Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural. University, Harbin, 150030, China.
College of Food Science, Northeast Agricultural. University, Harbin, 150030, China.
Food Chem Toxicol. 2021 Mar;149:112027. doi: 10.1016/j.fct.2021.112027. Epub 2021 Jan 27.
T-2 toxin is an inevitable environmental and grain pollutant, which can cause kidney damage, but the mechanism is not clear. In this study, male mice were administered with T-2 toxin at 0, 0.5, 1.0, 2.0 mg/kg body weight (BW) for 28 days. We found that T-2 toxin induced renal structural damage, downregulated BW and kidney coefficient, impaired renal function accompanied by oxidative stress and apoptosis. Meanwhile, T-2 toxin increased nuclear Nrf2 protein expression and the mRNA expressions of its downstream target genes. The correlation analysis indicated that apoptosis and Nrf2 pathway were positively correlated with oxidative stress. These results suggested that the nephrotoxicity of T-2 toxin in mice caused by oxidative stress-mediated apoptosis is related to Nrf2 pathway.
T-2 毒素是一种不可避免的环境和粮食污染物，可引起肾脏损伤，但机制尚不清楚。在这项研究中，雄性小鼠连续 28 天经口灌胃给予 T-2 毒素 0、0.5、1.0、2.0mg/kg 体重。结果发现，T-2 毒素诱导了肾脏结构损伤，下调了体重和肾脏系数，损害了肾功能，同时伴有氧化应激和细胞凋亡。同时，T-2 毒素增加了核 Nrf2 蛋白表达及其下游靶基因的 mRNA 表达。相关性分析表明，细胞凋亡和 Nrf2 通路与氧化应激呈正相关。这些结果提示，T-2 毒素诱导的氧化应激介导的细胞凋亡引起的小鼠肾毒性与 Nrf2 通路有关。
