Dmd057190 1219..1226

نویسندگان

  • Kyunghee Yang
  • Kim L. R. Brouwer
چکیده

Inhibition of bile acid transport by troglitazone (TGZ) and its major metabolite, TGZ sulfate (TS), may lead to hepatocellular accumulation of toxic bile acids; TS accumulation and hepatotoxicity may be associated with impaired TS biliary excretion. This study evaluated the impact of impaired transport of breast cancer resistance protein (Bcrp) and multidrug resistance–associated protein 2 (Mrp2) on the hepatobiliary disposition of generated metabolites, TS and TGZ glucuronide (TG). Sandwich-cultured hepatocytes (SCH) from Mrp2-deficient (TR) rats in combination with Bcrp knockdown using RNA interference were employed. The biliary excretion index (BEI) of generated TS was not significantly altered by impaired Bcrp (20.9 to 21.1%) and/or Mrp2 function (24.4% and 17.5% in WT and TR rat SCH, respectively). Thus, loss-of-function of Mrp2 and/or Bcrp do not appear to be risk factors for increased hepatocellular TS accumulation in rats, potentially because of a compensatory transporter(s) that excretes TS into bile. Further investigations revealed that the compensatory TS biliary transporter was not the bile salt export pump (Bsep) or P-glycoprotein (P-gp). Interestingly, TGZ sulfation was significantly decreased in TR compared with WT rat SCH (total recovery: 2.8 versus 5.0% of TGZ dose), resulting in decreased hepatocellular TS accumulation, even though sulfotransferase activity in TR rat hepatocyte S9 fraction was similar. Hepatocellular TG accumulation was significantly increased in TR compared with WT rat SCH due to increased glucuronidation and negligible TG biliary excretion. These data emphasize that the interplay between metabolite formation and excretion determines hepatocellular exposure to generated metabolites such as TS and TG.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Working Draft , Standard for Programming Language

declarator, 184, 1224access-specifier, 235, 1226additive-expression, 118, 1217alias-declaration, 140, 1220alignment-specifier, 176, 1223and-expression, 122, 1217asm-definition, 173, 1222assignment-expression, 125, 1218assignment-operator, 125, 1218attribute, 176, 1223attribute-argument-clause, 176, 1223attribute-declaration, 140, 1220attribute-lis...

متن کامل

miR-1226 targets expression of the mucin 1 oncoprotein and induces cell death.

The MUC1 oncoprotein is aberrantly overexpressed in human carcinomas and hematologic malignancies. Micro-RNAs (miRNAs) have been implicated in the suppression and induction of oncogenesis. The present studies demonstrate that the MUC1 mRNA 3' untranslated region (3'UTR) contains a highly conserved motif for binding of a novel miRNA, miR-1226, that has no known targets. The results show that miR...

متن کامل

Continuity of care: a multidisciplinary review.

http://bmj.com/cgi/content/full/327/7425/1219 Updated information and services can be found at: These include: Data supplement http://bmj.com/cgi/content/full/327/7425/1219/DC1 "List of reviewed articles" References http://bmj.com/cgi/content/full/327/7425/1219#otherarticles 6 online articles that cite this article can be accessed at: http://bmj.com/cgi/content/full/327/7425/1219#BIBL This arti...

متن کامل

Thorough QT/QTc Evaluation of the Cardiac Safety of Secnidazole at Therapeutic and Supratherapeutic Doses in Healthy Individuals

SYM-1219, a novel oral granule formulation of secnidazole, is under development as single-dose treatment for bacterial vaginosis. This 4-way, randomized, crossover study evaluated the effects of SYM-1219 on electrocardiographic (ECG) parameters in 52 healthy subjects. Subjects were administered single doses of SYM-1219, 2 g (proposed therapeutic dose), 6 g (supratherapeutic dose), placebo, and ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2014