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dc.contributor.authorTapia-Rojas C.
dc.contributor.authorMira R.G.
dc.contributor.authorTorres A.K.
dc.contributor.authorJara C.
dc.contributor.authorPérez M.J.
dc.contributor.authorVergara E.H.
dc.contributor.authorCerpa W.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:29:14Z
dc.date.available2020-09-02T22:29:14Z
dc.date.issued2017
dc.identifier10.1002/bdr2.1172
dc.identifier.citation109, 20, 1623-1639
dc.identifier.issn24721727
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6375
dc.descriptionAdolescence is a period of multiple changes where social behaviors influence interpersonal-relations. Adolescents live new experiences, including alcohol consumption which has become an increasing health problem. The age of onset for consumption has declined in the last decades, and additionally, the adolescents now uptake greater amounts of alcohol per occasion. Alcohol consumption is a risk factor for accidents, mental illnesses or other pathologies, as well as for the appearance of addictions, including alcoholism. An interesting topic to study is the damage that alcohol induces on the central nervous system (CNS) in the young population. The brain undergoes substantial modifications during adolescence, making brain cells more vulnerable to the ethanol toxicity. Over the last years, the brain mitochondria have emerged as a cell organelle which is particularly susceptible to alcohol. Mitochondria suffer severe alterations which can be exacerbated if the amount of alcohol or the exposure time is increased. In this review, we focus on the changes that the adolescent brain undergoes after drinking, placing particular emphasis on mitochondrial damage and their consequences against brain function. Finally, we propose the mitochondria as an important mediator in alcohol toxicity and a potential therapeutic target to reduce or treat brain conditions associated with excessive alcohol consumption. © 2017 Wiley Periodicals, Inc.
dc.language.isoen
dc.publisherJohn Wiley and Sons Inc.
dc.subjectadolescence
dc.subjectalcohol
dc.subjectalcoholism
dc.subjectbinge-drinking
dc.subjectmitochondria
dc.subjectoxidative stress
dc.subjectalcohol
dc.subjectantioxidant
dc.subjectneurotransmitter
dc.subjectprostaglandin synthase
dc.subjectreactive oxygen metabolite
dc.subjectvoltage dependent anion channel
dc.subjectalcohol
dc.subjectadolescent
dc.subjectalcohol consumption
dc.subjectalcohol intoxication
dc.subjectalcohol withdrawal syndrome
dc.subjectalcoholism
dc.subjectbinge drinking
dc.subjectbody temperature
dc.subjectbrain cell
dc.subjectbrain function
dc.subjectbrain intoxication
dc.subjectcalcium homeostasis
dc.subjectcell damage
dc.subjectcell death
dc.subjectcentral nervous system
dc.subjectcentral nervous system depression
dc.subjectcerebellum
dc.subjectconsciousness disorder
dc.subjectemotional disorder
dc.subjecthangover
dc.subjecthippocampus
dc.subjecthuman
dc.subjectmental disease
dc.subjectmitochondrial damage
dc.subjectmitochondrial membrane
dc.subjectmitochondrial permeability
dc.subjectoxidative stress
dc.subjectperception
dc.subjectphysical capacity
dc.subjectpublic health problem
dc.subjectReview
dc.subjectrisk factor
dc.subjectsynapse
dc.subjectalcohol intoxication
dc.subjectbrain
dc.subjectdrinking behavior
dc.subjectdrug effect
dc.subjectmitochondrion
dc.subjectpathology
dc.subjectsocial behavior
dc.subjectAdolescent
dc.subjectAlcohol Drinking
dc.subjectAlcoholic Intoxication
dc.subjectBrain
dc.subjectEthanol
dc.subjectHumans
dc.subjectMitochondria
dc.subjectRisk Factors
dc.subjectSocial Behavior
dc.titleAlcohol consumption during adolescence: A link between mitochondrial damage and ethanol brain intoxication
dc.typeReview


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