T-2 toxin, one member of the type A trichothecene family, induces the apoptosis of human hepatocytes (L02) and murine Leydig cells (TM3), as well as mitochondrial dysfunctions. In the present study, we attempted to investigate whether T-2 toxin toxicity is related to mitochondrial dysfunction and mitophagy. We found that T-2 toxin might induce autophagy and mitophagy in TM3 cells (TM3) in a concentration-dependent manner. In addition, T-2 toxin could induce mitochondrial dysfunction, depolarization, and fission concentration-dependently. The inducible effects of T-2 toxin on mitophagy, mitochondrial dysfunction, and cell apoptosis could all be significantly reversed by autophagy inhibitor, 3 MA. Finally, DRP-1 participated in the inducible effects of T-2 toxin on TM3 cell mitophagy, mitochondrial dysfunction, and cell apoptosis. In summary, mitophagy and mitochondrial dysfunction are essential mechanisms of the toxicity induced by T-2 toxin. Thus, our findings provide a rationale for further studies on selectively targeting mitophagy to improve mitochondrial dysfunction and to protect cells from T-2 toxin-induced toxicity.

中文翻译：

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T-2毒素诱导的依赖DRP-1的线粒体吞噬导致小鼠Leydig细胞（TM3）凋亡。

T-2毒素是A型单丝孢菌素家族的成员，它诱导人肝细胞（L02）和鼠Leydig细胞（TM3）的凋亡以及线粒体功能障碍。在本研究中，我们试图研究T-2毒素毒性是否与线粒体功能障碍和线粒体吞噬有关。我们发现T-2毒素可能以浓度依赖的方式诱导TM3细胞（TM3）中的自噬和线粒体。另外，T-2毒素可诱导线粒体功能障碍，去极化和裂变浓度依赖性。自噬抑制剂3 MA可显着逆转T-2毒素对线粒体，线粒体功能障碍和细胞凋亡的诱导作用。最后，DRP-1参与了T-2毒素对TM3细胞线粒体，线粒体功能障碍和细胞凋亡的诱导作用。总之，线粒体和线粒体功能障碍是T-2毒素诱导的毒性的重要机制。因此，我们的发现为进一步研究选择性靶向线粒体以改善线粒体功能障碍并保护细胞免受T-2毒素诱导的毒性提供了理论基础。