XXXX treatment potentiates excretion of mutagenic urine in @entity41553 -treated Fischer 344 @entity35 .

@entity21750 @entity41553 @entity10664 @entity41554 @entity51224 @entity12472 @entity35 @entity53172
@entity12472 ( @entity10664 ), an s- @entity21750 herbicide, is a widespread environmental contaminant. The hepatocarcinogenic component of technical grade @entity53172 , @entity41553 ( @entity41554 , 19.5%), is a byproduct of @entity51224 synthesis and is found at production sites. This study explores the effect of @entity10664 treatment on the bioactivation of the promutagen, @entity41554 . Male Fischer 344 @entity35 (5 weeks old) were administered 50 mg/kg of @entity10664 by gavage for 5 weeks. At 1, 3, and 5 weeks, both DMSO-control and @entity10664 -pretreated @entity35 were treated p.o. with 75 mg/kg of @entity41554 and were housed in metabolism cages for urine collection. Sulfatase- and beta-glucuronidase-treated, concentrated urine was bioassayed for urinary mutagens in a microsuspension modification of the Salmonella assay with and without metabolic activation. No significant change in mutagen excretion was observed in @entity10664 -treated @entity35 ; however, an elevation in direct-acting urine mutagens from @entity35 receiving @entity10664 and @entity41554 at weeks 1 (359 +/- 68 vs. 621 +/- 96 revertants/ml) and 5 (278 +/- 46 vs. 667 +/- 109 revertants/ml) of treatment was observed. The increase in production of urinary mutagens was accompanied by an elevation in small intestinal nitroreductase activity. Increases in large intestinal nitroreductase and beta-glucuronidase were observed after 5 weeks. There was no apparent effect of @entity10664 following 5 weeks of treatment on the production of @entity41554 -derived hepatic DNA adducts. @entity10664 treatment modifies intestinal enzymes responsible for promutagen bioactivation, and potentiates the excretion of mutagenic urine in @entity41554 -treated animals.
