Maternal BDE-209 exposure during lactation perturbs steroidogenesis, germ cell kinetics and THRα1 expression in testes of prepubertal mice offspring. (December 2018)

• Record Type: Journal Article
• Authors: Sarkar, Debarshi; Singh, Vinay Kumar; Singh, Shio Kumar
• Is Part Of: Food and chemical toxicology. Volume 122(2018)
• Page Start: 104
• Page End: 119
• Publication Date: 2018-12
• Subjects: BDE-209 -- Mice -- SF-1 -- Steroidogenesis -- Testis -- THRα1; Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2018.10.025
• Languages: English
• ISSNs: 0278-6915

Abstract

Abstract: 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. Highlights: Maternal exposure to BDE-209 affects testis histopathology in mice offspring. Downregulation in SF-1 expression is responsible for decreased steroidogenesis. BDE-209-exposed mice offspring show decreased steroidogenesis. Maternal exposure to BDE-209 perturbs germ cell kinetics in mice offspring. Expression of THRα1 in testis is decreased in offspring of treated dams.