Tris (2-chloroethyl) phosphate (TCEP), a commonly used organophosphate flame retardant, has garnered considerable concern owing to its pervasive presence in the environment and its toxic effects on living organisms. The perpetuation of populations and species hinges on successful reproduction, yet research into the mechanisms underlying reproductive toxicity remains scant, particularly in aquatic species. In this work, zebrafish embryos were exposed to TCEP (0, 0.8, 4, 20, and 100 µg/L) for 120 days until sexual maturation, and multiple reproductive endpoints were investigated in male zebrafish. Our results showed that the body weight, body length, and gonadal-somatic index (GSI) were remarkably decreased in all TCEP treatment groups (except GSI in the 0.8 µg/L TCEP-treated group). Long-term exposure to TCEP led to reduced reproductive capacity of male zebrafish, as evidenced by decreased fertilization. Histological observation gave an indication of delayed testicular development and inhibited spermatogenesis under TCEP stress. The content of testosterone (T) was significantly elevated in all TCEP treatment group, whereas 17 β-estradiol (E2) levels remained stable. Transcriptome analysis revealed a lot of downregulated genes involved in steroid hormone biosynthesis, energy metabolism, and sperm motility, which might account for the imbalance of steroid hormone levels, retarded spermatogenesis and declined fertilization success. Overall, these findings offered a thorough understanding of the mechanisms underlying the male reproductive toxicity caused by TCEP, highlight the risk of TCEP on reproductive health of fish.

中文翻译：

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揭示雄性斑马鱼在整个生命周期中暴露于环境相关浓度的磷酸三（2-氯乙基）酯所诱导的生殖毒性机制


磷酸三（2-氯乙基）酯 （TCEP） 是一种常用的有机磷酸盐阻燃剂，由于其在环境中的普遍存在及其对生物体的毒性作用而引起了相当大的关注。种群和物种的延续取决于成功的繁殖，但对生殖毒性潜在机制的研究仍然很少，尤其是在水生物种中。在这项工作中，斑马鱼胚胎暴露于 TCEP （0、0.8、4、20 和 100 μg/L） 120 天直至性成熟，并研究了雄性斑马鱼的多个生殖终点。我们的结果显示，所有 TCEP 治疗组的体重、体长和性腺体指数 （GSI） 均显著降低 （0.8 μg/L TCEP 治疗组的 GSI 除外）。长期暴露于 TCEP 导致雄性斑马鱼的繁殖能力下降，受精减少就是证明。组织学观察表明在 TCEP 应激下睾丸发育延迟和精子发生受到抑制。所有 TCEP 治疗组睾酮 （T） 含量均显著升高，而 17 β-雌二醇 （E2） 水平保持稳定。转录组分析显示，许多下调的基因参与类固醇激素的生物合成、能量代谢和精子活力，这可能是类固醇激素水平失衡、精子发生迟缓和受精成功率下降的原因。总体而言，这些发现提供了对 TCEP 引起的雄性生殖毒性潜在机制的透彻理解，突出了 TCEP 对鱼类生殖健康的风险。