**1. Introduction**

Cadmium (Cd) is a widespread environmental toxicant that poses a serious threat to human health [1]. Due to its high solubility in water, Cd can easily enter the human body through the food chain from polluted soils and water [2]. Cd exposure will cause metabolic dysfunction and eventually lead to irreversible damage to multiple organs [3,4]. About 50–70% of the absorbed heavy metal accumulates in the kidney and liver [5]. Acute Cd exposure primarily results in liver accumulation and hepatic injury [6]. The liver has been considered one of the main target organs of Cd [7]. Recent research has shown that acute Cd exposure leads to severe hepatic injury, accompanied by oxidative damage, inflammation, and apoptosis [8]. Therefore, reducing oxidative damage, ameliorating inflammatory response, and preventing the development of hepatocyte apoptosis may be practical strategies for the treatment of Cd-induced hepatic injury.

**Citation:** Wang, J.; Fang, Z.; Li, Y.; Sun, L.; Liu, Y.; Deng, Q.; Zhong, S. Ameliorative Effects of Oyster Protein Hydrolysates on Cadmium-Induced Hepatic Injury in Mice. *Mar. Drugs* **2022**, *20*, 758. https://doi.org/10.3390/md20120758

Academic Editors: Donatella Degl'Innocenti and Marzia Vasarri

Received: 7 October 2022 Accepted: 28 November 2022 Published: 30 November 2022

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Protein hydrolysates from oysters (*Crassostrea hongkongensis*) have multiple health benefits, including anti-oxidation [9], anti-inflammatory [10], anti-apoptosis [11], anticancer, and other properties [12]. In previous studies, oyster-derived hydrolysates have been shown to be protective against D-galactosamine(D-GalN)-induced hepatic injury [13]. The peptides (SCAP1, SCAP3, and SCAP7) produced from oyster protein hydrolysis (OPs) present strong antioxidant and anti-cancer properties [14]. In addition, OPs are considered to be a safe and effective dietetic treatment for alcoholic liver disease by declining ethanolinduced oxidative stress and inflammation [15]. In addition, oyster ferritin was found to efficiently reduce the damage of heavy metals in mice [16]. The evidence suggests that OPs might be a potential candidate for ameliorating Cd-induced hepatic injury. Therefore, this study aimed to investigate the ameliorative effect of OPs on hepatic oxidative damage, inflammation, and apoptosis in Cd-exposed mice.
