Atrazine treatment potentiates excretion of mutagenic urine in 2, 6-dinitrotoluene-treated fischer 344 rats
✍ Scribed by S. E. George; R. W. Chadwick; M. J. Kohan; J. C. Allison; S. H. Warren; R. W. Williams
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 660 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0893-6692
No coin nor oath required. For personal study only.
✦ Synopsis
Atrazine (ATZ), an striazine herbicide, is a widespread environmental contaminant. The hepatocarcinogenic component of technical grade dinitrotoluene, 2,6dinitrotoluene (2,6-DNT, 19.5%), is a byproduct of trinitrotoluene synthesis and is found at production sites. This study explores the effect of change in mutagen excretion was observed in ATZtreated rats; however, an elevation in directclcting urine mutagens from rats receiving ATZ and 2,6-DNT at weeks 1 (359 ? 68 vs. 621 ? 96 r e vertants/ml) and 5 (278 ? 46 vs. 667 ? 109 revertants/ml) of treatment was observed. The in-ATZ treatment on the bioactivation of the promutagen, 2,6-DNT. Male Fischer 344 rats (5 weeks old) were administered 50 mg/kg of ATZ by gavage for 5 weeks. At 1, 3, and 5 weeks, both DMSOcontrol and ATZ-pretreated rats were treated p.0.
with 75 mg/kg of 2,6-DNT and were housed in metabolism cages for urine collection. Sulfataseand P-glucuronidase-treated, concentrated urine was bioassayed for urinary mutagens in a microsuspension modification of the Salmonella assay with and without metabolic activation. No significant crease in production of urinary mutagens was accompanied by an elevation in small intestinal nitroreductase activity. Increases in large intestinal nitroreductase and hlucuronidase were observed after 5 weeks. There was no apparent effect of ATZ following 5 weeks of treatment on the production of 2,6-DNTderived hepatic DNA adducts. ATZ treatment modifies intestinal enzymes responsible for promutagen bioactivation, and potentiates the excretion of mutagenic urine in 2,6-DNT-treated animals.