生物技术进展 ›› 2021, Vol. 11 ›› Issue (2): 204-213.DOI: 10.19586/j.2095-2341.2020.0140

• 研究论文 • 上一篇    下一篇

十溴联苯醚(BDE-209)短期暴露对成年期小鼠的免疫毒性研究

廖桃桃1,汤俊杰1,史潇翔1,张伟杰2,茆广华1*,吴向阳1*   

  1. 1.江苏大学环境与安全工程学院, 江苏 镇江 212013;
    2.江苏大学食品与生物工程学院, 江苏 镇江 212013
  • 收稿日期:2020-10-27 出版日期:2021-03-25 发布日期:2020-11-27
  • 通讯作者: 茆广华 E-mail: maoyun82@sina.com;吴向阳 E-mail:wuxy@ujs.edu.cn
  • 作者简介:廖桃桃 E-mail: ltt4328@126.com
  • 基金资助:
    江苏省自然科学青年基金(BK20160497);江苏大学高级人才启动基金(15JDG031)。

Study on the Immunotoxicity of Short-term Exposure of Decabromodiphenyl Ether (BDE-209) in Adult Mice

LIAO Taotao, TANG Junjie, SHI Xiaoxiang, ZHANG Weijie, MAO Guanghua,  WU Xiangyang   

  1. 1.School of the Environment and Safety Engineering, Jiangsu University, Jiangsu Zhenjiang 212013, China;
    2.School of the Food and Biological Engineering, Jiangsu University, Jiangsu Zhenjiang 212013, China
  • Received:2020-10-27 Online:2021-03-25 Published:2020-11-27

摘要: 为了探讨十溴联苯醚(BDE-209)短期暴露对成年期小鼠免疫毒性及机体自我修复能力的影响,构建了雌性Balb/c小鼠BDE-209短期暴露及恢复模型。分别于给药结束后的第1 d和第21 d考察脏器指数、免疫球蛋白、淋巴细胞增殖、脂质过氧化、免疫细胞因子及相关基因变化;在此基础上,采用综合生物标志物响应结合主成分和析因分析综合评估BDE-209对成年期小鼠的免疫毒性。结果显示,BDE-209可降低小鼠的免疫器官指数,并伴随氧化损伤;BDE-209可刺激IgG分泌,抑制脾淋巴细胞增殖;BDE-209可改变Th1、Th2细胞相关细胞因子分泌及基因表达,进而引起Th1/Th2失衡。综合分析表明,BDE-209的免疫毒性在暴露结束21 d后可得到改善,BDE-209的暴露剂量和是否度过恢复期之间存在交互影响。结果表明,BDE-209短期暴露对成年期小鼠具有免疫毒性,但该毒性效应可通过机体的自我修复得到一定程度的改善。

关键词: 十溴联苯醚, 免疫毒性, 综合生物标志物响应, 自我修复

Abstract: To investigate the immunotoxicity of short-term exposure to decabromodiphenyl ether (BDE-209) and its self-recovery in adult mice, a model of short-term exposure of BDE-209 in female Balb/c mice was established. Organ index, immunoglobulin, lymphocyte proliferation, lipid peroxidation, immune cytokine and genes were investigated on 1 d and 21 d after the end of administration, respectively. And integrated evaluation was conducted by integrated biomarker responses combined with principal component analysis and factorial analysis. The results showed that BDE-209 could reduce the index of immune organs, accompanied by oxidative damage. BDE-209 could stimulate the secretion of IgG and inhibit the proliferation of spleen lymphocytes. BDE-209 could change the secretion of cytokines and gene expression related to Th1 and Th2 cells, causing Th1/Th2 imbalance. The comprehensive analysis showed that the immunotoxicity of BDE-209 was reduced 21 days after the end of exposure, and there was an interaction between the exposure dose of BDE-209 and whether the recovery period was passed. The results showed that short term exposure to BDE-209 has immunotoxicity in adult mice, but this effect could be reduced to some extent by self-recovery.

Key words: decabromodiphenyl ether, immunotoxicity, integrated biomarker responses, self-recovery