1. Fluoride exposure during puberty induces testicular impairment via ER stress-triggered apoptosis in mice.
- Author
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Wang R, Gong W, Jiang Y, Yin Q, Wang Z, Wu J, Zhang M, Li M, Liu Y, Wang J, Chen Y, and Ji Y
- Subjects
- Animals, Male, Mice, Sexual Maturation drug effects, Heat-Shock Proteins metabolism, Heat-Shock Proteins genetics, Sperm Count, Spermatogenesis drug effects, Endoplasmic Reticulum Stress drug effects, Apoptosis drug effects, Testis drug effects, Testis metabolism, Fluorides toxicity, Endoplasmic Reticulum Chaperone BiP
- Abstract
Fluoride, a ubiquitous environmental compound, carries significant health risks at excessive levels. This study investigated the reproductive toxicity of fluoride exposure during puberty in mice, focusing on its impact on testicular development, spermatogenesis, and underlying mechanisms. The results showed that fluoride exposure during puberty impaired testicular structure, induced germ cell apoptosis, and reduced sperm counts in mice. Additionally, the SOD activity and GSH content were significantly decreased, while MDA content was significantly elevated in the NaF group. Immunohistochemistry showed an increase in the number of cells positive for GRP78, a key ER stress marker. Moreover, qRT-PCR and Western blot analyses confirmed the upregulation of both Grp78 mRNA and protein expression, as well as increased mRNA expression of other ER stress-associated genes (Grp94, chop, Atf6, Atf4, and Xbp1) and enhanced protein expression of phosphorylated PERK, IRE1α, eIF2α, JNK, XBP-1, ATF-6α, ATF-4, and CHOP. In conclusion, our findings demonstrate that fluoride exposure during puberty impairs testicular structure, induces germ cell apoptosis, and reduces sperm counts in mice. ER stress may participate in testicular cell apoptosis, and contribute to the testicular damage and decreased sperm counts induced by fluoride., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)
- Published
- 2024
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