Detoxification activity of bioactive food compounds against ethanol-induced injuries and hangover symptoms: A review

Abstract

Alcohol drinking is a popular activity among adolescents in many countries, largely due to its pleasant, relaxing effects. As a major concern, ethanol consumption put the drinkers at risk of nutrients' deficiency due to the disordered eating, anorexia, and malabsorption of nutrients. Moreover, alcohol drinking may lead to the development of hangover symptoms including diarrhea, thirsty, fatigue, and oxidative stress. A broad range of functional food components with antioxidant and/or anti-inflammatory properties including pectin, aloe vera polysaccharides, chito-oligosaccharides, and other herbal components have been explored due to their detoxification effects against ethanol. The underlying anti-hangover mechanisms include reducing the intestinal absorption of ethanol or its metabolites, increasing the activity of ethanol metabolizing enzymes, development of fatty acid β-oxidation in mitochondria, inhibition of inflammatory response, blocking the target receptors of ethanol in the body, and possession of antioxidant activity under the oxidative stress developed by ethanol consumption. Therefore, the development of bioactive food-based therapeutic formula can assist clinicians and also drinkers in the alleviation of alcohol side effects.

Keywords: anti‐hangover agents; bioactive food compounds; detoxification; ethanol; food supplementation; nutrient deficiency.

FIGURE 1

A summary of potential long‐term health effects of excessive alcohol drinking on some main organs.

FIGURE 2

Metabolism of ethanol into acetaldehyde by two enzymatic pathways. In the liver, alcohol dehydrogenase (ADH) plays a major role, while cytochrome P450 (CYP2E1) plays a minor role.

FIGURE 3

Mitochondrial fatty acid beta‐oxidation and its role in ethanol‐induced fatty liver. Fatty acids enter into the cell. In the cytoplasm, fatty acids are converted to fatty Acyl‐CoA by acyl‐CoA synthase and then transferred to the mitochondrial matrix by VDAC, CPT I, CACT, and CPT II, step by step. Acyl‐CoA then undergoes β‐oxidation to produce acetyl‐CoA for tricarboxylic acid cycle. These are the normal mechanisms for fatty acid catabolism. In the presence of alcohol, these mechanisms are impaired, resulting in morphologic changes in the liver cells and the accumulation of fats. ACS, Acyl‐CoA synthase; CPT, carnitine O‐palmitoyltransferase; CACT, carnitine‐acylcarnitine translocase; VDAC, voltage‐dependent anion channel.

FIGURE 4

The role of pectin in enhancing the viscosity of intestinal mucus and its inhibitory impacts on absorption of ethanol or ethanol‐derived metabolites. These inhibitory effects ultimately reduce lipogenesis in the liver.