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短期十溴联苯醚(BDE-209)暴露对中年雌性 Balb/c 小鼠引起的持续免疫损伤。

Persistent immune injury induced by short-term decabromodiphenyl ether (BDE-209) exposure to female middle-aged Balb/c mice.

机构信息

School of the Environment and Safety Engineering, Jiangsu University, Zhenjiang, Jiangsu, China.

The Laboratory Animal Research Center of Jiangsu University, Zhenjiang, Jiangsu, China.

出版信息

Environ Sci Pollut Res Int. 2023 Nov;30(51):111325-111343. doi: 10.1007/s11356-023-30148-w. Epub 2023 Oct 9.

DOI:10.1007/s11356-023-30148-w
PMID:37814044
Abstract

Decabromodiphenyl ether (BDE-209), widely used in various industries for its excellent flame-retardant performance, could be enriched in humans and is closely associated with immune impairment. In addition, immune system is gradually declined and becoming more sensitive to environmental pollutants in the ageing process. Therefore, the immunotoxicity of BDE-209 (4, 40, and 400 mg/kg/day) to middle-aged mice and its recovery and susceptibility was first to be comprehensively investigated in this study. The results showed that BDE-209 exposure could lead to oxidative injury to immune organs (spleen, thymus, and liver), impair humoral (immunoglobulins), cellular (lymphopoiesis), and non-specific immunity, and disturb the expressions of the genes related to Th1/Th2 balance (T helper cells) in the middle-aged mice. In addition, Integrated Biomarker Response (IBR) indicated that BDE-209-induced immune impairment was challenging to self-regulated, and even exacerbated after 21 days of recovery and oxidative injury in immune organs could be the main reason. Furthermore, factorial analysis showed that middle-aged mice exposed to BDE-209 suffered from greater immune impairment than adult mice, and the immune impairment in aged mice is more difficult to be self-repaired than that in adult mice. It can be seen that the aged tend to suffer from BDE-209-induced persistent immune impairment and health threats.

摘要

十溴二苯醚(BDE-209)因其出色的阻燃性能而被广泛应用于各个行业,它可能在人体内积累,并与免疫损伤密切相关。此外,在衰老过程中,免疫系统逐渐衰退,对环境污染物更加敏感。因此,本研究首次全面研究了 BDE-209(4、40 和 400mg/kg/天)对中年小鼠的免疫毒性及其恢复和敏感性。结果表明,BDE-209 暴露会导致免疫器官(脾脏、胸腺和肝脏)氧化损伤,损害体液(免疫球蛋白)、细胞(淋巴生成)和非特异性免疫,并扰乱与 Th1/Th2 平衡(辅助性 T 细胞)相关的基因表达。此外,综合生物标志物反应(IBR)表明,BDE-209 引起的免疫损伤难以自我调节,甚至在 21 天恢复期后会加剧,而免疫器官的氧化损伤可能是主要原因。此外,因子分析表明,暴露于 BDE-209 的中年小鼠比成年小鼠遭受更大的免疫损伤,老年小鼠的免疫损伤比成年小鼠更难自我修复。由此可见,老年人更容易受到 BDE-209 引起的持续免疫损伤和健康威胁。

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