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Updated: Jun 4, 2026

A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model
Published on: February 6, 2018
Fenvalerate induces germ cell apoptosis in mouse testes through the Fas/FasL signaling pathway
Xian-Feng Zhao1, Qun Wang, Yan-Li Ji
1Department of Toxicology, Anhui Medical University, 230032, Hefei, China.
Abstract:
Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with fenvalerate (15 or 60 mg/kg) by gavage for 28 days. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). The number of TUNEL+ germ cells per tubule and the percentage of tubules with TUNEL+ germ cells were significantly increased in testes of mice treated with fenvalerate in a dose-dependent manner. TUNEL+ germ cells were observed mainly in stages VII-VIII and also stages IX-XII seminiferous tubules in testes. Additional experiments showed that fenvalerate increased the level of active caspase-8 and caspase-3 in testes. In addition, fenvalerate upregulated the expression of Fas and FasL in testes. No significant difference on the expression of Bcl-2 and Bax in testes was observed between fenvalerate-treated mice and controls. Fenvalerate did not affect the leakage of cytochrome c from mitochondria into cytoplasm. In addition, fenvalerate did not cause the activation of caspase-9 in testes. Taken together, these results suggest that fenvalerate induces germ cell apoptosis in testes through the Fas/FasL signaling pathway.
Insights
Fenvalerate exposure significantly increases germ cell apoptosis in male mice testes. This occurs via the Fas/FasL signaling pathway, impacting male reproductive health.
Area of Science:
- Toxicology
- Reproductive Biology
- Cellular Biology
Background:
- Fenvalerate is an insecticide with known adverse effects on male reproduction.
- The precise mechanisms underlying fenvalerate's impact on spermatogenesis are not fully understood.
- Investigating germ cell apoptosis is crucial for understanding male reproductive toxicity.
Purpose of the Study:
- To investigate the effects of fenvalerate exposure on germ cell apoptosis in adult male mice testes.
- To elucidate the specific molecular pathways involved in fenvalerate-induced germ cell death.
- To determine the dose-dependent effects of fenvalerate on testicular germ cells.
Main Methods:
- Adult male mice were administered fenvalerate (15 or 60 mg/kg) via gavage for 28 days.
- Germ cell apoptosis was quantified using terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) assay.
- Levels of caspases (caspase-8, caspase-3, caspase-9), Fas, FasL, Bcl-2, Bax, and cytochrome c were analyzed.
Main Results:
- Fenvalerate treatment significantly increased the number of TUNEL+ germ cells in a dose-dependent manner.
- Apoptotic germ cells were predominantly observed in seminiferous tubule stages VII-VIII and IX-XII.
- Fenvalerate upregulated active caspase-8 and caspase-3, and increased Fas and FasL expression without altering Bcl-2/Bax or cytochrome c release.
Conclusions:
- Fenvalerate induces germ cell apoptosis in mouse testes.
- The Fas/FasL signaling pathway is critically involved in fenvalerate-induced testicular toxicity.
- These findings highlight a potential mechanism for fenvalerate's adverse effects on male fertility.
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