AI Article Synopsis
- Chronic fluoride exposure (above 1.5 ppm) leads to health issues by causing oxidative stress and damaging DNA beyond repair.
- In a study, Swiss albino mice exposed to 15 ppm fluoride for 8 months showed damage in various organs, along with increased oxidative stress indicators like GSH depletion and lipid peroxidation.
- The research found that fluoride exposure altered the expression of key DNA repair genes Ogg1 and Rad51, with hypermethylation affecting Rad51, potentially linking fluoride-induced neurotoxicity to epigenetic changes.
Article Abstract
Chronic exposure to fluoride (F) beyond the permissible limit (1.5 ppm) is known to cause detrimental health effects by induction of oxidative stress-mediated DNA damage overpowering the DNA repair machinery. In the present study, we assessed F induced oxidative stress through monitoring biochemical parameters and looked into the effect of chronic F exposure on two crucial DNA repair genes Ogg1 and Rad51 having important role against ROS induced DNA damages. To address this issue, we exposed Swiss albino mice to an environmentally relevant concentration of fluoride (15 ppm NaF) for 8 months. Results revealed histoarchitectural damages in liver, brain, kidney and spleen. Depletion of GSH, increase in lipid peroxidation and catalase activity in liver and brain confirmed the generation of oxidative stress. qRT-PCR result showed that expressions of Ogg1 and Rad51 were altered after F exposure in the affected organs. Promoter hypermethylation was associated with the downregulation of Rad51. F-induced DNA damage and the compromised DNA repair machinery triggered intrinsic pathway of apoptosis in liver and brain. The present study indicates the possible association of epigenetic regulation with F induced neurotoxicity.
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| http://dx.doi.org/10.1016/j.ecoenv.2020.110962 | DOI Listing |
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