Objective To evaluate the effects of exposure to decabromodiphenyl ether (BDE209) of mothers during pregnancy and lactation on serum thyroid hormone (TH) concentrations of offspring mice at puberty and adulthood.
Methods Thirty specific pathogen free female Kunming mice of 8 weeks old were used as F0 generation and randomly divided into control, low exposure, and high exposure groups after mating, with 10 mice in each group. The control group was fed with peanut oil at 0.01 L/kg (in terms of body weight, thereafter), and the exposure groups were given BDE209 at 50 and 300μg/kg by intragastric administration once a day until postnatal day 21 (PND21, puberty) of F1 generation offspring mice, establishing a F0 generation exposure model from pregnancy to lactation. Then, thirty female Kunming mice of the F1 generation of 8 weeks old were randomly divided into control, low exposure, and high exposure groups after mating and received the same treatments as the F0 generation until PND21 of F2 generation offspring mice, establishing a F1 generation exposure model from pregnancy to lactation. The body weights of mice were measured on PND21 and PND60 (adulthood) of F1 and F2 generation offspring mice. The serum levels of total thyroxine (T4), total triiodothyronine (T3), free thyroxine (FT4), and free triiodothyronine (FT3) were measured by direct chemiluminescence immunoassay at the same time points.
Results Compared with the control group, the body weights and the litter sizes of the F0 and F1 generation mother mice were significantly decreased in the low and high BDE209 exposure groups; the body weights of the F1 and F2 generation offspring mice in the low and high BDE209 exposure groups significantly decreased on PND21 (Ps ＜ 0.05). Compared with the control group, the low and high BDE209 exposures significantly increased the T4 concentrations of the F1 generation offspring mice by 21.1% and 37.2% on PND21, respectively; the high BDE209 exposure significantly increased the T4 concentration of the F1 generation offspring mice by 23.2% on PND60 (Ps ＜ 0.05). Compared with the control group, the low and high BDE209 exposures significantly increased the FT4 concentrations of the F1 generation offspring mice by 22.7% and 53.9% on PND21, respectively; the high BDE209 exposure significantly increased the FT4 concentration of the F1 generation offspring mice by 16.7% on PND60 (Ps ＜ 0.05). Compared with the control group, the high BDE209 exposure significantly increased the T3 and FT3 concentrations of the F1 generation offspring mice by 22.8% and 33.8% on PND21, respectively (Ps ＜ 0.05). Compared with the control group, the low and high BDE209 exposures significantly increased the T4 concentrations of the F2 generation offspring mice by 19.5% and 48.2% on PND21 and by 19.2% and 29.2% on PND60, respectively (Ps ＜0.05). Compared with the control group, the low and high BDE209 exposures significantly increased the FT4 concentrations of the F2 generation offspring mice by 27.4% and 65.3% on PND21, respectively; the high BDE209 exposure significantly increased the FT4 concentration of the F2 generation offspring mice by 32.5% on PND60 (Ps ＜ 0.05). Compared with the control group, the low and high BDE209 exposures significantly increased the T3 concentrations of the F2 generation offspring mice by 10.8% and 19.8% on PND21, respectively; the high BDE209 exposure significantly increased the FT3 of the F2 generation offspring mice by 20.2% on PND60 (Ps ＜0.05).
Conclusion Exposure to BDE209 during pregnancy and lactation has significant toxicity on TH homeostasis, which may lead to disorder in TH level during puberty and adulthood of the offspring.
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