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Published on: February 6, 2018
Flurochloridone induced abnormal spermatogenesis by damaging testicular Sertoli cells in mice
Weiqi Sun1, Fang Tian2, Hongjie Pan2
1School of Public Health/MOE Key Laboratory for Public Health Safety/ Collaborative Innovation Center of Social Risks Governance in Health, Fudan University, Shanghai 200032, China; Shanghai Municipal Center for Disease Control and Prevention, Shanghai 200336, China.
Background:
Flurochloridone (FLC), a selective herbicide used on a global scale, has been reported to have male reproductive toxicity whose evidence is limited, but its mechanism remains unclear. The present study was conducted to systematically explore the male reproductive toxicity of FLC, including sperm quality, spermatogenesis, toxicity targets, and potential mechanisms.
Methods:
Male C57BL/6 mice aged 6-7 weeks received gavage administration of FLC (365/730 mg/kg/day) for 28 consecutive days. Then, the tissue and sperm of mice were collected for analysis. We measured the gonadosomatic index and analyzed sperm concentration, motility, malformation rate, and mitochondrial membrane potential (MMP). Spermatocyte immunofluorescence staining was performed to analyze meiosis. We also performed pathological staining on the testis and epididymis tissue and TUNEL staining, immunohistochemical analysis, and ultrastructural observation on the testicular tissue.
Results:
Results showed that FLC caused testicular weight reduction, dysfunction, and architectural damage in mice, but no significant adverse effect was found in the epididymis. The exposure interfered with spermatogonial proliferation and meiosis, affecting sperm concentration, motility, kinematic parameters, morphology, and MMP, decreasing sperm quality. Furthermore, mitochondrial damage and apoptosis of testicular Sertoli cells were observed in mice treated with FLC.
Conclusion:
We found that FLC has significant adverse effects on spermatogonial proliferation and meiosis. Meanwhile, apoptosis and mitochondrial damage may be the potential mechanism of Sertoli cell damage. Our study demonstrated that FLC could induce testicular Sertoli cell damage, leading to abnormal spermatogenesis, which decreased sperm quality. The data provided references for the toxicity risk and research methods of FLC application in the environment.
Insights
Flurochloridone (FLC) herbicide exposure significantly harms male mouse reproductive health, impairing sperm quality and spermatogenesis by damaging Sertoli cells and mitochondria. This study clarifies FLC
Area of Science:
- Environmental Toxicology
- Reproductive Toxicology
- Herbicide Safety
Background:
- Flurochloridone (FLC) is a widely used herbicide with suspected, yet poorly understood, male reproductive toxicity.
- Limited evidence necessitates a comprehensive investigation into FLC's effects on male reproductive health and its underlying mechanisms.
Purpose of the Study:
- To systematically evaluate the male reproductive toxicity of Flurochloridone (FLC) in mice.
- To elucidate the specific impacts of FLC on sperm quality, spermatogenesis, and identify potential toxicity targets and mechanisms.
Main Methods:
- Male C57BL/6 mice were administered varying doses of FLC (365/730 mg/kg/day) via gavage for 28 days.
- Analysis included gonadosomatic index, sperm parameters (concentration, motility, morphology, mitochondrial membrane potential), meiosis assessment, and testicular/epididymal tissue examination (pathology, TUNEL, immunohistochemistry, ultrastructure).
Main Results:
- FLC exposure led to reduced testicular weight, dysfunction, and structural damage, while the epididymis remained largely unaffected.
- Spermatogonial proliferation and meiosis were disrupted, resulting in decreased sperm quality (concentration, motility, morphology, mitochondrial membrane potential).
- Mitochondrial damage and apoptosis in testicular Sertoli cells were observed in FLC-treated mice.
Conclusions:
- FLC significantly impairs spermatogonial proliferation and meiosis, leading to reduced sperm quality.
- Apoptosis and mitochondrial damage in Sertoli cells are identified as potential mechanisms for FLC-induced reproductive toxicity.
- This study demonstrates FLC's capacity to induce Sertoli cell damage, disrupt spermatogenesis, and decrease sperm quality, providing crucial data for environmental risk assessment.
