The biological activity of synthetic 24,25 and 25,26 diOHD3 was studied in vitamin D-deficient rats. The purpose of this study was to investigate the influence of small doses of both metabolites (0.125-0.250 mug) upon intestinal calcium transport and bone calcium mobilization. Both metabolites were able to increase calcium absorption in rats maintained on a calcium-deficient diet, but failed to do it in rats on a normal calcium diet. Bilateral nephrectomy suppressed this effect. The "bone calcium mobilization" of both derivatives was measured in vitamin D and calcium- or phosphorus-deprived rats after one intravenous dose. When serum calcium was initially low, 24,25 and 25,26 diOHD3 increased serum calcium moderately, but the increment was only significant with 24,25 diOHD3. When serum calcium was normal before the injection, both metabolites decreased serum calcium significantly, and the decrease was greater with 24,25 diOHD3. Intraperitoneal administration of the metabolites for 5 consecutive days produced a significant increase of calcium in serum and bone ash.

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1. A radioimmunoassay of 25,26-dihydroxycholecalciferol has been developed with an antiserum raised in a sheep, tritiated 1,25-dihydroxycholecalciferol as tracer and synthetic 25,26-dihydroxycholecalciferol as standard. The metabolite was purified from serum extracts by Sephadex LH 20 and high-pressure liquid chromatography; recovery was monitored with biologically generated, tritiated 25,26-dihydroxycholecalciferol. 2. The mean +/- SEM concentration of 25,26-dihydroxycholecalciferol in serum from 18 healthy subjects was 587 +/- 65 pmol/l. Seven Asian patients with osteomalacia due to vitamin D deficiency had very low or undetectable (< 96--231 pmol/l) circulating 25,26-dihydroxycholecalciferol concentrations. 3. The metabolite was detectable in the sera from seven anephric patients (mean 262 +/- 43 pmol/l), indicating that extrarenal sites for the 26-hydroxylation of 25-hydroxycholecalciferol exist in man. 4. A strong positive correlation between the concentrations of 25-hydroxycholecalciferol and those of 25,26-dihydroxycholecalciferol in serum was obtained. Thus it appears that in man the production of this dihydroxy metabolite of vitamin D depends on the concentration of its precursor, 25-hydroxycholecalciferol.

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