT hypocalcemic activity was between 1 and 5 MRC u/1.73 m2. No significant differences in the effects on serum calcium of either 10, 25, 75 or 150 MRC u/1.73(2) m could be found. The threshold for pTCT hypophosphatemic activity was between 10 and 25 MRC u/1.73 m2 with, similary, no dose-response relationship for doses varying from 25 to 150 MRC u/1.73 m2. The present data demonstrate the high sensitivity of children, especially those younger than 3 years, to pTCT; furthermore, the lack of a dose-response relationship indicates that the pharmacological use of pTCT in pediatrics at doses higher than 10 to 25 MRC u/1.73 m2 is unnecessary.

Adolescent↗
PubMed1978

The in vitro production and activity of 24, 25-dihydroxycholecalciferol in cartilage and calvarium.

Previously reported results from our laboratory have indicated that 24, 25-dihydroxycholecalciferol can be formed in vitro during incubations of cartilage tissue or cartilage cells with 25-hydroxycholecalcified. They have also demonstrated the high potency of this dihydroxymetabolite of vitamin D3 in stimulating in vitro the sulfate incorporation into proteoglycans of cartilage cells in culture and in decreasing in vitro the parathyroid hormone action on rat calvarium phosphatases activities. The present report shows that 24, 25-)OH)2 D3 can also be produced during rat calvarium incubations with 25-hydroxycholecalciferol and that therefore calvarium as well as cartilage might be both a site of formation and a site of action for 24, 25-(OH)2 D3. The review of recent experimental and clinical investigations strongly suggests that this metabolite has a physiological significance and may be specifically active on some parameters of bone mineralization. Further studies on the cartilage and calvarium abilities to convert 25-hydroxycholecalciferol into 24, 25-(OH)2 D3 shows that this transformation occurs in the mitochondrial fraction but that it does not seem modified by factors known to control the 25-hydroxycholecalciferol metabolism in the kidney. Finally the analysis of experimental and clinical results published so far does not yet bring enough information to understand the significance of this extrarenal metabolism of 25-hydroxycholecalciferol.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1977

Phosphatase content of rat calvaria after in vivo administration of vitamin D3 metabolites.

The effects of acute or chronic administration of small doses (130 pmol) of 25-hydroxycholecalciferol, 24,25-dihydroxycholecalciferol, and 1,25-dihydroxycholecalciferol on rat calvaria acid and alkaline phosphatase activities were investigated in weanling male albino Wistar rats raised on a vitamin D-deficient, low-calcium diet. The results indicate that each of these active metabolites has a different effect on calvarial phosphatase activities. 25-hydroxycholecalciferol causes a significant increase, and 24,25-dihydroxycholecalciferol a decrease in the enzymatic activity. In animals treated with 1,25-dihydroxycholecalciferol these activities are lower after one injection, but after seven daily doses they are not different from those of ethanol-injected control rats. The observed changes do not seem to be related to changes in serum calcium and/or phosphorus concentrations.

Acid Phosphatase↗
PubMed1977

Maintenance of a calcemic response to parathyroid hormone in D-deficient rats by the prevention of severe hyperparathyroidism.

Parathyroid gland transplanted rats and hypophysectomized rats were raised from weaning on a diet without vitamin D and low in calcium (0.02%) for 4 weeks. At the enn of this period the animals of both experimental groups, when compared to their respective controls (i.e., sham-operated animals for parathyroid-transplanted ones, and hypophysectomized plus bovine growth hormone-supplemented ones for hypophysectomized rats) were characterized by (a) moderate or absent secondary hyperparathyroidism; (b) near normal bone calcium content; and (c) a maintained responsiveness to the calcemic effect of parathyroid extract (PTE). The PTE action is a bone effect that does not require the presence of the kidneys and is not related to changes in serum calcium and/or phosphorus concentrations. These results indicate that when severe hyperparathyroidism is prevented, the sensitivity of bone to the calcemic action of PTE can be maintained in D-deficient calcium-deprived rats. They also suggest that in these animals the main factor leading to resistance to PTH is the state of severe chronic hyperparathyroidism.

Animals↗