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Updated: Jul 25, 2026
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Cresyl Diphenyl Phosphate exposure induces reproductive functional defects in men and male mice
Danni Jiang1, Yang Xu2, Xiaojuan Han1
1Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, 107 Wenhua West Road, Ji'nan, Shandong 250012, China.
Abstract:
Cresyl Diphenyl Phosphate (CDP), as a novel organophosphate esters (OPEs), achieves widely used and exposed in multiple industries. However, its male reproductive toxicity and underlying mechanism remains unclear. In vivo, male mice were gavaged with CDP (0, 4, 20, or 100 mg/kg/d) for 8 weeks. And we treated TM3, TM4 and GC-2 cells with 0, 10, 25, and 50 μM CDP for 24 h to detect its reproductive toxicity effect in vitro. In our study, we revealed that CDP inhibited proliferation and induced apoptosis in mice testis and GC-2 cells, thereby leading to the decreased sperm quality. In mechanism, CDP trigger the oxidative stress and ROS production, thus partially causing DNA damage and cell apoptosis. Moreover, CDP exposure causes injury to Ledyig cells and Sertoli cells, thus disturbing the testicular microenvironment and inhibiting spermatogonia proliferation. In conclusion, this research reveals multiple adverse impacts of CDP on the male reproductive system and calls for further study of the toxicological effects of CDP on human health.
Insights
Cresyl diphenyl phosphate (CDP) exposure harms male fertility by reducing sperm quality and damaging testicular cells. This organophosphate ester causes oxidative stress, DNA damage, and disrupts the testicular environment.
Area of Science:
- Environmental toxicology
- Reproductive toxicology
- Cell biology
Background:
- Organophosphate esters (OPEs), including Cresyl Diphenyl Phosphate (CDP), are widely used industrially.
- The male reproductive toxicity and specific mechanisms of CDP exposure are not well understood.
Purpose of the Study:
- To investigate the male reproductive toxicity of Cresyl Diphenyl Phosphate (CDP) in vivo and in vitro.
- To elucidate the underlying mechanisms of CDP-induced reproductive toxicity.
Main Methods:
- Male mice were exposed to varying doses of CDP (0-100 mg/kg/d) for 8 weeks.
- Testicular cells (TM3, TM4, GC-2) were treated with CDP (0-50 μM) for 24 hours.
- Sperm quality, cell proliferation, apoptosis, oxidative stress, ROS production, DNA damage, and testicular cell injury were assessed.
Main Results:
- CDP exposure significantly inhibited proliferation and induced apoptosis in mouse testes and GC-2 cells, leading to decreased sperm quality.
- CDP triggered oxidative stress and reactive oxygen species (ROS) production, contributing to DNA damage and cell apoptosis.
- CDP caused injury to Leydig and Sertoli cells, disrupting the testicular microenvironment and inhibiting spermatogonia proliferation.
Conclusions:
- Cresyl Diphenyl Phosphate (CDP) exerts multiple adverse effects on the male reproductive system.
- CDP-induced reproductive toxicity is mediated by oxidative stress, DNA damage, and disruption of the testicular microenvironment.
- Further research is warranted to assess the toxicological risks of CDP to human health.
