Pendimethalin induces apoptosis in testicular cells via hampering ER-mitochondrial function and autophagy

Jiyeon Ham, Whasun Lim, Gwonhwa Song

    Research output: Contribution to journalArticlepeer-review

    14 Citations (Scopus)

    Abstract

    Pendimethalin (PDM) is a dinitroaniline crop pesticide that is extensively utilized worldwide. However, the reproductive toxicity and cellular mechanisms of PDM have not been identified. Therefore, we elucidated the adverse effects of PDM on the reproductive system using mouse testicular Leydig and Sertoli cells (TM3 and TM4 cells, respectively). Our results demonstrated that PDM suppressed the viability and proliferation of TM3 and TM4 cells. Additionally, PDM induced cytosolic calcium upregulation and permeabilization of mitochondrial membrane potential in both TM3 and TM4 cells. We also verified that PDM activates the endoplasmic reticulum (ER) stress pathway and autophagy. Furthermore, we confirmed that activation of ER stress and autophagy were blocked by 2-aminoethoxydiphenyl borate (2-APB) treatment. Finally, we confirmed PDM-induced cell cycle arrest and apoptosis in TM3 and TM4 cells. Thus, we first demonstrated that PDM impedes the survival of testis cells, and further, their function.

    Original languageEnglish
    Article number116835
    JournalEnvironmental Pollution
    Volume278
    DOIs
    Publication statusPublished - 2021 Jun 1

    Bibliographical note

    Funding Information:
    This research was supported by the National Research Foundation of Korea (NRF) grant funded by the Ministry of Science and ICT (MSIT) (grant number: 2018R1C1B6009048 ) and suppported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Minisry of Education (grant number: 2020R1A6A3A13074214 ).

    Publisher Copyright:
    © 2021 Elsevier Ltd

    Keywords

    • Autophagy
    • ER stress
    • Herbicides
    • Inositol 1,4,5-triphosphate receptors
    • Pendimethalin

    ASJC Scopus subject areas

    • Toxicology
    • Pollution
    • Health, Toxicology and Mutagenesis

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