Prevention of Brain Damage Triggered by Alcohol Consumption during Adolescence: Focus on Oxidative Stress

BUJÁN, GE; GUELMAN, LR; SERRA, HA; MOLINA, SJ

CURRENT PHARMACEUTICAL DESIGN.

BENTHAM SCIENCE PUBL LTD

Lugar: Oak Park; Año: 2019 vol. 25 p. 4782 - 4790

1381-6128

Alcohol consumption usually begins in human adolescence, often in a "binge like" manner. However, although alcohol abuse has a high prevalence at this stage, its effects have been hardly examined in the developing brain. Several authors have reported that alcohol intake during specific periods of development might induce brain damage. Although the mechanisms are poorly understood, it has been postulated that neuroinflammatory processes as well as 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 ROS production. However, only few studies have measured brain ROS levels in experimental animals exposed to alcohol during development. Moreover, although neuroprotective agents may be relevant tools useful to reduce alcohol-induced neurodegeneration, restore cognitive function and improve treatment outcomes for alcoholism, few data are available in the literature. The present paper reviews significant evidences about the mechanisms involved in alcohol-induced brain damage on developing individuals as well as the effect of different potential neuroprotectants that have shown to be able to prevent alcohol-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) or the antioxidant properties of the female hormone estradiol, are some of the therapeutic strategies that could have some clinical relevance in the treatment of alcoholism.