T-2毒素在谷物和饲料中广泛存在，具有毒性强、脱毒困难等特点，长期暴露于该毒素中将严重抑制动物生长，给畜牧业生产带来巨大经济损失。最近的研究表明，T-2毒素引起细胞产生氧化应激是其一个重要的毒性作用机制。但T-2毒素是如何诱导细胞产生氧化应激的机制尚不清楚。我们前期研究表明，T-2毒素能引起GH3细胞线粒体膜电位明显降低、氧化应激的产生、显著上调与ROS产生密切相关的线粒体呼吸链酶复合物亚基NDUFS3表达。本研究在前期基因组和蛋白组学基础上，以NDUFS3为切入点，应用染色质免疫共沉淀技术、RNA干扰、蛋白超表达、电镜等技术，并结合线粒体膜电位、ATP含量、形态变化和氧化应激指标等阐释该毒素作用下，线粒体亚基在线粒体功能障碍和氧化应激中的作用及其与调控呼吸链亚基表达的转录因子TFAM和上游信号通路cAMP/PKA-CREB-PGC-1α间的相互作用，为毒素预防和保证动物健康奠定坚实基础。

T-2 toxin is widespread in cereals and feed, which has strong toxicity. And the toxicity of T-2 toxin is difficult to be reduced. Long-term exposure to the toxin will seriously inhibit the growth of animals, which will result in huge economic losses in livestock production. Recent studies showed that T-2 toxin could cause oxidative stress in cells, which has been regarded to be an important mechanism to explain the toxic effects of the toxin. However, to T-2 toxin, the mechanism by which way induces oxidative stress still remains unclear. Our previous studies have shown that, in GH3 cells, T-2 toxin could result in the significant decrease of mitochondrial membrane potential, the oxidative stress, and the significant increase of the mitochondrial respiratory chain enzyme complex subunits NDUFS3. As known, NDUFS3 is closely related to the production of ROS. In the present study, based on the genomic and proteomic studies, NDUFS3 will be selected to investigate its potential role in mitochondrial dysfunction, oxidative stress and the transcription factor (TFAM) and the upstream signaling pathway cAMP/PKA-CREB-PGC-1α mediating the expression of respiratory chain subunits by using various techniques, such as the chromatin immunoprecipitation technique, RNA interference, overexpression of protein and electron microscopy. Various parameters including the mitochondrial membrane potential, ATP content, morphological changes and the parameters of the oxidative stress were detected to reveal the potential role of NDUFS3. The present study will throw a new light to the prevention of T-2 toxin and the ensurance of animal health.