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.