Exposure to the fungicide prothioconazole and its metabolite prothioconazole-desthio induced hepatic metabolism disorder and oxidative stress in mice.

ABSTRACT

Prothioconazole (PTC), as a popular triazole fungicide, with its main metabolite prothioconazole desthio (PTC-d), have attracted widespread concern due to their widely use and toxicological effects on non-target organisms. However, toxic effects of study analyzed PTC and PTC-d on the hepatic metabolism of mammalian still remains unclear. In this study, we conducted the study of the C57BL/6 mice which oral exposure to 30 mg/kg PTC and PTC-d via metabolomic analysis. In the liver, the metabolomics profile unveiled that exposure to 30 mg/kg PTC and PTC-d led to significantly altered 13 and 28 metabolites respectively, with 6 metabolites in common including significant decreased d-Fructose, Glutathione, showing the change of carbohydrate, lipid and amino acid metabolism. Via the further exploration of genes related to hepatic glycolipid metabolism and the biomarkers of oxidative stress, we found that liver was potentially damaged after exposure to 5 and 30 mg/kg PTC and PTC-d. Particularly, it was proved that PTC-d caused more adverse effect than its parent compound PTC on hepatotoxicity, and high concentration PTC or PTC-d exposure is more harmful than low concentration exposure.