Artículo
Prevention of Brain Damage Triggered by Alcohol Consumption during Adolescence: Focus on Oxidative Stress
Fecha de publicación:
08/2019
Editorial:
Bentham Science Publishers
Revista:
Current Pharmaceutical Design
ISSN:
1381-6128
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
Alcohol consumption, in particular ethanol (EtOH), typically begins in human adolescence, often in a “binge like” manner. However, although EtOH abuse has a high prevalence at this stage, the effects of exposure during adolescence have been less explored than prenatal or adult age exposure. Several authors have reported that EtOH intake during specific periods of development might induce brain damage. Although the mechanisms are poorly understood, it has been postulated that oxidative stress may play a role. In fact, some of these studies revealed a decrease in brain antioxidant enzymes’ level and/or an increase in reactive oxygen species (ROS) production. Nevertheless, although existing literature shows a number of studies in which ROS were measured in developing animals, fewer reported the measurement of ROS levels after EtOH exposure in adolescence. Importantly, neuroprotective agents aimed to these potential targets may be relevant tools useful to reduce EtOH-induced neurodegeneration, restore cognitive function and improve treatment outcomes for alcohol use disorders (AUDs). The present paper reviews significant evidences about the mechanisms involved in EtOH-induced brain damage, as well as the effect of different potential neuroprotectants that have shown to be able to prevent EtOH-induced oxidative stress. A selective inhibitor of the endocannabinoid anandamide metabolism, a flavonol present in different fruits (quercetin), an antibiotic with known neuroprotective properties (minocycline), a SOD/catalase mimetic, a potent antioxidant and anti-inflammatory molecule (resveratrol), a powerful ROS scavenger (melatonin), an isoquinoline alkaloid (berberine), are some of the therapeutic strategies that could have some clinical relevance in the treatment of AUDs. As most of these works were performed in adult animal models and using EtOH-forced paradigms, the finding of neuroprotective tools that could be effective in adolescent animal models of voluntary EtOH intake should be encouraged.
Palabras clave:
ADOLESCENCE
,
BEHAVIOR
,
DEVELOPMENT
,
ETHANOL
,
NEUROPROTECTION
,
OXIDATIVE STRESS
Archivos asociados
Licencia
Identificadores
Colecciones
Articulos(CEFYBO)
Articulos de CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Articulos de CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Citación
Buján, Gustavo Ezequiel; Serra, H.A.; Molina, Sonia Jazmín; Guelman, L.R.; Prevention of Brain Damage Triggered by Alcohol Consumption during Adolescence: Focus on Oxidative Stress; Bentham Science Publishers; Current Pharmaceutical Design; 25; 45; 8-2019; 4782-4790
Compartir
Altmétricas