US EPA

2157179 

Journal Article 

Abstract 

Metabolism and excretion of 2,4,5,2',5'-pentachlorobiphenyl (PCB) in male rat 

Chen, PR; Matthews, HB 

1974 

1 

Toxicology and Applied Pharmacology
ISSN: 0041-008X
EISSN: 1096-0333 

29 

1 

88 

English 

WOS:A1974T653800040 

is part of a larger document 3378179 Abstracts of papers for the Thirteenth Annual Meeting of the Society of Toxicology, Washington, D.C. March 10–14, 1974

The metabolism and excretion of [14C]PCB in male rats was followed as part of a pharma­ cokinetic study. After iv doses of 0.6 or 6.0 mg/kg, excretion of PCB occurred primarily in the feces of rats with about 50% excreted during the first 3 days after dosing. Another 12% was excreted in feces during the next 4 days. About 5% of the dose of PCB was excreted in the urine during the first 24 hr with only an additional 1% excreted thereafter. Analysis of radio­ activity excreted in the feces revealed the presence of 2 metabolites as well as significant amounts of parent PCB. Both metabolites were isolated and analyzed by chemical ionization mass spectroscopy (MS). The data obtained from MS indicated the major metabolite was a mono­ hydroxylated-PCB and the minor metabolite was a dihydroxy analog. NMR studies are in progress to determine the positions of the hydroxyl groups. Analysis of urinary radioactivity revealed the presence of only 1 metabolite, a glucuronide conjugate. That metabolism is closely coupled to excretion is suggested by the fact that no metabolites of PCB were found in liver and other tissues. The size of the dose apparently had no effect on the rate of excretion. During the first 24 hr, the rate of excretion of PCB and metabolites in the feces was markedly increased by animal pretreatment with an inducer, phenobarbital, and decreased by an inhibitor, SKF-525A, of the hepatic microsomal mixed-function oxidases. In conclusion, PCB is excreted primarily via the biliary route in rats. Excretion occurs both in the form of hydroxylated metabolites and as unchanged PCB, and the excretion rate is sensitive to the effects of an inducer or inhibitor of the hepatic microsomal hydroxylating enzymes. 

Thirteenth Annual Meeting of the Society of Toxicology 

Washington, D.C. 

March 10–14, 1974