Increase in renal glutathione in cholestatic liver disease is due to a direct effect of bile acids

American Journal of Physiology - Renal Physiology

Volumn 283, Issue 6 52-6, 2002, Pages

  Purucker, Edmund ^a   Marschall, Hanns Ulrich ^b   Geier, Andreas ^a   Gartung, Carsten ^a   Matern, Siegfried ^a  

^a RWTH AACHEN UNIVERSITY   (Germany)

^b KAROLINSKA INSTITUTE   (Sweden)

Author keywords

Bile duct ligation; Glutathione depletion; Sodium excretion; glutamylcysteine synthetase

Indexed keywords

ANION; BILE ACID; BUTHIONINE SULFOXIMINE; CARRIER PROTEIN; GLUTAMATE CYSTEINE LIGASE; GLUTATHIONE; GLUTATHIONE DISULFIDE; GLUTATHIONE SYNTHASE; GLYCINE; MESSENGER RNA; ORGANIC COMPOUND; SODIUM; TAURINE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BLOOD LEVEL; CHRONIC LIVER DISEASE; CONTROLLED STUDY; ENZYME INHIBITION; ENZYME SPECIFICITY; GLUTATHIONE METABOLISM; INTRAHEPATIC CHOLESTASIS; KIDNEY; KIDNEY DYSFUNCTION; MALE; NONHUMAN; PRIORITY JOURNAL; RAT; SODIUM EXCRETION; SODIUM RETENTION; SODIUM URINE LEVEL; URINE VOLUME;

EID: 0036890295     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.00237.2001     Document Type: Article

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