Aged Garlic Extract Prevents Alcohol‐Induced Cytotoxicity through Induction of Aldehyde Dehydrogenase 2 in the Liver of Mice

Abstract

Scope Acetaldehyde is a highly toxic primary metabolite of ethanol, and converts to nontoxic acetic acid by aldehyde dehydrogenase (ALDH). Accumulation of acetaldehyde causes significant damage to human body. Aged garlic extract (AGE) is a functional food material and possesses various health beneficial effects. This study investigates whether AGE contributes to acetaldehyde detoxification through ALDH induction and its underlying mechanism. Methods and results C57BL/6J mice are orally administrated 10–1000 mg kg−1 body weight (BW) of AGE for 1 week before ethanol administration. AGE suppresses ethanol‐caused accumulation of acetaldehyde level in the plasma through inducing mitochondrial ALDH2 but not cytosolic ALDH1A1. AGE also induces antioxidant enzymes, heme oxygenase‐1, and NAD(P)H:quinone oxidoreductase 1, resulting in prevention of lipid peroxidation in the liver. In HepG2 cells, AGE prevents ethanol‐ and acetaldehyde‐caused cytotoxicity. AGE induces mitochondrial ALDH2 through activating nuclear factor‐erythroid 2‐related factor 2 (Nrf2). AGE inhibits protein degradation of Nrf2 and enhances protein degradation of kelch‐like ECH‐associated protein 1. Furthermore, S‐allyl cysteine and S‐allyl mercaptocysteine as the bioactive compounds in AGE also induce ALDH2 and Nrf2. Conclusion AGE prevents acetaldehyde‐induced hepatotoxicity through enhancing acetaldehyde detoxification through Nrf2‐dependent induction of mitochondrial ALDH2.

Aqueous extract of Laurus nobilis leaf accelerates the alcohol metabolism and prevents liver damage in single-ethanol binge rats

“…In this study, oral administration of LN reduced the AST, ALT, and γ-GT activities in the serum of ethanol-administered rats. This is consistent with a recent study that examined the effects of aged garlic extract on alcohol-induced liver damage [ 37 ]. γ-GT is a membrane enzyme involved in glutathione homeostasis.…”