Uncoupling as initiating event in mitochondrial dysfunction after diuron exposure

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Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.contributorCenter for Evaluation of Environmental Impact on Human Health (TOXICAM)-
Autor(es): dc.creatorSeloto, Danielle Gabriel-
Autor(es): dc.creatorRios Rossi Lima, Thania-
Autor(es): dc.creatorde Camargo, João Lauro Vianna-
Autor(es): dc.creatorPereira, Lilian Cristina-
Data de aceite: dc.date.accessioned2025-08-21T15:28:45Z-
Data de disponibilização: dc.date.available2025-08-21T15:28:45Z-
Data de envio: dc.date.issued2025-04-29-
Data de envio: dc.date.issued2023-12-31-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.1080/01480545.2024.2404129-
Fonte completa do material: dc.identifierhttps://hdl.handle.net/11449/297446-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/297446-
Descrição: dc.descriptionDiuron, a herbicide derived from urea, has been shown to induce urinary bladder urothelial tumors in rodents, leading the U.S. Environmental Protection Agency (USEPA) to designate it as a ‘known/likely’ human carcinogen. In our laboratory, a series of studies investigating the carcinogenic mode of action (MoA) of Diuron have consistently revealed its cytotoxic effects on the urinary bladder urothelium. Prolonged exposure to relatively high doses of Diuron results in urothelial necrosis, regenerative hyperplasia, and eventually, the development of tumors. The hypothesis posited is that Diuron and its metabolites exert toxicity by causing damage to mitochondria, a phenomenon referred to as mitotoxicity. Our research focuses on evaluating how Diuron and its metabolites affect mitochondria isolated from both the urothelium and the liver, the primary organ for Diuron biotransformation. In this context, we present and discuss data pertaining to mitochondria isolated from the liver of Wistar rats exposed to Diuron or its metabolites 3-(3,4-diclorofenil)-1-metilureia (DCPMU) or 3,4-dichloroaniline (DCA) at concentrations ranging from 0.5 to 500 µM in vitro. The findings indicate that, at concentrations of 100 and 500 µM, the tested chemicals induce uncoupling of oxidative phosphorylation, as evidenced by the dissipation of mitochondrial membrane potential and basal oxygen consumption. Notably, at 500 µM, DCA causes mitochondrial swelling, a morphofunctional indicator of severe organelle damage. These outcomes underscore the classification of Diuron and its metabolites, DCA and DCPMU, as mitotoxic to liver cells, given the pronounced mitochondrial dysfunction they induce.-
Descrição: dc.descriptionMedical School São Paulo State University (UNESP), São Paulo-
Descrição: dc.descriptionCenter for Evaluation of Environmental Impact on Human Health (TOXICAM), São Paulo-
Descrição: dc.descriptionSchool of Agriculture São Paulo State University (UNESP), São Paulo-
Descrição: dc.descriptionMedical School São Paulo State University (UNESP), São Paulo-
Descrição: dc.descriptionSchool of Agriculture São Paulo State University (UNESP), São Paulo-
Formato: dc.format1382-1392-
Idioma: dc.languageen-
Relação: dc.relationDrug and Chemical Toxicology-
???dc.source???: dc.sourceScopus-
Palavras-chave: dc.subjectDCA-
Palavras-chave: dc.subjectDCPMU-
Palavras-chave: dc.subjectDiuron-
Palavras-chave: dc.subjectMitochondrial damage-
Palavras-chave: dc.subjectmitotoxicants-
Palavras-chave: dc.subjecttoxicity mechanisms-
Título: dc.titleUncoupling as initiating event in mitochondrial dysfunction after diuron exposure-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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