T-2 toxin causes dysfunction of Sertoli cells by inducing oxidative stress

T-2 toxin is an inevitable mycotoxin in food products and feeds. It is a proven toxicant impairing the male reproductive system. However, previous studies have concentrated on the toxic effect of T-2 toxin on Leydig cells, with little attention on the Sertoli cell cytotoxicity. Therefore, this study aimed to establish the toxic mechanism of T-2 toxin on Sertoli cells. The Sertoli cell line (TM4 cell) was cultured and exposed to different concentrations of T-2 toxin with/without N-acetyl-L-cysteine (NAC) for 24 h. A CCK-8 assay then measured the cell viability. In addition, the expression of TM4 cell biomarkers (FSHR and ABP) and functional factors (occludin (Ocln), zonula occluden-1 (ZO-1), Connexin 43 (Cx-43), and N-Cadherin (N-cad)) were measured by qRT-PCR and Western blotting. The oxidative stress status (ROS, MDA, CAT, and SOD) and apoptosis rate, including the caspase-9, 8, and 3 activities in TM4 cells, were analyzed. We established that (1): T-2 toxin decreased TM4 cells viability and the half-maximal inhibitory concentration was 8.10 nM. (2): T-2 toxin-induced oxidative stress, evidenced by increased ROS and MDA contents, and inhibited CAT and SOD activities. (3): T-2 toxin inhibited FSHR, ABP, ocln, ZO-1, Cx-43, and N-Cad expressions. (4): T-2 toxin promoted TM4 cell apoptosis and caspase-9, 8, and 3 activities. (5): N-acetyl-L-cysteine relieved oxidative stress, functional impairment, and apoptosis in TM4 cells treated with T-2 toxin. Thus, T-2 toxin induced TM4 cell dysfunction through ROS-induced apoptosis. [Display omitted] •T-2 toxin induced TM4 cell oxidative stress.•T-2 toxin caused TM4 cell dysfunction and apoptosis.•T-2 toxin caused TM4 cell dysfunction and apoptosis by inducing oxidative stress.