The metabolism of imidacloprid by aldehyde oxidase contributes to its clastogenic effect in New Zealand rabbits

Publication date: May–June 2018 Source:Mutation Research/Genetic Toxicology and Environmental Mutagenesis, Volumes 829–830 Author(s): Alexander I. Vardavas, Eren Ozcagli, Persefoni Fragkiadaki, Polychronis D. Stivaktakis, Manolis N. Tzatzarakis, Athanasios K. Alegakis, Fotini Vasilaki, Kostas Kaloudis, John Tsiaoussis, Dimitrios Kouretas, Christina Tsitsimpikou, Félix Carvalho, Aristidis M. Tsatsakis Imidacloprid (IMI) is a systemic, chloro-nicotinyl insecticide classified in Regulation N° 1272/2008 of the European Commision as “harmful if swallowed and very toxic to aquatic life, with long-lasting effects”. IMI is metabolized in vitro both by aldehyde oxidase (AOX) (reduction) and by cytochrome P450s enzymes (CYPs). In the present study, the AOX inhibitor sodium tungstate dihydrate (ST) was used to elucidate the relative contribution of CYP 450 and AOX metabolic pathways on IMI metabolism, in male rabbits exposed to IMI for two months. To evaluate the inhibition effectiveness, various metabolite concentrations in the IMI and IMI + ST exposed groups were monitored. DNA damage was also evaluated in micronucleus (MN) and single cell electrophoresis (SCGC) assays in both groups, along with oxidative stress (OS) with the inflammatory status of the exposed animals, in order to clarify which metabolic pathway is more detrimental in this experimental setting. A significant increase in the frequency of binucleated cells with MN (BNMN, 105%) and micronucle...
Source: Mutation Research Genetic Toxicology and Environmental Mutagenesis - Category: Genetics & Stem Cells Source Type: research