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NADPH oxidase contributes to oxidative damage and mitochondrial impairment induced by acute ethanol treatment in rat hippocampal neurons

dc.contributor.authorPérez M.J.
dc.contributor.authorLoyola R.
dc.contributor.authorCanelo F.
dc.contributor.authorAranguiz A.
dc.contributor.authorTapia-Monsalves C.
dc.contributor.authorOsorio-Fuentealba C.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:26:01Z
dc.date.available2020-09-02T22:26:01Z
dc.date.issued2020
dc.identifier10.1016/j.neuropharm.2020.108100
dc.identifier.citation171, , -
dc.identifier.issn00283908
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5868
dc.descriptionAcute ethanol treatment induces neurodegeneration in cultured neurons and can lead to brain damage in animal models. Neuronal cells exposed to ethanol showed an increase in reactive oxygen species (ROS), oxidative damage and mitochondrial impairment contributing to synaptic failure. However, the underlying mechanisms of these events are not well understood. Here, we studied the contribution of NADPH oxidase, as a relevant source of ROS production in the brain, to mitochondrial impairment and oxidative stress induced by ethanol. We used primary hippocampal neurons subjected to an acute treatment of ethanol at increasing concentrations (25, 50, and 75 mM, 24 h), and we evaluated ROS production, mitochondrial function, and synaptic vesicle activity. Our studies showed that after ethanol administration, hippocampal neurons presented an increase in ROS levels, mitochondrial dysfunction, calcium handling defects, and synaptic impairment. Interestingly, treatment with the NADPH inhibitor, apocynin, significantly prevented oxidative stress, mitochondrial dysfunction, and the impairment of synaptic vesicle activity induced by ethanol treatment. These results indicate that NADPH oxidase could be a key participant in the molecular mechanism by which alcohol affects the brain. © 2020 Elsevier Ltd
dc.language.isoen
dc.publisherElsevier Ltd
dc.subjectAlcohol
dc.subjectMitochondria
dc.subjectNADPH oxidase
dc.subjectOxidative stress
dc.subjectadenosine triphosphate
dc.subjectalcohol
dc.subjectapocynin
dc.subjectmitochondrial permeability transition pore
dc.subjectreactive oxygen metabolite
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbioenergy
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectcytosol
dc.subjectembryo
dc.subjectenzyme inhibition
dc.subjectenzyme mechanism
dc.subjectenzyme synthesis
dc.subjectfluorescence
dc.subjecthippocampus
dc.subjectincubation time
dc.subjectlimit of quantitation
dc.subjectmitochondrion
dc.subjectnerve cell culture
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectrat
dc.subjectsynapse vesicle
dc.subjectultraviolet spectrophotometry
dc.subjectWestern blotting
dc.titleNADPH oxidase contributes to oxidative damage and mitochondrial impairment induced by acute ethanol treatment in rat hippocampal neurons
dc.typeArticle


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