研究报告
罗妮娜.碘代乙酸体外暴露诱导斑马鱼(Danio rerio)淋巴细胞内源性凋亡可能机理研究[J].环境科学学报,2016,36(6):2290-2296
碘代乙酸体外暴露诱导斑马鱼(Danio rerio)淋巴细胞内源性凋亡可能机理研究
- Intrinsic apoptosis mechanism of zebrafish (Danio rerio) lymphocytes induced by iodine acetic acid exposure in vitro
- 摘要：以斑马鱼(Danio rerio)为试验生物,经淋巴细胞体外暴露试验,从细胞内源性凋亡角度,研究了饮用水消毒副产物-碘代乙酸诱导斑马鱼淋巴细胞损伤的致毒机理.结果表明,在碘代乙酸的环境浓度1μg·L-1下暴露24、36、48和96 h后,细胞凋亡率从对照组的3.52%分别增加到15.89%、22.47%、40.76%和52.13%,与对照组差异均为极显著(p<0.01);线粒体膜电位分别较对照组下降了32.9%、50.1%、68.6%和81.5%,与对照组差异均为极显著(p<0.01);细胞色素C的相对释放量分别增加了0.85、1.37、1.86和2.66倍,与对照组差异均为极显著(p<0.01).暴露36、48和96 h后,Caspase-3酶活性分别增加了0.49、0.86和1.43倍,与对照组差异均为极显著(p<0.01);Caspase-9酶活性分别增加了0.73、1.41和1.88倍,与对照组差异均为极显著(p<0.01);抑制凋亡Bcl-2基因的相对表达量分别下降27.0%、35.3%和52.3%,与对照组差异均为极显著(p<0.01);而促进凋亡的Bax基因相对表达量分别增加1.1、2.3和3.2倍,与对照组差异均为极显著(p<0.01).碘代乙酸体外诱导斑马鱼淋巴细胞凋亡的可能机制是,线粒体膜电位的崩溃导致细胞色素C持续从线粒体中释放,进而引起细胞凋亡下游通路的变化;Bcl-2基因和Bax基因明显参与了对凋亡的调控.此外,Caspase-9酶的活化导致Caspase-3酶活化,最终引起细胞凋亡.
- Abstract：Zebrafish (Danio rerio) lymphocytes were used to investigate the possible apoptosis mechanism induced by a disinfection byproduct, iodine acetic acid exposure in vitro. The results showed that 1 μg·L-1, the environmental concentration of iodine acetic acid exposure induced the apoptosis of zebrafish lymphocytes in vitro. After the exposure for 24, 36, 48 and 96 hours, the apoptosis percentages were added to 15.89%, 22.47%, 40.76% and 52.13% (p<0.01), respectively, while the control apoptosis percentage was 3.52% according to the flow cytometric analysis. The mitochondrial membrane potential decreased by 32.9%, 50.1%, 68.6% and 81.5% (p<0.01), respectively, as compared with control group. However, their relative cytochrome C levels were 1.85, 2.37, 2.86 and 3.66 times higher than that of the control (p<0.01). After the exposure for 36, 48 and 96 hours, the relative Caspase-3 activities were 1.49, 1.86 and 2.43 times higher than that of the control (p<0.01), while the relative Caspase-9 activities were 1.73, 2.41 and 2.88 times higher than that of the control (p<0.01); the relative expressions of Bcl-2 gene decreased 27.0%, 35.3% and 52.3% (p<0.01); the relative expressions of Bax gene increased 1.1, 2.3 and 3.2 times (p<0.01), respectively. The possible mechanism of zebrafish lymphocytes intrinsic apoptosis induced by iodine acetic acid exposure in vitro was that the disruption of mitochondrial membrane potential resulted in cytochrome C release from mitochondrial to cytoplasm to change the downstream apoptosis pathway. Both Bcl-2 gene and Bax gene were obviously involved in this process. The activated Caspase-9 caused Caspase-3 activation, leading to apoptosis.
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