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A schematic diagram of the proposed mechanisms by which SeMet ameliorates T-2 toxin-induced liver injury by inhibiting ROS-induced mitochondrial-caspase apoptosis pathway. R0S: reactive oxygen species, T-AOC: total antioxidant capacity, GSH-Px: glutathione peroxidase, MDA: malondialdehyde, SeMet: selenomethionine, Bcl-2: B-cell lymphoma-2, Bax: Bcl-2-Associated X, cytC: Cytochrome C, apaf-1: apoptotic protease activating factor 1
