Decabromodiphenyl ether (BDE-209), a congener of polybrominated diphenyl ethers (PBDEs), is used as flame retardant and affects thyroid homeostasis. Thyroid hormones (THs) play crucial role in Leydig cell differentiation and steroidogenesis during early life. Present study examined the effect of maternal BDE-209 exposure during lactation on testicular steroidogenesis and spermatogenesis in relation to thyroid hormone receptor alpha 1 (THRα1) and possible mechanism(s) of its action in prepubertal Parkes mice offspring. Lactating female Parkes mice were orally gavaged with 500, and 700 mg/kg body weight of BDE-209 in corn oil from postnatal day (PND) 1 to PND 28. Lactating mothers and male pups were sacrificed on PND 28. Maternal BDE-209 exposure markedly affected testicular histopathology, steroidogenesis and germ cell dynamics with downregulated expressions of various steroidogenic markers in mice offspring. Serum THs levels were markedly reduced in both pups and lactating mothers compared to controls. Expression of proliferating cell nuclear antigen and THRα1 also deceased in testes of BDE-209-exposed mice offspring. In silico analysis by molecular docking was performed successfully for steroidogenic facor-1 (SF-1) and THRα1 with BDE-209 and T₃. Maternal BDE-209 exposure during lactation affects testicular steroidogenesis, spermatogenesis and expression of THRα1 in prepubertal mice offspring through downregulation of SF-1.

十溴二苯醚（BDE-209）是多溴二苯醚（PBDEs）的同类物，被用作阻燃剂并影响甲状腺的稳态。甲状腺激素（THs）在生命早期的Leydig细胞分化和类固醇生成中起着至关重要的作用。本研究检查了哺乳期母体BDE-209暴露对与甲状腺激素受体α1（THRα1）有关的睾丸类固醇生成和精子生成的作用及其在青春期前Parkes小鼠后代中作用的可能机制。从出生后第1天到PND 28，口服给雌性Parkes雌鼠口服500和700 mg / kg体重的BDE-209玉米油，在PND 28处死哺乳的母鼠和雄性幼崽。母体BDE-209暴露明显影响睾丸组织病理学，类固醇生成和生殖细胞动力学，并在小鼠后代中下调了多种类固醇生成标记的表达。与对照组相比，幼崽和哺乳期母亲的血清THs水平均明显降低。在暴露于BDE-209的小鼠后代的睾丸中，增殖细胞核抗原和THRα1的表达也下降。通过类固醇合成facor-1（SF-1）和THRα1与BDE-209和T ₃的分子对接成功地进行了计算机分析。哺乳期母体BDE-209暴露通过下调SF-1来影响青春期前小鼠后代睾丸类固醇生成，精子生成和THRα1的表达。