Neuroprotective Effects of Boric Acid against Fluoride Toxicity on Rat Synaptosomes

Abstract

Objective: Fluoride toxicity primarily contributes to the production of reactive oxygen and nitrogen derivatives, trigger the cell death pathways by causing lipid peroxidation and DNA damage. Boric acid (BA) contributes to preservation of membrane integrity and function and maintenance of redox balance due to its high affinity to some metabolites in the organism. The aim of this study was to investigate the protective effect of BA on neurodegenerative processes against the toxic effects of sodium fluoride (NaF) administered at different doses on rat brain synaptosomes.Material and Methods: Synaptosomes obtained from the rat frontal cortex were administered at different doses of sodium fluoride (NaF) to determine the most toxic dose of NaF. Determined toxic dose of NaF for synaptosomes and BA concentrations were administered in vitro at 37°C for 30min and then the parameters of malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, Na/K ATPase activity and DNA fragmentation value were measured spectrophotometrically.Results: There was a statistically significant difference between measured parameters, when the 80mg/L NaF group was compared with the control group. We found that 10 and 25 mM BA treatment provided a significant improvement in MDA, SOD, Na/K ATPase and DNA fragmentation compared to the 80mg/L NaF group. The 5 mM BA concentration was not found effective dose according to other doses. Conclusion: In conclusion, BA has potential for neuroprotective effects against cellular damage caused by NaF. The results suggest that the BA can be a neuroprotective therapeutic agent for fluoride toxicity.