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目的应用小鼠胚胎干细胞(mESC)作为模型探讨T-2毒素对mESC的作用靶点与作用机制。方法选用0.5 ng/ml T-2毒素处理分化过程中的mESC 24、72和120 h,流式细胞术检测mESC的活性氧簇(ROS)的生成,比色法检测mESC的抗氧化防御酶活性,包括超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)的活力变化,以及脂质过氧化产物丙二醛(MDA)的含量。结果 0.5 ng/ml T-2毒素作用72与120 h,mESC中ROS大量蓄积,抗氧化防御酶(SOD、GPx)活力下降,MDA增加,其效应呈现时间依赖关系。自由基清除剂(Trolox,200μmol/L)预处理可以降低T-2毒素对mESC抗氧化防御酶活力的抑制作用,减轻T-2毒素引起的mESC中ROS的蓄积以及MDA的增加。结论低剂量T-2毒素染毒引起mESC的氧化损伤是其发育毒性的重要机制之一。
Objective To investigate the target and mechanism of T-2 toxin mESC by using mouse embryonic stem cells (mESC) as a model. Methods The mESCs during differentiation were treated with 0.5 ng / ml T-2 toxin for 24, 72 and 120 h. The generation of reactive oxygen species (ROS) in mESCs was detected by flow cytometry. The antioxidant enzyme activities of mESCs , Including changes in the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx), as well as the content of malondialdehyde (MDA), a lipid peroxidation product. Results After 72 and 120 h exposure to 0.5 ng / ml T-2 toxin, the ROS accumulation in mESCs was significantly reduced. The activities of antioxidant enzymes SOD and GPx were decreased and the MDA content increased. The effect was time-dependent. Pretreatment with free radical scavenger (Trolox, 200 μmol / L) could reduce the inhibitory effect of T-2 toxin on the antioxidant enzyme activity of mESC and reduce the accumulation of ROS and the increase of MDA in mESC induced by T-2 toxin. Conclusion The oxidative damage of mESC induced by low dose T-2 toxin is one of the important mechanisms of its developmental toxicity.