## 1 Introduction  
A moderate amount of alcohol can promote the body's metabolism rate and reduce the risk of cardiovascular difficulties. However, long-term, heavy alcohol consumption can cause hangovers and other health issues including hepatitis, liver cirrhosis and fatty liver, muscle pain, etc. [1, 2, 3]. A meta-analysis and case-cohort study indicated that heavy alcohol drinking is associated with being a major risk factor for gastric cancer [4, 5]. In 2014, gastric cancer was the second most common cause of morbidity and the third most common cause of mortality in South Korea [6]. Numerous mechanisms are known to explain alcohol-induced hepatotoxicity, among these, the generation of reactive oxygen species (ROS) leads to oxidative stress, which is one of the most extensively studied mechanisms [7, 8]. In addition, the antioxidant level of the liver cells is inhibited by ethanol-induced oxidative stress [9, 10]. Liver is a primary organ that regulates alcohol metabolism as it contains an abundant amount of alcohol metabolizing enzymes [11]. Alcohol can be metabolized by oxidative and non-oxidative pathways in the liver [12]. These pathways involve several enzymes such as alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), microsomal ethanol oxidizing system (MEOS, CYP2E1), and catalase (less significant) [13]. The most important pathway for alcohol metabolism is represented by alcohol dehydrogenase and acetaldehyde dehydrogenase enzymes widely distributed in the liver. ADH enzymes oxidize ethanol into acetaldehyde, which is broken down further into acetate by ALDH enzymes [14; 15]. In addition, the chronic use of alcohol promotes the production of ROS [16]. Moreover, in mitochondria, NADH is reoxidized into NAD+, which causes an imbalance in the intracellular redox state that leads to an increase in oxidative stress [17]. The excessive consumption of alcohol also increases the activity of cytochrome P450 2E1 (CYP2E1) but not ADH, and this activated enzyme can produce acetaldehyde via the formation of ROS [18]. Large amounts of ROS can cause cellular dysfunction and could eventually lead to cell death [19]. In higher concentrations, both acetaldehyde and ROS can cause harmful effects such as nausea, vomiting, sweating, and a rapid pulse. Therefore, it is important to eliminate excess ethanol and acetaldehyde from our body to prevent severe liver damage [20]. For thousands of years, herbal remedies have been used to cure alcoholic disorders in several cultures. _Terminalia ferdinandiana_, commonly known as the Kakadu plum (KKD), is traditionally the most popular fruit in Australian Aboriginal populations. KKD is found mostly in the Northern Territory (NT) and Western Australia (WA), and is considered to be a medicine rather than food by certain tribes [21; 22; 23]. In WA, KKD is known as the bush plum, billygoat plum, gubinge, and Nyaninyari [3]. In the NT, the Aboriginal people use this fruit as an important commercial product to provide them with a livelihood [23]. The KKD was traditionally used as a refreshing drink for children and adults in WA: it was consumed for energy and refreshment on hunting trips [24]. The fruit contains a large amount of vitamin C (L-ascorbic acid) along with a wide range of phytochemicals, such as phenolic compounds and flavonoids, which includes gallotannins, elgalotannins, elgalotannis, phenolic acids, proanthocyanidins, ellagic and gallic acid [25; 26]. _T. ferdinandiana_ is a potential antioxidant [27; 28; 29] and possesses pharmacological activities against cancer [30], rheumatoid arthritis [31], inflammation [32], bacteria [33], and so on. An investigation revealed that ascorbic acid from _T. ferdinandiana_ has a protective effect against the chronic toxicity of acetaldehyde, which arises from heavy alcohol drinking. In contrast, the levels of ascorbic acid in the body are known to be lowered in alcoholics [34]. However, the protective mechanism of KKD on ethanol metabolism have not yet been reported.