The Effects of a Diphosphonate and Dietary Calcium on the Metabolism of Vitamin D3 (Cholecalciferol) in the Chick

1975 ◽  
Vol 49 (5) ◽  
pp. 391-400
Author(s):  
Carol M. Taylor ◽  
E. Barbara Mawer ◽  
A. Reeve

1. Vitamin D-deficient chicks, maintained on a diet adequate in calcium and treated with ethane-1-hydroxy-1,1-diphosphonate for 2 days before a single oral dose of cholecalciferol (vitamin D3), converted the vitamin into 24,25-dihydroxycholecalciferol instead of into the normal metabolite 1,25-dihydroxycholecalciferol. 2. This inhibition of the renal 1-hydroxylase disappeared on withdrawal of the diphosphonate. 3. Kidneys from chicks given diphosphonate for 12 days converted 25-hydroxycholecalciferol into 24,25-dihydroxycholecalciferol on incubation in vitro. 4. The inhibition of the 1-hydroxylase was markedly accelerated by treating the birds with cholecalciferol. 5. No inhibition of renal 1-hydroxylation was observed in birds maintained on a diet low in calcium. 6. A possible mechanism producing this effect is discussed.

Author(s):  
Cora M. Best ◽  
Robert Sherwood ◽  
Janet A. Novotny ◽  
Sheng Zhang ◽  
Eva K. Pressman ◽  
...  

1977 ◽  
Vol 53 (5) ◽  
pp. 439-446
Author(s):  
R. Lorentzon ◽  
S.-E. Larsson

1. Chromatography measurements indicated that adult rats converted 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol at a lower rate than that reported earlier for young animals. In serum, less-polar metabolites were found which probably represented vitamin D esters and vitamin D3. 2. A low dietary intake of calcium resulted in an evident increase in the fraction corresponding to 1,25-dihydroxycholecalciferol in the kidneys and also in the intestinal mucosa and serum. 3. Inclusion of 0·67 mmol of cadmium/l of drinking water at a low dietary intake of calcium resulted in an increased accumulation of both cadmium and zinc in the kidneys and liver compared with values at a normal dietary calcium intake. 4. At a normal dietary calcium intake, cadmium exposure caused inhibited production of 1,25-dihydroxycholecalciferol by the kidneys and an increased accumulation of 24,25-dihydroxycholecalciferol, vitamin D3 and vitamin D esters in the serum. 5. The inhibitory effect of cadmium on the renal conversion of 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol was almost completely counteracted by a simultaneous low dietary calcium intake. Cadmium-exposed, calcium-deficient animals also showed a maintained accumulation of 1,25-dihydroxycholecalciferol in the intestinal mucosa.


1973 ◽  
Vol 30 (03) ◽  
pp. 494-498 ◽  
Author(s):  
G de Gaetano ◽  
J Vermylen

SummaryThrombelastograms of both native blood and re-calcified platelet-rich plasma samples taken from subjects given a single oral dose of aspirin (1 gram) were not significantly different from the pretreatment recordings. Aspirin also did not modify the thrombelastogram when preincubated in vitro with platelet-rich plasma at concentrations inhibiting the platelet “release reaction” by collagen. Thrombelastography therefore cannot evaluate the effect of aspirin on platelet function.


1995 ◽  
Vol 319 (2) ◽  
pp. 535-539 ◽  
Author(s):  
M.J. Beckman ◽  
J.A. Johnson ◽  
J.P. Goff ◽  
T.A. Reinhardt ◽  
D.C. Beitz ◽  
...  

1974 ◽  
Vol 46 (4) ◽  
pp. 433-448 ◽  
Author(s):  
J. Silver ◽  
G. Neale ◽  
G. R. Thompson

1. The metabolism of radioactive cholecalciferol was studied in control and phenobarbitone-treated rats and pigs. 2. Treatment with phenobarbitone enhanced the appearance in plasma of 25-hydroxycholecalciferol (peak IV on silicic acid chromatography), and of more-polar metabolites (peak V), but not of the most-polar metabolites (peak VI). Peak IV had the chromatographic properties of authentic 25-hydroxycholecalciferol (25-HCC) and had biological activity. 3. There was no effect on the appearance of peaks V and VI in plasma after an injection of radioactive 25-HCC. 4. Treatment with phenobarbitone enhanced the excretion of metabolites of radioactive vitamin D3 in bile. These metabolites were largely water-soluble conjugates of peaks IV, V and VI, which included glucuronides. Peak IV in bile was not identical with 25-HCC. 5. Prolonged treatment with phenobarbitone depleted the tissue radioactivity of rats given radioactive vitamin D3.


1986 ◽  
Vol 374 (1) ◽  
pp. 199-203 ◽  
Author(s):  
Elizabeth Suwita ◽  
Daniel M. Lapadula ◽  
Mohamed B. Abou-Donia

1985 ◽  
Vol 40 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
Ana R. de Boland ◽  
Ricardo Boland

Cultures of vitamin D-deficient chick soleus muscle and 12 day-old chick embryo myoblasts were used to characterize the effects of 1,25-dihydroxy-vitamin D3 and 25-hydroxy-vitamin D3 on muscle cell Ca metabolism. Physiological amounts of both sterols increased the rate and extent of 45Ca uptake by cultures. However. 1.25(OH)2D3 was significantly more effective than 25 OHD3. The greater potency of 1,25(OH)2D3 to increase Ca uptake could be shown after various treatment intervals of cultures and using a wide concentration range of both derivatives. Information about Ca pools affected by vitamin D3 metabolites was obtained through kinetic analysis of Ca efflux in cultured myoblasts. Cytoplasmic and mitochondria Ca pools were identified on the basis of their half-times of desaturation and by selective inhibition of plasma membrane and mitochondrial Ca transport with LaCl3 and Ruthenium Red, respectively. The data suggests that 1,25(OH)2D3 acts on muscle cellular Ca by increasing Ca efflux and influx through mitochondrial and plasma membranes whereas the predominant effect of 25 OHD3 is to increase Ca influx into mitochondria.


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