Oxidative Stress-Induced Brain Damage Triggered by Voluntary Ethanol Consumption during Adolescence: A Potential Target for Neuroprotection?

Title:Oxidative Stress-Induced Brain Damage Triggered by Voluntary Ethanol Consumption during Adolescence: A Potential Target for Neuroprotection?

Volume: 25 Issue: 45

Author(s): Gustavo E. Buján, Hector A. Serra, Sonia J. Molina and Laura R. Guelman*

Affiliation:

• Universidad de Buenos Aires, Facultad de Medicina, 1 Cátedra de Farmacología, Buenos Aires,Argentina

Keywords: Ethanol, behavior, oxidative stress, neuroprotection, development, adolescence.

Abstract: 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.

Cite this article as:

Buján E. Gustavo , Serra A. Hector , Molina J. Sonia and Guelman R. Laura *, Oxidative Stress-Induced Brain Damage Triggered by Voluntary Ethanol Consumption during Adolescence: A Potential Target for Neuroprotection?, Current Pharmaceutical Design 2019; 25 (45) . https://dx.doi.org/10.2174/1381612825666191209121735

DOI https://dx.doi.org/10.2174/1381612825666191209121735	Print ISSN 1381-6128
Publisher Name Bentham Science Publisher	Online ISSN 1873-4286