Studies on the mechanism of estradiol-17.BETA.-D-glucuronide-induced cholestasis in the rat.
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The effects of estradiol-17β-D-glucuronide (E<SUB>2</SUB> 17G) on bile excretion were studied in the rat and primary cultured rat hepatocytes.<BR>E<SUB>2</SUB> 17G induced an immediate, reversible and dose-dependent inhibition of bile flow.<BR>Electron microscopy revealed significant reduction of alkaline phosphatase activity on bile canaliculi during cholestasis without their ultrastructural alterations, and also showed no marked changes either of structure or permeability of tight junctions to Lanthanum.<BR>The radioactivity of intravenously-administrated <SUP>14</SUP>C-taurocholate (<SUP>14</SUP>C-TC) increased immediately in the liver homogenate and then showed a rebound elevation in serum with E<SUB>2</SUB> 17G treatment.<BR>In primary cultured rat hepatocytes the uptake of E<SUB>2</SUB> 17G into hepatocytes demonstrated Michaelis-Menten kinetics and a mutual inhibition between E<SUB>2</SUB> 17G and TC was observed.<BR>These data suggest that inhibitions of both bile acid secretion into bile canaliculi and, in some extent, inhibition of bile acid uptake of into hepatocytes are major factors in E<SUB>2</SUB> 17G-induced cholestasis in the rat.
- 社団法人 日本肝臓学会の論文
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- Studies on the mechanism of estradiol-17.BETA.-D-glucuronide-induced cholestasis in the rat.