β-Naphthoflavone and ethanol reverse mitochondrial dysfunction in a parkinsonian model of neurodegeneration

The 1-methyl-4-phenylpyridinium (MPP+) is a parkinsonian-inducing toxin that promotes neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it was reported that some Cytochrome P450 (CYP) isoforms, such as CYP 2D6 or 2E1, may be involved in the developmen...

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Detalhes bibliográficos
Autores: Fernández Abascal, Jesús, Chiaino, Elda, Frosini, Maria, Davey, Gavin P, Valoti, Massimo
Formato: artículo
Fecha de publicación:2020
País:España
Recursos:Universidad Pablo de Olavide (UPO)
Repositorio:RIO. Repositorio Institucional Olavide
Idioma:inglés
OAI Identifier:oai:rio.upo.es:10433/22761
Acesso em linha:https://hdl.handle.net/10433/22761
Access Level:acceso abierto
Palavra-chave:CYP 2D6
CYP 2E1
CYP induction
Cytochrome P-450 system
MPP+ toxicity
Mitochondrial kinetics
Neurodegeneration
Neuroprotection
Descrição
Resumo:The 1-methyl-4-phenylpyridinium (MPP+) is a parkinsonian-inducing toxin that promotes neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it was reported that some Cytochrome P450 (CYP) isoforms, such as CYP 2D6 or 2E1, may be involved in the development of this neurodegenerative disease. In order to study a possible role for CYP induction in neurorepair, we designed an in vitro model where undifferentiated neuroblastoma SH-SY5Y cells were treated with the CYP inducers β-naphthoflavone (βNF) and ethanol (EtOH) before and during exposure to the parkinsonian neurotoxin, MPP+. The toxic effect of MPP+ in cell viability was rescued with both βNF and EtOH treatments. We also report that this was due to a decrease in reactive oxygen species (ROS) production, restoration of mitochondrial fusion kinetics, and mitochondrial membrane potential. These treatments also protected complex I activity against the inhibitory effects caused by MPP+, suggesting a possible neuroprotective role for CYP inducers. These results bring new insights into the possible role of CYP isoenzymes in xenobiotic clearance and central nervous system homeostasis.