蒋荣娟, 赵超超, 王程强, 宋家乐, 钱波. 孕哺期十溴联苯醚暴露对子鼠神经甾体水平和学习记忆能力的影响[J]. 环境与职业医学, 2020, 37(9): 909-914. DOI: 10.13213/j.cnki.jeom.2020.20137
引用本文: 蒋荣娟, 赵超超, 王程强, 宋家乐, 钱波. 孕哺期十溴联苯醚暴露对子鼠神经甾体水平和学习记忆能力的影响[J]. 环境与职业医学, 2020, 37(9): 909-914. DOI: 10.13213/j.cnki.jeom.2020.20137
JIANG Rong-juan, ZHAO Chao-chao, WANG Cheng-qiang, SONG Jia-le, QIAN Bo. Effects of decabromodiphenyl ether exposure during pregnant and lactating periods on neurosteroid and learning and memory ability of offspring mice[J]. Journal of Environmental and Occupational Medicine, 2020, 37(9): 909-914. DOI: 10.13213/j.cnki.jeom.2020.20137
Citation: JIANG Rong-juan, ZHAO Chao-chao, WANG Cheng-qiang, SONG Jia-le, QIAN Bo. Effects of decabromodiphenyl ether exposure during pregnant and lactating periods on neurosteroid and learning and memory ability of offspring mice[J]. Journal of Environmental and Occupational Medicine, 2020, 37(9): 909-914. DOI: 10.13213/j.cnki.jeom.2020.20137

孕哺期十溴联苯醚暴露对子鼠神经甾体水平和学习记忆能力的影响

Effects of decabromodiphenyl ether exposure during pregnant and lactating periods on neurosteroid and learning and memory ability of offspring mice

  • 摘要: 背景

    十溴联苯醚(BDE209)的神经发育毒性机制尚不清楚,研究资料提示神经甾体紊乱可能是其诱发神经发育毒性的重要原因。

    目的

    探索BDE209对神经甾体水平的影响,以及神经甾体紊乱在BDE209诱发神经发育毒性中的作用。

    方法

    60只ICR雌鼠随机分为0、225、900 mg·kg-1 BDE209染毒组,受孕成功后经口灌胃母鼠BDE209至子鼠出生后第21天。每个剂量组选取24只子鼠,通过Morris水迷宫实验检测子鼠学习记忆能力,使用酶联免疫吸附试验测定子鼠大脑和血清孕酮(PROG)、3α-5α四氢孕酮(3α-5α-THP)、脱氢表雄酮(DHEA)、孕烯醇酮(PREG)水平,采用JC-1荧光探针检测子鼠海马线粒体膜电位。

    结果

    水迷宫实验结果显示:各组逃避潜伏期随着训练天数增加均呈下降趋势,与训练第1天相比,训练第4天,对照组、225 mg·kg-1染毒组和900 mg·kg-1染毒组逃避潜伏期分别下降51.34%,27.20%和16.87%。水迷宫实验第5天,225、900 mg·kg-1染毒组象限穿越次数与对照组相比分别下降51.81%和67.47%,象限停留时间分别下降48.45%和77.47%,平台穿越次数分别下降64.29%和75.00%(均P < 0.05)。大脑神经甾体检测结果显示,与对照组相比:225、900 mg·kg-1染毒组PROG分别下降36.51%和69.28%,3α-5α-THP分别下降31.84%和57.43%,DHEA分别下降31.13%和60.15%,PREG分别下降31.17%和68.07%(均P < 0.05)。血清神经甾体检测结果显示,与对照组相比:225、900 mg·kg-1染毒组PROG分别下降29.49%和63.44%,3α-5α-THP分别下降25.12%和53.71%,DHEA分别下降29.09%和56.97%,PREG分别下降25.39%和47.07%(均P < 0.05)。海马线粒体膜电位检测结果显示:225、900 mg·kg-1染毒组线粒体膜电位与对照组相比分别下降10.06%和25.58%(均P < 0.05)。

    结论

    BDE209具有神经发育毒性,孕哺期BDE209染毒可能通过诱发神经甾体紊乱从而抑制子鼠学习记忆能力。

     

    Abstract: Background

    Decabromodiphenyl ether (BDE209) has neurodevelopmental toxicity, but the associated mechanism is not clear. Previous studies have shown that neurosteroid disorder may be one of the main reasons.

    Objective

    This experiment explores the effect of BDE209 on neurosteroid levels, and the role of neurosteroid disorder in neurodevelopmental toxicity induced by BDE209.

    Methods

    Sixty female ICR mice were randomly divided into 0, 225, and 900 mg·kg-1 BDE209 exposure groups. After conception, the pregnant mice were administered with BDE209 by oral gavage to 21 days after offspring birth. Twenty-four offspring mice of each group were selected, their learning and memory ability was tested by Morris water maze, their levels of progesterone (PROG), 3α-5α-tetrahydroprogesterone (3α-5α-THP), dehydroepiandrosterone (DHEA), and pregnenolone (PREG) in brain and serum were detected by enzyme-linked immunosorbent assay, and mitochondrial membrane potential in hippocampus was detected using a JC-1 fluorescence probe.

    Results

    The water maze experiment results showed that the escape latencies of the designed groups decreased with prolonged training days, and the decreases on day 4 versus day 1 of the control group, the 225 mg·kg-1 exposure group, and the 900 mg·kg-1 exposure group were 51.34%, 27.20%, and 16.87%, respectively. On day 5 of the water maze experiment, compared with the control group, the number of quadrant crossing of the 225 and 900 mg·kg-1 exposure groups were decreased by 51.81% and 67.47%, the quadrant staying time by 48.45% and 77.47%, and the number of platform crossing by 64.29% and 75.00%, respectively (P < 0.05). The brain neurosteroid test results showed that compared with the control group, the PROG of the 225 and 900 mg·kg-1 exposure groups were decreased by 36.51% and 69.28%, the 3α-5α-THP by 31.84% and 57.43%, the DHEA by 31.13% and 60.15%, and PREG by 31.17% and 68.07%, respectively (P < 0.05). The serum neurosteroid test results showed that compared with the control group, the PROG of the 225 and 900 mg·kg-1 exposure groups were decreased by 29.49% and 63.44%, the 3α-5α-THP by 25.12% and 53.71%, the DHEA by 29.09% and 56.97%, and the PREG by 25.39% and 47.07%, respectively (P < 0.05). The mitochondrial membrane potential test results showed that the mitochondrial membrane potential of the 225 and 900 mg·kg-1 exposure groups were decreased by 10.06% and 25.58% compared with the control group respectively (P < 0.05).

    Conclusion

    BDE209 has neurodevelopmental toxicity, and BDE209 exposure during pregnancy and lactation may inhibit learning and memory ability of offspring mice by inducing neurosteroid disorder.

     

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