Triphenyl phosphate induced reproductive toxicity through the JNK signaling pathway in Caenorhabditis elegans

  • J Hazard Mater. 2023 Mar 15:446:130643. doi: 10.1016/j.jhazmat.2022.130643.
Chongli Shi  1 ,  Chen Wang  2 ,  Lingjun Zeng  1 ,  Yi Peng  1 ,  Yeyong Li  1 ,  Haibin Hao  3 ,  Yang Zheng  1 ,  Chao Chen  4 ,  Haibo Chen  5 ,  Jin Zhang  1 ,  Minghui Xiang  1 ,  Yuan Huang  1 ,  Hui Li  6
Affiliations
  • 1. Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China.
  • 2. Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China. Electronic address: [email protected].
  • 3. Department of Critical Care Medicine, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing 210000, China.
  • 4. State Key Laboratory of Bioreactor Engineering, Biomedical Nanotechnology Center, Shanghai Collaborative Innovation Center for Biomanufacturing, School of Biotechnology, East China University of Science and Technology, Shanghai 200237, China.
  • 5. State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment, South China Institute of Environmental Sciences. Ministry of Ecology and Environment, Guangzhou 510655, China.
  • 6. Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China. Electronic address: [email protected].
PMID: 36586333 DOI: 10.1016/j.jhazmat.2022.130643
Abstract

Triphenyl phosphate (TPHP) is a widely used aryl organophosphate flame retardant (OPFR) that has attracted attention due to its frequent detection in the environment and living organisms. To date, the reproductive toxicity of TPHP has been investigated in organisms, but its molecular mechanisms are not fully understood. Caenorhabditis elegans (C. elegans) is the ideal animal for the study of reproductive toxicity following environmental pollutants, with short generation times, intact reproductive structures, and hermaphroditic fertilization. This study aimed to explore the reproductive dysfunction and molecular mechanisms induced by TPHP exposure in C. elegans. Specifically, exposure to TPHP resulted in a reduction in the number of eggs laid and developing embryos in utero, an increase in the number of apoptotic gonadal cells, and germ cell cycle arrest. The JNK signaling pathway is a potential pathway inducing reproductive toxicity following TPHP exposure based on transcriptome Sequencing (RNA-seq). Moreover, TPHP exposure induced down-regulation of vhp-1 and kgb-2 gene transcription levels, and the knockout of vhp-1 and kgb-2 in the mutant strains exhibited more severe toxicity in apoptotic gonad cells, embryos, and eggs developing in utero, suggesting that vhp-1 and kgb-2 genes play a crucial role in TPHP-induced reproductive toxicity. Our data provide convergent evidence showing that TPHP exposure results in reproductive dysfunction through the JNK signaling pathway and improve our understanding of the ecotoxicity and toxicological mechanisms of aryl-OPFRs.

Keywords
JNK signaling pathway; Potential health risks; Reproductive toxicity; Triphenyl phosphate.
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