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 c
Modulation of 2,6-dinitrotoluene genotoxicity by alachlor treatment of Fischer 344 rats
โ Scribed by S. Elizabeth George; Joycelyn C. Allison; Lance R. Brooks; Brent T. Eischen; Michael J. Kohan; Sarah H. Warren; Leon C. King
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 145 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0893-6692
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โฆ Synopsis
Due to its widespread use as a preemergent herbi-DNA-alachlor adducts formed in vitro, no hepatic cide, alachlor has been detected as a groundwater DNA adducts were detected in vivo in these two contaminant. The procarcinogen, 2,6-dinitrotolu-treatment groups. Interestingly, a significant inene (DNT), a by-product of the munitions industry crease in excretion of mutagenic urine from DNTand a precursor to polyurethane production, is treated rats was observed following 3 weeks of found in the manufacturing waste stream. This study alachlor treatment in the absence of S9 (690 { 130 explores the effect of alachlor treatment on the bio-vs. 339 { 28 revertants/ml) which corresponded activation of DNT by examining urine mutagenicity, to increased DNT-related hepatic DNA adduct forintestinal enzymes, and hepatic DNA adducts to mation (5.90 { 0.88 adducts/10 8 nucleotides vs. detect changes in metabolism. Five-week-old male 10.56 1 {0.59 adducts/10 8 nucleotides [relative rats were treated daily by gavage with 50 mg/kg adduct level (RAL)]). Elevation in the production of of alachlor for up to 5 weeks while control animals mutagenic urine from control and treated animals received an equal volume of peanut oil. At 1, 3, was linked to increases in intestinal nitroreductase and 5 weeks following the initial alachlor dose, and b-glucuronidase activities; however, the only animals were administered p.o. 75 mg/kg DNT or significant alachlor-related effects were an increase DMSO. Urine was collected for 24 hr in metabolism in small intestinal 1-week b-glucuronidase and 5cages. Following incubation with sulfatase and b-week dehydrochlorinase activities. The increased glucuronidase, urines were individually concen-urine mutagenicity and hepatic DNA adduct formatrated by C-18 solid phase extraction, dried under tion indicates that alachlor has a transient effect on N 2 , and prepared for bioassay in Salmonella typhi-DNT bioactivation that apparently is unrelated to murium strain TA98 with and without metabolic acti-intestinal bioactivation. Environ. Mol. Mutagen. vation. Urine from peanut oil-and alachlor-treated 31: 274 -281, 1998. แญง
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