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Updated: Apr 17, 2026
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
2,2',4,4'-Tetrabromodiphenyl ether disrupts spermatogenesis, impairs mitochondrial function and induces apoptosis of
Shaoping Huang1, Yiqiang Cui2, Xuejiang Guo2
1State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Jiangsu, China; Department of Human Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, Jiangsu, China.
Abstract:
Our objective was to explore molecular markers and mechanism of BDE47 on spermatogenesis in mammals. Adult male SD rats were gavaged daily with corn oil containing 0, 0.001, 0.03, 1 or 20mg BDE47/kg bw for eight weeks. Testes morphology was analyzed using electron microscopy, TUNEL, immunohistochemistry and morphometry. Differential proteome profile and western blotting were applied to determine molecular markers and protein expression. GC1-spg cells (mouse spermatogonial cells) were used to verify mechanism of BDE47. Data showed BDE47 reduced tubular epithelial thickness, impaired mitochondrial function and induced apoptosis in early leptotene spermatocytes. Proteomic study identified 70 differential spots corresponding to 64 proteins. 20 proteins related to apoptosis, 15 located in mitochondria. Exposure of GC1-spg cells showed BDE47 induced apoptosis, impaired mitochondria and decreased Bcl-2 in cells. Data indicate that BDE47 disrupts spermatogenesis, impairs mitochondrial function and induces apoptosis of early leptotene spermatocytes in rats probably via mitochondrial pathway.
Insights
Polybrominated diphenyl ether 47 (BDE47) exposure in rats reduced sperm production by damaging testicular tissue and impairing mitochondria. This study suggests BDE47 disrupts mammalian spermatogenesis through a mitochondrial-mediated apoptosis pathway.
Area of Science:
- Environmental toxicology
- Reproductive biology
- Molecular toxicology
Background:
- Polybrominated diphenyl ethers (PBDEs) are flame retardants with potential endocrine-disrupting effects.
- BDE47 is a common PBDE congener found in the environment and human tissues.
- Limited data exist on the specific mechanisms by which BDE47 affects male reproductive function.
Purpose of the Study:
- To investigate the effects of BDE47 exposure on spermatogenesis in male rats.
- To identify molecular markers and elucidate the mechanism underlying BDE47-induced reproductive toxicity.
- To assess the impact of BDE47 on testicular morphology, apoptosis, and mitochondrial function.
Main Methods:
- Adult male Sprague-Dawley rats were exposed to varying doses of BDE47 for eight weeks.
- Testicular morphology was analyzed using electron microscopy, TUNEL assay, immunohistochemistry, and morphometry.
- Proteomic profiling and Western blotting were employed to identify differential protein expression.
- GC1-spg cells were used to validate the mechanism of BDE47 action.
Main Results:
- BDE47 exposure led to reduced tubular epithelial thickness and impaired mitochondrial function in rat testes.
- Apoptosis was induced in early leptotene spermatocytes following BDE47 exposure.
- Proteomic analysis identified 64 differentially expressed proteins, with many related to apoptosis and mitochondrial function.
- In vitro studies confirmed BDE47 induced apoptosis, mitochondrial dysfunction, and decreased Bcl-2 expression in spermatogonial cells.
Conclusions:
- BDE47 disrupts spermatogenesis in rats by inducing apoptosis in early spermatocytes and impairing mitochondrial function.
- The mechanism likely involves the mitochondrial pathway, leading to decreased Bcl-2 expression.
- These findings highlight the reproductive risks associated with BDE47 exposure.
