Dietary Selenium Deficiency Facilitated Reduced Stomatin and Phosphatidylserine Externalization, Increasing Erythrocyte Osmotic Fragility in Mice

Selenium (Se) is an essential trace element that maintains normal physiological functions in organisms. Since the discovery of glutathione peroxidase (GSH-PX), public interest in selenoproteins has gradually increased. Based on previous studies, dietary Se maintains erythrocyte homeostasis through selenoprotein-induced mediation of redox reactions. Furthermore, both the surface phosphatidylserine (PS) and intramembrane stomatin contents can be used as indicators of erythrocyte osmotic fragility. This study focused on the mechanism by which dietary Se deficiency increases erythrocyte osmotic fragility. We fed Se-deficient grain to mice for 8 weeks to establish a Se deficiency model in mice. We measured Se levels in the blood as well as the activities of antioxidant enzymes associated with selenoproteins in a Se-deficient environment. We used Western blotting, routine blood analysis, and other methods to detect red blood cell oxidative stress levels, membrane stomatin levels, and PS externalization. Fresh blood was collected to test erythrocyte osmotic fragility. The results showed that antioxidant enzyme activity was affected by dietary Se deficiency. Oxidative stress increased lipid peroxidation and the ROS content in the blood of the mice. Under such conditions, decreased PS exposure and stomatin content in the erythrocyte membrane eventually affected the structure of the erythrocyte membrane and increased erythrocyte osmotic fragility.