Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis


Ommati M. M., Sabouri S., Sun Z., Zamiri M. J., Retana-Marquez S., Ahmadi H. N., ...daha çox

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, vol.271, 2024 (SCI-Expanded, Scopus) identifier identifier identifier

  • Nəşrin Növü: Article / Article
  • Cild: 271
  • Nəşr tarixi: 2024
  • Doi nömrəsi: 10.1016/j.ecoenv.2024.115947
  • jurnalın adı: ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
  • Jurnalın baxıldığı indekslər: Science Citation Index Expanded (SCI-EXPANDED), Scopus, PASCAL, Aerospace Database, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), Artic & Antarctic Regions, BIOSIS, CAB Abstracts, Chemical Abstracts Core, Chimica, Communication Abstracts, EMBASE, Environment Index, Food Science & Technology Abstracts, Geobase, Greenfile, Metadex, Pollution Abstracts, Veterinary Science Database, Directory of Open Access Journals, Civil Engineering Abstracts
  • Açıq Arxiv Kolleksiyası: Məqalə
  • Adres: Yox

Qısa məlumat

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.