Metabolism of 22-oxacalcitriol by a vitamin D-inducible pathway in cultured parathyroid cells

Journal Article

Catabolism of 22-oxacalcitriol (OCT) in parathyroid cells was compared to that of the parent hormone, 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Catabolism of both compounds was greatly accelerated by pretreatment of the cells with 1,25-(OH)2D3 or OCT. The rate of degradation of OCT was slightly greater than that of 1,25-(OH)2D3. Excess unlabeled OCT or 1,25-(OH)2D3 inhibited metabolism of both tritiated substrates. Ketoconazole, a cytochrome P450 inhibitor, blocked catabolism of both compounds. The major OCT metabolite appeared to be 1,20-dihydroxy-22,23,24,25,26,27-hexanor-vitamin D3 which was not active in suppressing PTH secretion. We conclude that OCT appears to be metabolized by the same vitamin D-inducible side chain oxidation pathway that catabolizes other vitamin D compounds and that its higher than expected suppression of PTH secretion is not due to slower cellular metabolism. © 1992.

Full Text

Duke Authors

Cited Authors

  • Brown, AJ; Berkoben, M; Ritter, C; Kubodera, N; Nishii, Y; Slatopolsky, E

Published Date

  • 1992

Published In

Volume / Issue

  • 189 / 2

Start / End Page

  • 759 - 764

PubMed ID

  • 1472047

International Standard Serial Number (ISSN)

  • 0006-291X

Digital Object Identifier (DOI)

  • 10.1016/0006-291X(92)92266-Z