## Abstract Aiming at new drugs to efficiently treat diseases, in which either increased or decreased levels of active vitamin D are desirable, we have designed some 400 structurally different azole‐type inhibitors and examined their capacity to selectively block vitamin D metabolism by CYP24 or sy
Vitamin D hydroxylases
✍ Scribed by Helen L. Henry
- Book ID
- 102878661
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 510 KB
- Volume
- 49
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
There are three mixed function oxidases which catalyze hydroxylations of vitamin D and its derivatives. These include the hepatic mitochondrial or microsomal vitamin D~3~‐25‐hydroxylase and the two renal mitochondrial enzymes which further hydroxylate 25‐hydroxyvitamin‐D~3~ (25‐OH‐D~3~) to form 24R,25‐dihydroxyvitamin D~3~ (24,25(OH)~2~D~3~) and 1,25‐dihydroxyvitamin D~3~ [1,25(OH)~2~D~3~], the primary steroid hormonal derivative of vitamin D~3~. All three enzymes are cytochrome P450 dependent. The two renal mitochondrial enzymes are regulated, usually in a reciprocal fashion. The intracellular signalling systems involved in this regulation include 1,25(OH)~2~D~3~ itself and both protein kinases A and C. Recent progress has been made in the purification and cloning of the vitamin D~3~‐25‐hydroxylase and the 25‐OH‐D~3~‐24‐hydroxylase. When the 25‐OH‐D~3~‐1‐hydroxylase is purified and cloned, efforts which have thus far been frustrated by its low abundance, fertile new ground for the study of the regulation of vitamin D metabolism at the molecular level will be opened up.
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Bone disease and low serum levels of 25-hydroxyvitamin D are prevalent in cholestatic syndromes such as primary biliary cirrhosis and biliary atresia. Defective hydroxylation, along with malabsorption of vitamin D, could be a factor in 25-hydroxyvitamin D depletion. To assess hepatic hydroxylation d
## Abstract Vitamin D wird im Organismus zunächst durch Sonnenbestrahlung, dann weiter in Leber und Niere durch Hydroxylierungen in ein steroidähnliches Hormon (Calcitriol) umgewandelt, das Calciumhaushalt, Knochenbildung sowie Zelldifferenzierungen und ‐proliferationen reguliert. Im Unterschied zu