The effect of omega-3 fatty acids on alcohol-induced damage

Abstract

Alcohol is the most widely consumed psychoactive substance in the world that has a severe impact on many organs and bodily systems, particularly the liver and nervous system. Alcohol use during pregnancy roots long-lasting changes in the newborns and during adolescence has long-term detrimental effects especially on the brain. The brain contains docosahexaenoic acid (DHA), a major omega-3 (n-3) fatty acid (FA) that makes up cell membranes and influences membrane-associated protein function, cell signaling, gene expression and lipid production. N-3 is beneficial in several brain conditions like neurodegenerative diseases, ameliorating cognitive impairment, oxidative stress, neuronal death and inflammation. Because alcohol decreases the levels of n-3, it is timely to know whether n-3 supplementation positively modifies alcohol-induced injuries. The aim of this review is to summarize the state-of-the-art of the n-3 effects on certain conditions caused by alcohol intake, focusing primarily on brain damage and alcoholic liver disease.

Keywords: brain damage; ethanol; liver disease; n-3; polyunsaturated fatty acids.

FIGURE 1

FASD and n-3 effects. Due to maternal ethanol intake, fetal glutathione decreases, oxidative stress augments, neuronal necrosis raises and LTP is impaired. Maternal n-3 enriched diet increases glutathione, decreases oxidative stress, reduces neuronal necrosis and rescues LTP, mitigating ethanol harmful effects. Created with www.Biorender.com.

FIGURE 2

Alcohol damage of neurogenic NSC differentiation and n-3 effects. Alcohol decreases G protein and AC activation, consequently cAMP signaling is downregulated and PKA and CREB phosphorylation are increased, having a negative impact on NSC differentiation. PDE activity is upregulated by alcohol. However, n-3 intake improves cAMP signaling, decreasing PKA/CREB that promotes NSC differentiation. Also, n-3 downregulates PDE. Created with www.Biorender.com.

FIGURE 3

Alcohol-induced hepatic steatosis and n-3 effects. The increase in SRBEP-1 and ROS by alcohol elevates liver FA biosynthesis and oxidative stress, respectively, and alcoholic PPARα rise reduces liver fat oxidation. The consequence is steatosis. N-3 enriched diet lowers SRBEP-1 and ROS, decreasing liver FA biosynthesis and oxidative stress. It also promotes liver fat oxidation by downregulating activation of PPARα. Altogether, n-3 ameliorates steatosis. Created with www.Biorender.com.