Selenium supplementation effect of selenium-chelating peptide from sturgeon (Acipenseridae) heads and prevention of liver injury in selenium-deficient mice

Abstract

Selenium deficiency leads to oxidative stress and inflammatory damage, while peptide–selenium chelation effectively alleviates this insufficiency. To develop novel selenium supplements from marine by-product resources, sturgeon head peptides (SHPs) were hydrolyzed with pepsin and a sturgeon head peptide–selenium (SHP-Se) chelate was also prepared. The protective effects of the SHP-Se chelate against oxidative stress and liver injury were investigated in a Se-deficient mouse model, which was successfully established by feeding adult Kunming mice a selenium-deficient diet (0.15 mg Se per kg diet) for 18 days. Concurrently, control mice (Se-sufficient, n = 10) were fed a standard diet. Forty Se-deficient mice were randomly divided into the model group, Na₂SeO₃ group, low-dose SHP-Se chelate group (SHP-Se-L), and high-dose SHP-Se chelate group (SHP-Se-H). After 20 days of treatment, liver selenium content in the Na₂SeO₃, SHP-Se-L, and SHP-Se-H groups significantly increased compared to the model group. Compared to the Na₂SeO₃ group, the SHP-Se-H group exhibited increases in serum catalase, superoxide dismutase (SOD), reduced glutathione, and glutathione peroxidase levels by 41.42%, 26.09%, 140.54%, and 41.49%, respectively, while malondialdehyde, alanine aminotransferase, and aspartate aminotransferase levels decreased by 62.14%, 65.1%, and 28.6%, respectively. H&E histopathological staining further demonstrated that SHP-Se was more effective than inorganic selenium in restoring tissue damage. Therefore, as a novel selenium supplement, the SHP-Se chelate can effectively prevent oxidative stress-induced liver injury and shows great potential for application in the development of functional foods for dietary selenium supplementation.