Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis
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)...
| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2024-02-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324000228 |
| _version_ | 1797328867529064448 |
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| author | Mohammad Mehdi Ommati Samira Sabouri Zilong Sun Mohammad Javad Zamiri Socorro Retana‑Marquez Hassan Nategh Ahmadi Qiyong Zuo Aziz Eftekhari Lizbeth Juárez-Rojas Yaser Asefi Lina Lei Shu-gang Cui Mohammad Hasan Jadidi Hong-wei Wang Reza Heidari |
| author_facet | Mohammad Mehdi Ommati Samira Sabouri Zilong Sun Mohammad Javad Zamiri Socorro Retana‑Marquez Hassan Nategh Ahmadi Qiyong Zuo Aziz Eftekhari Lizbeth Juárez-Rojas Yaser Asefi Lina Lei Shu-gang Cui Mohammad Hasan Jadidi Hong-wei Wang Reza Heidari |
| author_sort | Mohammad Mehdi Ommati |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-08T06:57:10Z |
| format | Article |
| id | doaj.art-af9fee3234dd4bc489783a677172757c |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-03-08T06:57:10Z |
| publishDate | 2024-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-af9fee3234dd4bc489783a677172757c2024-02-03T06:34:24ZengElsevierEcotoxicology and Environmental Safety0147-65132024-02-01271115947Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosisMohammad Mehdi Ommati0Samira Sabouri1Zilong Sun2Mohammad Javad Zamiri3Socorro Retana‑Marquez4Hassan Nategh Ahmadi5Qiyong Zuo6Aziz Eftekhari7Lizbeth Juárez-Rojas8Yaser Asefi9Lina Lei10Shu-gang Cui11Mohammad Hasan Jadidi12Hong-wei Wang13Reza Heidari14Henan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, China; Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Corresponding author at: Henan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, China.College of Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, ChinaCollege of Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, ChinaDepartment of Animal Sciences, Shiraz University, Shiraz, IranDepartment of Biology of Reproduction, Autonomous Metropolitan University-Iztapalapa, Mexico City, MexicoCollege of Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, China; College of Animal Science and Veterinary Medicine, Shiraz University, Shiraz, IranHenan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, ChinaDepartment of Biochemistry, Faculty of Science, Ege University, Izmir, Turkey; Nanotechnology and Biochemical Toxicology (NBT) Center, Azerbaijan State University of Economics (UNEC), Baku AZ1001, AzerbaijanDepartment of Biology of Reproduction, Autonomous Metropolitan University-Iztapalapa, Mexico City, MexicoDepartment of Genetics, Ahar Branch, Islamic Azad University, Ahar, IranThe First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471000, ChinaHenan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, ChinaComparative Medicine and Animal Resources Centre, McGill University, Montreal, CanadaHenan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan 471000, China; Corresponding authors.Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Corresponding authors.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.http://www.sciencedirect.com/science/article/pii/S0147651324000228Antioxidant signaling pathwayBarrier disintegrityEndotoxemiaFluorosisSpermatotoxicity |
| spellingShingle | Mohammad Mehdi Ommati Samira Sabouri Zilong Sun Mohammad Javad Zamiri Socorro Retana‑Marquez Hassan Nategh Ahmadi Qiyong Zuo Aziz Eftekhari Lizbeth Juárez-Rojas Yaser Asefi Lina Lei Shu-gang Cui Mohammad Hasan Jadidi Hong-wei Wang Reza Heidari Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis Ecotoxicology and Environmental Safety Antioxidant signaling pathway Barrier disintegrity Endotoxemia Fluorosis Spermatotoxicity |
| title | Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis |
| title_full | Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis |
| title_fullStr | Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis |
| title_full_unstemmed | Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis |
| title_short | Inactivation of Mst/Nrf2/Keap1 signaling flexibly mitigates MAPK/NQO-HO1 activation in the reproductive axis of experimental fluorosis |
| title_sort | inactivation of mst nrf2 keap1 signaling flexibly mitigates mapk nqo ho1 activation in the reproductive axis of experimental fluorosis |
| topic | Antioxidant signaling pathway Barrier disintegrity Endotoxemia Fluorosis Spermatotoxicity |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324000228 |
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