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DOI 10.1002/bdr2.1172

Медицинская библиотека · Birth defects research · 2017

Alcohol consumption during adolescence: A link between mitochondrial damage and ethanol brain intoxication.

Tapia-Rojas Cheril, Mira Rodrigo G, Torres Angie K, Jara Claudia, Pérez María José, Vergara Erick H, Cerpa Waldo, Quintanilla Rodrigo A

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Аннотация

Adolescence 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.

Для цитирования: Tapia-Rojas Cheril, Mira Rodrigo G, Torres Angie K, Jara Claudia, Pérez María José, Vergara Erick H, Cerpa Waldo, Quintanilla Rodrigo A. Alcohol consumption during adolescence: A link between mitochondrial damage and ethanol brain intoxication.. Birth defects research. 2017. DOI: 10.1002/bdr2.1172.

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