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dc.contributor.authorStivaktakis, Polychronis D.
dc.contributor.authorTzatzarakis, Manolis N.
dc.contributor.authorAlegakis, Athanasios K.
dc.contributor.authorVasilaki, Fotini
dc.contributor.authorKaloudis, Kostas
dc.contributor.authorVardavas, Alexander I.
dc.contributor.authorTsiaoussis, John
dc.contributor.authorKouretas, Dimitrios
dc.contributor.authorTsitsimpikou, Christina
dc.contributor.authorCarvalho, Felix
dc.contributor.authorTsatsakis, Aristidis M.
dc.contributor.authorOzcagli, Eren
dc.contributor.authorFragkiadaki, Persefoni
dc.date.accessioned2021-03-05T11:59:46Z
dc.date.available2021-03-05T11:59:46Z
dc.identifier.citationVardavas A. I. , Ozcagli E., Fragkiadaki P., Stivaktakis P. D. , Tzatzarakis M. N. , Alegakis A. K. , Vasilaki F., Kaloudis K., Tsiaoussis J., Kouretas D., et al., "The metabolism of imidacloprid by aldehyde oxidase contributes to its clastogenic effect in New Zealand rabbits", MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, cilt.829, ss.26-32, 2018
dc.identifier.issn1383-5718
dc.identifier.otherav_aae3065b-5a40-4d47-9195-a01d06170de2
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/114111
dc.identifier.urihttps://doi.org/10.1016/j.mrgentox.2018.03.002
dc.description.abstractImidacloprid (IMI) is a systemic, chloro-nicotinyl insecticide classified in Regulation No 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 micronuclei (MN, 142%) was observed after exposure to IMI (p 0.05), which indicates no cytotoxic effect. Similarly, comet results show that the IMI group exhibited the highest achieved tail intensity, which reached 70.7% over the control groups, whereas in the IMI + ST groups the increase remained at 48.5%. No differences were observed between all groups for oxidative-stress biomarkers. The results indicate that the AOX metabolic pathway plays a more important role in the systemic toxicity of IMI.
dc.language.isoeng
dc.subjectMeslek Bilimleri
dc.subjectBİYOTEKNOLOJİ VE UYGULAMALI MİKROBİYOLOJİ
dc.subjectMikrobiyoloji
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectGENETİK VE HAYAT
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectTOKSİKOLOJİ
dc.subjectFarmakoloji ve Toksikoloji
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectTıbbi Genetik
dc.subjectEczacılık
dc.subjectFarmasötik Toksikoloji
dc.subjectYaşam Bilimleri
dc.subjectBiyoteknoloji
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectTemel Bilimler
dc.titleThe metabolism of imidacloprid by aldehyde oxidase contributes to its clastogenic effect in New Zealand rabbits
dc.typeMakale
dc.relation.journalMUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
dc.contributor.departmentTechnical University Of Crete , ,
dc.identifier.volume829
dc.identifier.startpage26
dc.identifier.endpage32
dc.contributor.firstauthorID253087


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