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

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