Procyanidins B2 reverses the T-2 toxin-induced mitochondrial apoptosis in TM3 Leydig cells

[Display omitted] •T-2 toxin induces oxidative stress in Leydig cells which leads to apoptosis which is underpinning mechanism for T-2 toxin-induced male reproductive toxicity.•Excessive reactive oxygen species induced by T-2 toxin is a pivotal factor for apoptosis in the Leydig cells.•T-2 toxin induced toxic responses in Leydig cells can be alleviated by procyanidins B2 (PB2) suggesting a potential utility of PB2 in dietary intervention of T-2 toxin induced toxicity. Procyanidins B2 (PB2) was found to block T-2 toxin-induced reproductive toxicity and may be used as a dietary preventive agent. We investigated the mechanism of PB2 in blocking the T-2 toxin-induced apoptosis in Leydig cells in conjunction with analysis of T-2 toxin induced proapoptotic responses in Leydig cells including induction of oxidative stresses. The stress inducible proteins ASK, p38 and JNK were increased in response to T-2 toxin and the induction was attenuated by PB2. Furthermore, we showed that T-2 toxin suppressed mitochondrial membrane potential, reduced the levels of the mitochondrial respiratory chain complex I-V, adversely affected the level of mitochondrial proteins CypD, Bax, Bak, Bcl-2, Bcl-xl, Bax/Bcl-2 and cyt c and these adverse effects were counteracted by PB2 in dose-dependent manner. In summary, our results showed great potential of PB2 in preventing T-2 toxin-induced toxicity in Leydig cells through its potent antioxidant property.