HT-2 toxin exposure induces mitochondria dysfunction and DNA damage during mouse early embryo development

Abstract

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.

Keywords: DNA damage; Embryo; HT-2; Mitochondria; Oxidative stress.