Authors
Guoqing Wang, Ruijie Ba, Bin Liu, Yan Wang, Shu Niu, Hedan Wan, Yuhui Du, Fangfang Yu, Guoyu Zhou, Jingyuan Zhu, Yue Ba
Published in
Chemico-biological interactions. Pages 112346. Sep 18, 2026. Epub Sep 18, 2026.
Abstract
Endemic fluorosis from high-fluoride groundwater is a global concern. While fluoride exposure is linked to male infertility, the mechanisms remain unclear. This study utilized male Sprague-Dawley (SD) rats and in vitro immortalized human testicular Sertoli (iHTS) cells to investigate the potential mechanisms underlying sodium fluoride (NaF)-induced testicular damage. In vivo, three-month NaF exposure caused testicular tissue disorganization, decreased sperm viability and motility, and increased sperm abnormalities. Furthermore, NaF exposure significantly altered the oxidative stress status in the rat testis, evidenced by decreased total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD), and glutathione (GSH) levels, along with increased malondialdehyde (MDA) content. Meanwhile, levels of pyroptosis-related proteins (AIM2, Cleaved Caspase-3, GSDME, and GSDME-N), as well as LDH, interleukin (IL)-1β, and IL-18, were significantly increased. Similar results were observed in vitro. Interestingly, knocking down AIM2 in NaF-treated iHTS cells significantly decreased the levels of Cleaved Caspase-3, GSDME, GSDME-N, IL-1β, IL-18, and LDH. Furthermore, inhibiting NaF-induced oxidative stress with N-acetylcysteine (NAC) effectively mitigated these NaF-induced protein and biochemical alterations. These findings suggest that excessive fluoride exposure induces oxidative stress in testicular tissue and cells, subsequently activating the AIM2/Caspase-3/GSDME pyroptotic axis, thereby leading to testicular damage.
PMID:
42759637
Bibliographic data and abstract were imported from PubMed on 19 Sep 2026.
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