Kashin-Beck Disease (KBD) is a chronic, degenerative, disabling, and endemic osteoarthropathy with unknown etiology, which is a serious threat to the health of people in endemic areas with KBD. Selenium (Se) deficiency and T-2 toxin were confirmed as important environmental factors of KBD by epidemiological studies. However, excessive apoptosis of chondrocytes in articular and epiphyseal plate cartilages are mainly pathological characteristics of KBD (Guo et al. 2014). The role of oxidative damage and T-2 toxin in KBD and the protective mechanism of Se is still unknown (Chen et al. 2012, Wang et al. 2013). Therefore, this study was conducted to explore the expression of GPX3 in KBD patients and further clarify the mechanism of GPX3 in cartilage injuries through establishing the chondrocytes model of oxidative damage and T-2 toxin.