T‐2 toxin‐induced femur lesion is accompanied by autophagy and apoptosis associated with Wnt/β‐catenin signaling in mice

T-2 toxin is one of the most common mycotoxins found in grain foods, animal feed, and other agricultural by-products causing food contamination and health threat. The skeletal system is the main target tissue for T-2 toxin. T-2 toxin exposure is also recognized as a potential contributor to multiple types of bone diseases, including Kashin-Beck disease. However, the mechanisms of T-2 toxin-induced bone toxicity remain unclear. In this study, 60 male C57BL/6 mice were exposed T-2 toxin with 0, 0.5, 1 or 2 mg/kg body weight by intragastric administration for 28 days, respectively. Femora were collected for the detections of femur lesion, bone formation factors, oxidative stress, autophagy, apoptosis, and Wnt/β-catenin signaling. Our research showed that T-2 toxin caused bone formation disorders, presenting as the reduction of the BMD and femur length, bone structure changes and abnormal bone formation proteins expressions, along with enhanced oxidative stress. Meanwhile, T-2 toxin increased expressions of autophagy-related proteins (Beclin 1, ATG5, p62, and LC3), and promoted apoptosis in mouse femur. Moreover, T-2 toxin suppressed the Wnt/β-catenin signaling and expressions of downstream target genes. Taken together, our data indicated T-2 toxin-induced femur lesion was accompanied by autophagy and apoptosis, which was associated with Wnt/β-catenin signaling.