Abstract
Bile acid synthesis, determined by conversion of [4-C-14]cholesterol into bile acids in rat and human hepatocytes and by measurement of mass production of bile acids in rat hepatocytes, was dose-dependently decreased by cyclosporin A, with 52% (rat) and 45% (human) inhibition at 10-mu-M. The decreased bile acid production in rat hepatocytes was due only to a fall in the synthesis of beta-muricholic and chenodeoxycholic acids (-64% at 10-mu-M-cyclosporin A), with no change in the formation of cholic acid. In isolated rat liver mitochondria, 26-hydroxylation of cholesterol was potently inhibited by the drug (concn. giving half-maximal inhibition = 4-mu-M). These results suggest that cyclosporin A blocks the alternative pathway in bile acid synthesis, which leads preferentially to the formation of chenodeoxycholic acid.
Original language | English |
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Pages (from-to) | 501-505 |
Number of pages | 5 |
Journal | Biochemical Journal |
Volume | 275 |
Publication status | Published - 15-Apr-1991 |
Keywords
- MICROSOMAL DRUG-METABOLISM
- PRIMARY MONOLAYER-CULTURES
- RAT HEPATOCYTES
- CHOLESTEROL 7-ALPHA-HYDROXYLASE
- IMMUNOSUPPRESSIVE AGENT
- RENAL-TRANSPLANTATION
- INVIVO
- 26-HYDROXYCHOLESTEROL
- HYDROXYLATION
- KETOCONAZOLE