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biliary fistula/glutathione

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Acyl-adenylates and acyl-CoA thioesters of bile acids (BAs) are reactive acyl-linked metabolites that have been shown to acylate the thiol group of glutathione (GSH); the reaction is catalyzed by glutathione S-transferase (GST) and the product is a thioester-linked BA-GSH conjugate. Such GSH
Acyl-adenylates and acyl-CoA thioesters of bile acids (BAs) are reactive acyl-linked metabolites that have been shown to undergo transacylation-type reactions with the thiol group of glutathione (GSH), leading to the formation of thioester-linked GSH conjugates. In the current study, we examined the

Excretion of sulfobromophthalein in rats with iodomethane-induced depletion of hepatic glutathione.

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Male urethane-anesthetized Wistar rats with biliary fistulas were infused for 60 min i.v. with sulfobromophthalein (BSP) or BSP-glutathione conjugate (BSP-GSH) at 594 nmol/100 g/min. Thirty minutes prior to the start of the infusion, 20 mg/kg iodomethane, dissolved in oliver oil, was given into the
The intracellular distribution of glutathione into kinetically distinct pools and the determinants of glutathione turnover were examined in vivo. Glutathione turnover was measured in individual, restrained rats with a biliary fistula by administration of acetaminophen to trap the previously labeled

The acute pancreatotoxic effects of the plant nitrile 1-cyano-2-hydroxy-3-butene.

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The effects of synthetic 1-cyano-2-hydroxy-3-butene (CHB), a racemic mixture of the (R)- and (S)-enantiomers, were studied in adult male rats. The compound given by gavage in olive oil at doses of 25-200 mg/kg causes toxic effects on the pancreas that resemble those seen when naturally occurring CHB
Urethane anesthetized Wistar rats with biliary fistulas were infused during 100 min with sulfobromophthalein (BSP), the glutathione conjugate of sulfobromophthalein (BSP-GSH), cholic acid (CA) and dehydrocholic acid (DCA). The dyes (594 nmol/100 g/min) and the bile acids (1200 nmol/100 g/min) were

Contribution of mrp2 in alterations of canalicular bile formation by the endothelin antagonist bosentan.

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OBJECTIVE Bosentan, a dual endothelin ET(A/B) receptor antagonist, may cause dose-dependent reversible cholestatic liver injury. We herein tested whether bosentan or metabolites, both eliminated in bile, induce alterations in bile secretion. METHODS Bile flow and output of bile constituents were
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