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The Effects of Benoxacor on the Liver and Gut Microbiome of C57BL/6 Mice
Journal article   Open access   Peer reviewed

The Effects of Benoxacor on the Liver and Gut Microbiome of C57BL/6 Mice

Derek Simonsen, Nicole Cady, Chunyun Zhang, Rachel L Shrode, Michael L McCormick, Douglas R Spitz Jr, Michael S Chimenti, Kai Wang, Ashutosh K Mangalam and Hans-Joachim Lehmler
Toxicological Sciences, Vol.186(1), pp.102-117
11/29/2021
DOI: 10.1093/toxsci/kfab142
PMCID: PMC9019840
PMID: 34850242
url
https://doi.org/10.1093/toxsci/kfab142View
Published (Version of record) Open Access

Abstract

The toxicity of many “inert” ingredients of pesticide formulations, such as safeners, is poorly characterized, despite evidence that humans may be exposed to these chemicals. Analysis of ToxCast data for dichloroacetamide safeners with the ToxPi tool identified benoxacor as the safener with the highest potential for toxicity, especially liver toxicity. Benoxacor was subsequently administered to mice via oral gavage for three days at concentrations of 0, 0.5, 5, and 50 mg/kg bodyweight (b.w.). Bodyweight-adjusted liver and testes weights were significantly increased in the 50 mg/kg b.w. group. There were no overt pathologies in either the liver or the intestine. 16S rRNA analysis of the cecal microbiome revealed no effects of benoxacor on α- or β-diversity; however, changes were observed in the abundance of certain bacteria. RNAseq analysis identified 163 hepatic genes affected by benoxacor exposure. Benoxacor exposure expressed a gene regulation profile similar to dichloroacetic acid and the fungicide sedaxane. Metabolomic analysis identified nine serum and fifteen liver metabolites that were affected by benoxacor exposure, changes that were not significant after correcting for multiple comparisons. The activity of antioxidant enzymes was not altered by benoxacor exposure. In vitro metabolism studies with liver microsomes and cytosol from male mice demonstrated that benoxacor is enantioselectively metabolized by cytochrome P450 enzymes (CYPs), carboxylesterases (CESs), and glutathione S-transferases (GSTs). These findings suggest that the minor toxic effects of benoxacor may be due to its rapid metabolism to toxic metabolites, such as dichloroacetic acid. This result challenges the assumption that inert ingredients of pesticide formulations are safe.
Agrochemicals biotransformation chiral does response environmental chemicals exposure

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