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dc.contributor.authorMiranda, Camila Araújo [UNESP]
dc.contributor.authorGuimarães, Anilda Rufino de Jesus Santos [UNESP]
dc.contributor.authorBizerra, Paulo Francisco Veiga [UNESP]
dc.contributor.authorMingatto, Fábio Erminio [UNESP]
dc.date.accessioned2020-12-12T02:47:51Z
dc.date.available2020-12-12T02:47:51Z
dc.date.issued2020-09-16
dc.identifierhttp://dx.doi.org/10.1080/15287394.2020.1805078
dc.identifier.citationJournal of Toxicology and Environmental Health - Part A: Current Issues, v. 83, n. 17-18, p. 616-629, 2020.
dc.identifier.issn1087-2620
dc.identifier.issn1528-7394
dc.identifier.urihttp://hdl.handle.net/11449/202023
dc.description.abstractDiazinon (DZN) is a broad-spectrum insecticide extensively used to control pests in crops and animals. Several investigators demonstrated that DZN produced tissue toxicity especially to the liver. In addition, the mitochondrion was implicated in DZN-induced toxicity, but the precise role of this organelle remains to be determined. The aim of this study was thus to examine the effects of DZN (50 to 150 μM) on the bioenergetics and mitochondrial permeability transition (MPT) associated processes in isolated rat liver mitochondria. DZN inhibited state-3 respiration in mitochondria energized with glutamate plus malate, substrates of complex I, and succinate, substrate of complex II of the respiratory chain and decreased the mitochondrial membrane potential resulting in inhibition of ATP synthesis. MPT was estimated by the extent of mitochondrial swelling, in the presence of 10 µM Ca2+. DZN elicited MPT in a concentration-dependent manner, via a mechanism sensitive to cyclosporine A, EGTA, ruthenium red and N-ethylmaleimide, which was associated with mitochondrial Ca2+ efflux and cytochrome c release. DZN did not result in hydrogen peroxide accumulation or glutathione oxidation, but this insecticide oxidized endogenous NAD(P)H and protein thiol groups. Data suggest the involvement of mitochondria, via apoptosis, in the hepatic cytotoxicity attributed to DZN.en
dc.format.extent616-629
dc.language.isoeng
dc.relation.ispartofJournal of Toxicology and Environmental Health - Part A: Current Issues
dc.sourceScopus
dc.subjectDiazinon
dc.subjectliver
dc.subjectmitochondrial membrane permeability transition
dc.subjectoxidative phosphorylation
dc.subjecttoxicity
dc.titleDiazinon impairs bioenergetics and induces membrane permeability transition on mitochondria isolated from rat liveren
dc.typeArtigo
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationDepartment of Animal Production College of Agricultural and Technological Sciences São Paulo State University (Unesp
dc.description.affiliationUnespDepartment of Animal Production College of Agricultural and Technological Sciences São Paulo State University (Unesp
dc.identifier.doi10.1080/15287394.2020.1805078
dc.identifier.scopus2-s2.0-85089456708
unesp.author.orcid0000-0003-3488-1814[4]
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