Lack of biliary excretion of Cd linked to an inherent defect of the canalicular isoform of multidrug resistance protein (cMrp) does not abnormally stimulate accumulation of Cd in the Eisai hyperbilirubinemic (EHB) rat liver

Archives of Toxicology

Volumn 71, Issue 5, 1997, Pages 336-339

  Sugawara, Naoki ^a   Lai, Yu Rong ^a   Arizono, Koji ^b   Kitajima, Toshiichi ^c   Inoue, Hideaki ^c  

^a SAPPORO MEDICAL UNIVERSITY   (Japan)

^b NAGASAKI UNIVERSITY   (Japan)

^c Lab of Pharmacokin and Pharmacol   (Japan)

Author keywords

ATP driven anion transport; Biliary excretion of Cd and glutathione; cMrp; EHB rat; Hepatic accumulation of Cd

Indexed keywords

CADMIUM; GLUTATHIONE; PROTEIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANION TRANSPORT; ARTICLE; BILIARY EXCRETION; BIOACCUMULATION; CONTROLLED STUDY; GENETIC DISORDER; HYPERBILIRUBINEMIA; MALE; MUTANT; NONHUMAN; PRIORITY JOURNAL; RAT; STRAIN DIFFERENCE;

ACETYLGLUCOSAMINE; ANIMALS; BILE; BILE CANALICULI; BILIRUBIN; BIOLOGICAL TRANSPORT; CADMIUM; DRUG RESISTANCE, MULTIPLE; GAMMA-GLUTAMYLTRANSFERASE; GLUTATHIONE; HYPERBILIRUBINEMIA; INTESTINES; KIDNEY; LIVER; MALE; RATS; RATS, SPRAGUE-DAWLEY;

ANIMALIA;

EID: 0030986126     PISSN: 03405761     EISSN: None     Source Type: Journal    
DOI: 10.1007/s002040050395     Document Type: Article

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