Diuron and its metabolites induce mitochondrial dysfunction-mediated cytotoxicity in urothelial cells

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MetadadosDescriçãoIdioma
Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.creatorLima, Thania Rios Rossi-
Autor(es): dc.creatorKohori, Natalia Akemi-
Autor(es): dc.creatorde Camargo, João Lauro Viana-
Autor(es): dc.creatorda Silva, Carla Adriene-
Autor(es): dc.creatorPereira, Lilian Cristina-
Data de aceite: dc.date.accessioned2025-08-21T21:25:53Z-
Data de disponibilização: dc.date.available2025-08-21T21:25:53Z-
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/10.1080/15376516.2023.2250430-
Fonte completa do material: dc.identifierhttps://hdl.handle.net/11449/301050-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/301050-
Descrição: dc.descriptionIn the environment, or during mammalian metabolism, the diuron herbicide (3-(3,4-dichlorophenyl)-1,1-dimethylurea) is transformed mainly into 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU) and 3,4-dichloroaniline (DCA). Previous research suggests that such substances are toxic to the urothelium of Wistar rats where, under specific exposure conditions, they may induce urothelial cell degeneration, necrosis, hyperplasia, and eventually tumors. However, the intimate mechanisms of action associated with such chemical toxicity are not fully understood. In this context, the purpose of the current in vitro study was to analyze the underlying mechanisms involved in the urothelial toxicity of those chemicals, addressing cell death and the possible role of mitochondrial dysfunction. Thus, human 1T1 urothelial cells were exposed to six different concentrations of diuron, DCA, and DCPMU, ranging from 0.5 to 500 µM. The results showed that tested chemicals induced oxidative stress and mitochondrial damage, cell cycle instability, and cell death, which were more expressive at the higher concentrations of the metabolites. These data corroborate previous studies from this laboratory and, collectively, suggest mitochondrial dysfunction as an initiating event triggering urothelial cell degeneration and death.-
Descrição: dc.descriptionSão Paulo State University (UNESP) Medical School-
Descrição: dc.descriptionCenter for Evaluation of Environmental Impact on Human Health (TOXICAM) UNESP Medical School-
Descrição: dc.descriptionSão Paulo State University (UNESP) School of Agriculture-
Descrição: dc.descriptionSão Paulo State University (UNESP) Medical School-
Descrição: dc.descriptionCenter for Evaluation of Environmental Impact on Human Health (TOXICAM) UNESP Medical School-
Descrição: dc.descriptionSão Paulo State University (UNESP) School of Agriculture-
Formato: dc.format32-45-
Idioma: dc.languageen-
Relação: dc.relationToxicology Mechanisms and Methods-
???dc.source???: dc.sourceScopus-
Palavras-chave: dc.subject1T1 cell culture-
Palavras-chave: dc.subjectdiuron and metabolites-
Palavras-chave: dc.subjectmitochondrial pathways-
Palavras-chave: dc.subjectMitotoxicants-
Palavras-chave: dc.subjecttoxicodynamics-
Título: dc.titleDiuron and its metabolites induce mitochondrial dysfunction-mediated cytotoxicity in urothelial cells-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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