题目：
Toxic effects of HT-2 toxin on mouse oocytes and its possible mechanisms
HT-2毒素对小鼠卵母细胞的毒性作用及其可能机制机制
句子翻译：
T-2 toxin is one of the type A trichothecene mycotoxins that is considered to be the most toxic of the trichothecenes. T-2 toxin has been shown to exert various toxic effects in farm animals and humans, as it induces lesions in the brain and in lymphoid, hematopoietic, and gastrointestinal tissues. HT-2 toxin is the major metabolite of T-2 toxin. There is little information regarding the effects of HT-2 toxin on the female reproductive system, particularly oocyte maturation. Thus, in this study, we investigated the toxic effects of HT-2 on mouse oocyte maturation and its possible mechanisms of action. HT-2 toxin exposure disrupted oocyte maturation, reduced actin expression in both the oocyte cortex and cytoplasm, and disrupted meiotic spindle morphology by reducing p-MAPK protein level. HT-2 toxin exposure also induced oxidative stress and resulted in oocyte apoptosis, as shown by ROS accumulation, increased SOD mRNA level, and the expression of the early apoptosis marker Annexin V and increased caspase-3 and bax mRNA levels. Additionally, HT-2 toxin exposure increased LC3 and ATG12 protein levels and lc3 and atg14 mRNA levels, which indicated that HT-2 toxin induced autophagy in mouse oocytes. We also examined for possible epigenetic modifications. Fluorescence intensity nalysis showed that 5mC level increased after HT-2 toxin exposure, whereas H3K9me2 and H3K27me3 levels decreased after HT-2 toxin exposure, which indicated that DNA and histone methylations were altered. Thus, our results indicated that HT-2 toxin exposure reduced mouse oocyte maturation capability by affecting cytoskeletal dynamics, apoptosis/autophagy, oxidative stress, and epigenetic modifications.
摘要：T-2毒素是一种被认为是毒性最强的A型毛霉烯真菌毒素。T-2毒素已被证明对农场动物和人类具有各种毒性作用，因为它会导致大脑、淋巴组织、造血组织和胃肠组织的损伤。HT-2毒素是T-2毒素的主要代谢产物。关于HT-2毒素对女性生殖系统的影响，特别是对卵母细胞成熟的影响，几乎没有资料。因此，在本研究中，我们研究了HT-2对小鼠卵母细胞成熟的毒性作用及其可能的作用机制。HT-2毒素暴露破坏了卵母细胞成熟，降低了卵母细胞皮质和细胞质中的肌动蛋白表达，并通过降低p-MAPK蛋白水平破坏了减数分裂纺锤体的形态。HT-2毒素暴露也诱导氧化应激并导致卵母细胞凋亡，表现为ROS积累、SOD mRNA水平升高、早期凋亡标志物膜联蛋白V的表达以及caspase-3和bax mRNA水平升高。此外，HT-2毒素暴露增加了LC3和ATG12蛋白水平以及LC3和atg14 mRNA水平，这表明HT-2毒素诱导小鼠卵母细胞自噬。我们还检查了可能的表观遗传修饰。荧光强度分析显示，HT-2毒素暴露后5mC水平升高，而H3K9me2和H3K27me3水平在HT-2毒素暴露后降低，这表明DNA和组蛋白甲基化发生了改变。因此，我们的研究结果表明，HT-2毒素暴露通过影响细胞骨架动力学、凋亡/自噬、氧化应激和表观修饰来降低小鼠卵母细胞成熟能力。
期刊Food and Chemical Toxicology 影响因子：4.679 发表于2017.12.26
词汇整理：