College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
Reprod Toxicol. 2019 Apr;85:104-109. doi: 10.1016/j.reprotox.2019.02.011. Epub 2019 Mar 1.
HT-2 toxin is one of the type A trichothecene mycotoxins existed in contaminated feed and has exerted various toxic effects on human and livestock, as it induces lesions in multiple tissues including reproductive system. However, till now it is still unclear about the toxicity of HT-2 on mammalian embryos. In this study, we showed that HT-2 treatment disrupted mouse early embryo development, and we also found the occurrence of oxidative stress, showing with the increased ROS level. This might be due to the mitochondria dysfunction, since the occurrence of aberrant mitochondria distribution was observed. Moreover, HT-2 exposure caused DNA damage, showing with the positive signal of γH2 A.X; and HT-2 treatment embryos showed increased LC3 positive signals, indicating the induction of autophagy, which further confirmed the occurrence of DNA damage. Thus, our results showed that HT-2 exposure impaired mouse embryo development by inducing oxidative stress, mitochondria dysfunction and DNA damage.
HT-2 毒素是存在于污染饲料中的 A 型单端孢霉烯族毒素之一，对人类和牲畜具有多种毒性作用，因为它会导致包括生殖系统在内的多种组织损伤。然而，到目前为止，关于 HT-2 对哺乳动物胚胎的毒性仍不清楚。在这项研究中，我们表明 HT-2 处理破坏了小鼠早期胚胎发育，我们还发现了氧化应激的发生，表现为 ROS 水平升高。这可能是由于线粒体功能障碍所致，因为观察到异常的线粒体分布。此外，HT-2 暴露会导致 DNA 损伤，表现为 γH2A.X 的阳性信号；并且 HT-2 处理的胚胎显示 LC3 阳性信号增加，表明自噬的诱导，进一步证实了 DNA 损伤的发生。因此，我们的结果表明，HT-2 暴露通过诱导氧化应激、线粒体功能障碍和 DNA 损伤来损害小鼠胚胎发育。
