Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis
Makaleler > Tam Makale · 2024
Yazarlar: Mohammad Mehdi Ommati, Samira Sabouri, Zilong Sun, Mohammad Javad Zamiri, Socorro Retana‑Marquez, Hassan Nategh Ahmadi, Qiyong Zuo, Azız EFTEKHARIMEHRABAD, Lizbeth Juárez-Rojas, Yaser Asefi, Lina Lei, Shu gang Cui, Shu gang Cui, Mohammad Hasan Jadidi, Hong wei Wang, Reza Heidari
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, SCI Expanded İndekslerine Giren Dergi, Uluslararası, Scopus, 2024, cilt 271, ss 115947-115947
DOI: 10.1016/j.ecoenv.2024.115947
Özet
Fluoride induced reprotoxicity through oxidative stress-mediated reproductive cell death. Hence, the current study evaluated the importance of the MST/Nrf2/MAPK/NQO-HO1 signaling pathway in fluorosis-induced reproductive toxicity. For this purpose, the reproductive toxicity of sodium fluoride (NaF) at physiological, biochemical, and intracellular levels was evaluated. In-vivo, NaF at 100 mg/L instigated physiological dysfunction, morphological, stereological, and structural injuries in the gut-gonadal axis of fluorosis mice through weakening the antioxidant signaling, Nrf2/HO-1/NQO1signaling pathway, causing the gut-gonadal barrier disintegrated via oxidative stress-induced inflammation, mitochondrial damage, apoptosis, and autophagy. Similar trends were also observed in-vitro in the isolated Leydig cells (LCs) challenging with 20 mg/L NaF. Henceforth, activating the cellular antioxidant signaling pathway, Nrf2/HO-1/NQO1, inactivating autophagy and apoptosis, or attenuating lipopolysaccharide (LPS) can be the theoretical basis and valuable therapeutic targets for coping with NaF-induced reproductive toxicity.