## 1 Introduction  
Ethanolamine glycerophospholipids (EtnGpls) are the major phospholipids present in biological membranes and can be classified into three subclasses based on differences in linkages at the _sn_-1 position of the glycerol moiety. Ethanolamine plasmalogen (PIsEtn) and phosphatidylethanolamine (PtdEtn) are the alkenyl and acyl forms of the EtnGpls, respectively. The ratio of PlsEtn-to-EtnGpl in the body varies depending on the tissue or organ. For example, in the human brain and nervous system, PlsEtn represents more than 60% of the total EtnGpls, whereas in the liver, it represents only 2-5% [1]. Owing to its alkenyl bond (vinyl-ether bond), PlsEtn possesses antioxidant properties, and its _sn_-2 position predominantly consists of polyunsaturated fatty acids (PUFA), including docosahexaenoicenoic acid (DHA; 22:6_sn_-3). Neurodegenerative disorders, such as Alzheimer's disease, result in decreased levels of PlsEtn, particularly PlsEtn-bearing DHA, in the brain and blood [2; 3; 4]. Endogenous plasmalogens, including choline plasmalogen, protect against hepatic steatosis and steatohepatitis in mice [5]. In some marine invertebrates, such as ascidian _Halocynthia roretzi_ and pacific oyster _Crassostrea gigas_, the majority of EtnGpl is present as PlsEtn [6]. Marine-derived PlsEtn exhibits various nutritional functions, including improving cognitive performance and intestinal impairments [1]. The alkenyl bond in plasmalogens is acid-labile, but plasmalogens contained in the diet are hardly degraded under stomach-like conditions (pH 1.0 at 37 \({}^{\circ}\)C for 1 h) because of the buffering action of the diets [7; 8; 9]. Ingested PlsEtn is digested into lysoPlsEtn and free fatty acid in the small intestine, and PlsEtn digests are absorbed and are subsequently resynthesized into PlsEtn preferentially with PUFA. Some ingested PlsEtn and lysoPlsEtn reach the large intestine. Therefore, ingested PlsEtn can function in both the body and intestines. PlsEtn mitigates LPS-induced damage in intestinal epithelial cells in vitro [10]. Administration of PlsEtn or lysoPlsEtn suppresses intestinal inflammatory injury in a mouse model of colitis and increases the cecal levels of short-chain fatty acids, which are produced by microbiota and enhance the intestinal barrier [11; 12]. PlsEtn protects HepG2 cells, which are used as an in vitro hepatic model, from lead-induced toxicity and subsequent oxidative stress [13]. Dietary PlsEtn enriched with eicosapentaenoic acid (EPA; 20:5_sn_-3) has been shown to mitigate atherosclerosis and hepatic steatosis in rodents subjected to a high-fat diet, and these effects are more pronounced than those observed with dietary EPA-ethyl ester [14; 15]. The proposed mechanism involves the enhancement of lipid and bile acid excretion in feces through the elevated hepatic expression of cytochrome P450 (CYP) 7A1. This process is achieved by the suppression of the farnesoid X receptor activation in the liver and the modification of microbiota abundance, which has bile salt hydrolase, thereby affecting secondary bile acid production. Although PlsEtn is present in the liver at low levels, it plays significant hepatic nutritional roles, including the enhancement of lipid metabolism and antioxidant activity. These effects may be exerted directly on the liver as well as through the gut-liver axis. Furthermore, the benefits conferred by dietary PlsEtn may mitigate liver impairment induced by excessive or prolonged drug dosage. Acetaminophen (_N_-acetyl-_p_-aminophenol, APAP) is a frequently used analgesic and antipyretic, and its overdose causes acute liver failure (ALF), chronic active hepatitis, cholestasis, and jaundice [16; 17]. Approximately 90% of the administered APAP is metabolized by UDP-glucuronosyltransferase and sulfotransferase into glucuronic acid and sulfate conjugates, respectively. Moreover, 5-9% of administered APAP is metabolized into the highly reactive intermediate _N_-acetyl-_p_-benzoquinone imine (NAQI) by the enzymatic reaction of CYP2E1 with APAP [18].