Wang Yan, Peng Xiaoli, Yang Zhuojun, Zhao Weiwei, Xu Wentao, Hao Junran, Wu Weihong, Shen Xiao Li, Luo Yunbo, Huang Kunlun
Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Toxins (Basel). 2017 May 18;9(5):167. doi: 10.3390/toxins9050167.
Ochratoxin A (OTA) is one of the most common and dangerous mycotoxins in the world. Previous work indicated that OTA could elicit spontaneous HR-like lesions formation , reactive oxygen species (ROS) play an important role in OTA toxicity, and their major endogenous source is mitochondria. However, there has been no evidence as to whether OTA induces directly PCD in plants until now. In this study, the presence of OTA in leaves triggered accelerated respiration, increased production of mitochondrial ROS, the opening of ROS-dependent mitochondrial permeability transition pores and a decrease in mitochondrial membrane potential as well as the release of cytochrome c into the cytosol. There were 42 and 43 significantly differentially expressed proteins identified in response to exposure to OTA for 8 and 24 h, respectively, according to iTRAQ analysis. These proteins were mainly involved in perturbation of the mitochondrial electron transport chain, interfering with ATP synthesis and inducing PCD. Digital gene expression data at transcriptional level was consistent with the cell death induced by OTA being PCD. These results indicated that mitochondrial dysfunction was a prerequisite for OTA-induced PCD and the initiation and execution of PCD via a mitochondrial-mediated pathway.
赭曲霉毒素A（OTA）是世界上最常见且危险的霉菌毒素之一。先前的研究表明，OTA可引发类似HR的自发损伤形成，活性氧（ROS）在OTA毒性中起重要作用，且其主要内源性来源是线粒体。然而，迄今为止，尚无证据表明OTA是否直接诱导植物程序性细胞死亡（PCD）。在本研究中，叶片中OTA的存在引发了呼吸加速、线粒体ROS产生增加、依赖ROS的线粒体通透性转换孔开放、线粒体膜电位降低以及细胞色素c释放到细胞质中。根据iTRAQ分析，分别在暴露于OTA 8小时和24小时后鉴定出42个和43个显著差异表达的蛋白质。这些蛋白质主要参与线粒体电子传递链的扰动、干扰ATP合成以及诱导PCD。转录水平的数字基因表达数据与OTA诱导的细胞死亡为PCD一致。这些结果表明，线粒体功能障碍是OTA诱导PCD以及通过线粒体介导的途径启动和执行PCD的先决条件。
