Selenium Improves Bone Microenvironment-Related Hematopoiesis and Immunity in T-2 Toxin-Exposed Mice

The T-2 toxin is one of the most frequent contaminants in the environment and agricultural production globally. It exerts a wide range of toxic effects. Selenium (Se), as an antioxidant, has the potential to be widely used to antagonize mycotoxin toxicity. To investigate the protective effects of Se on bone microenvironment (BM)-related hematopoiesis and immunity after T-2 toxin exposure, 36 male mice were treated with the T-2 toxin (1 mg/kg) and/or Se (0.2 mg/kg) by intragastric administration for 28 days. The results showed that Se alleviated T-2 toxin-induced cytopenia and splenic extramedullary hematopoiesis. Se also significantly relieved T-2 toxin-induced immunosuppression, as assessed by immune factors and lymphocytes. Furthermore, Se also attenuated oxidative stress and apoptosis and improved the BM in T-2 toxin-exposed mice. Therefore, Se improves BM-related hematopoiesis and immunity after T-2 toxin exposure. This study provides references for identifying the toxic mechanism and screening potential therapeutic drugs of the T-2 toxin.