| Literature DB >> 33086928 |
Jose Serrano1, Richard C Kolanczyk1, Brett R Blackwell1, Barbara R Sheedy1, Mark A Tapper1.
Abstract
Thiacloprid (THI) is a widely used neonicotinoid insecticide where concerns have been raised regarding low absorption by crops, substantial distribution in surrounding areas, and potential adverse effects to terrestrial and aquatic organisms.Prior to this study, there was very limited information addressing the ex vivo (precision-cut liver slices) metabolism of THI by fish species and the metabolic pathways regulating its potential for adverse effects.The in vitro and ex vivo biotransformation pathway of THI is defined by the formation of three primary metabolites (TM1, TM2 and TM3) via separate paths differentiated by reductive decyanation, reductive dechlorination with hydration and dealkylation processes, respectively.Kinetic rates were calculated for the rat microsomal decyanation of THI into TM1 (Km = 299.2 µM and Vmax = 5.3 pmol/min/mg), and for the dealkylation of THI into TM3 (Km = 368.9 µM and Vmax = 3.95 pmol/min/mg).Formation confirmation and identity inference of THI metabolites in absence of standards were achieved by LC-UV and High Resolution-MS strategies.The in vitro and ex vivo metabolic products of THI are conserved both across species (rat and Rainbow trout) and levels of biological organization (microsomes and liver slices), as previously reported for the neonicotinoid insecticides Imidacloprid and Acetamiprid.Entities:
Keywords: Chloropyridinyl neonicotinoids; in vitro/ex vivo metabolism; microsomal fraction; precision-cut slices; rainbow trout; rat; thiacloprid; uHPLC-HR-MS
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Year: 2021 PMID: 33086928 PMCID: PMC9536423 DOI: 10.1080/00498254.2020.1840658
Source DB: PubMed Journal: Xenobiotica ISSN: 0049-8254 Impact factor: 1.997