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Adolescence binge alcohol consumption induces hippocampal mitochondrial impairment that persists during the adulthood

dc.contributor.authorTapia-Rojas C.
dc.contributor.authorTorres A.K.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:29:14Z
dc.date.available2020-09-02T22:29:14Z
dc.date.issued2019
dc.identifier10.1016/j.neuroscience.2019.03.018
dc.identifier.citation406, , 356-368
dc.identifier.issn03064522
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6376
dc.descriptionBinge alcohol drinking is a well characterized consumption pattern related with drinking five or more alcoholic beverages during a short period of time followed by a non-drinking period. Several studies showed that this pattern of alcohol intake is becoming very popular among adolescents. However, little is known about the cellular mechanisms involved in ethanol toxicity under these conditions and if these negative changes could be extending to the adulthood. We previously reported that adolescent binge-ethanol consumption impairs brain function acutely. More importantly, we found that animals exposed to this alcohol treatment showed a decrease in the ATP production that remain over time. Therefore, in the present study, we will evaluate the mitochondrial and oxidative alterations that could occur in the adult hippocampus of rats exposed to a unique binge-drinking episode during the adolescence. Our results indicate that adult hippocampus after one adolescent binge-drinking episode presents an increase in the reactive oxygen species production accompanied of mitochondrial dysfunction. Adolescent binge-like ethanol exposure reduced the expression of the mitochondrial respiration complexes, induced mitochondrial depolarization, increased mitochondrial calcium levels, and reduced ATP production in the adult hippocampus. Altogether, our results indicate that adolescence binge alcohol drinking affects the electron transport chain components expression resulting in mitochondrial failure and loss of calcium buffering in the adult hippocampus. Therefore, we reported for first time that adolescent binge-alcohol consumption has severe repercussions on mitochondrial bioenergetics during the adulthood; and that this is not a transitory change until the state of drunkenness disappears as previously believed. © 2019 Elsevier Ltd
dc.language.isoen
dc.publisherElsevier Ltd
dc.subjectadolescence
dc.subjectalcohol
dc.subjectbinge-drinking
dc.subjecthippocampus
dc.subjectmitochondria
dc.subjectadenosine triphosphate
dc.subjectalcohol
dc.subjectcalcium
dc.subjectreactive oxygen metabolite
dc.subjectreactive oxygen metabolite
dc.subjectadolescent
dc.subjectadult
dc.subjectadulthood
dc.subjectalcohol consumption
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbinge drinking
dc.subjectbrain function
dc.subjectcalcium cell level
dc.subjectcognitive defect
dc.subjectcontrolled study
dc.subjectdepolarization
dc.subjectdisorders of mitochondrial functions
dc.subjectelectron transport
dc.subjectexposure
dc.subjectmitochondrial respiration
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectrat
dc.subjectadverse event
dc.subjectage
dc.subjectanimal
dc.subjectbinge drinking
dc.subjectcomplication
dc.subjectdrinking behavior
dc.subjectdrug effect
dc.subjecthippocampus
dc.subjectmale
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectorgan culture technique
dc.subjectpathology
dc.subjectSprague Dawley rat
dc.subjectAge Factors
dc.subjectAlcohol Drinking
dc.subjectAnimals
dc.subjectBinge Drinking
dc.subjectHippocampus
dc.subjectMale
dc.subjectMitochondria
dc.subjectOrgan Culture Techniques
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectReactive Oxygen Species
dc.titleAdolescence binge alcohol consumption induces hippocampal mitochondrial impairment that persists during the adulthood
dc.typeArticle


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