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

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

  • 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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