Record Display for the EPA National Library Catalog

RECORD NUMBER: 4 OF 7

OLS Field Name OLS Field Data
Main Title Effect of Pretreatment on the Biliary Excretion of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin, 2,3,7,8-Tetrachlorodibenzofuran, and 3,3',4,4'-Tetrachlorobiphenyl in the Rat.
Author McKinley, M. K. ; Kedderis, L. B. ; Birnbaum, L. S. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Environmental Toxicology Div. ;ManTech Environmental Technology, Inc., Research Triangle Park, NC. ;Duke Univ., Durham, NC. School of the Environment. ;North Carolina Univ. at Chapel Hill.
Publisher c1993
Year Published 1993
Report Number EPA/600/J-94/073;
Stock Number PB94-141413
Additional Subjects Bilary tract ; Tetrachlorodibenzodioxin ; Polychlorobiphenyl compounds ; Tissue distribution ; Metabolism ; Bile ; Feces ; High pressure liquid chromatography ; Reprints ;
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB94-141413 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 05/14/1994
Collation 10p
Abstract
The laterally halogenated chemicals 2,3,7,8-tetrachlorodibenzofuran (TCDF) and 3,3',4,4'-tetrachlorobiphenyl (TCB) exhibit the same spectrum of toxic effects as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the prototype and most toxic member of the halogenated aromatic hydrocarbon family. The biliary elimination of TCDF, TCDD, and TCB was examined as an indirect measure of metabolism. Male F344 rats were anesthetized with pentobarbital, the bile duct was cannulated, and 0.1 micromol (3H)TCDD, (14C)TCDF, or (14C)TCB/kg body wt was administered iv. To determine if TCDF was able to induce its own metabolism in vivo, a single dose of 1.0 micromol TCDF/kg was administered to rats by oral gavage 3 days prior to iv injection of 0.1 or 0.3 micromol (14C)TCDF/kg. Biliary excretion and hepatic concentrations of (14C)TCDF were significantly increased in the pretreated animals. These results suggest an autoinduction of TCDF metabolism.