Abstract

Background: Sodium fluoride (NaF) is a well-known environmental pollutant prevalently found in drinking water and is also used for the treatment of dental problems. It promotes oxidative stress and disrupts tissue homeostasis in the vital organs of the body including kidney and liver. Two antioxidants, namely mangiferin and genistein, have been reported to exert protective effect against NaF-induced oxidative insult. These two polyphenols are known to modulate intracellular gene expressions under different pathophysiological states.
Methods and findings: The present study was designed to investigate the attenuative role of mangiferin and genistein against NaF induced cytotoxicity on normal kidney epithelial (NKE) cells. Several free radical scavenging assays indicate that both the polyphenolic compounds are effective in scavenging free radicals in cell free system. Further, dose and time dependent studies revealed that 500 μM NaF exposure for 16 hours optimally induced 50% cell death. Along with these data, several other assays investigating FRAP LDH leakage, lipid peroxidation, apoptosis, ROS generation, endogenous antioxidant system, mitochondrial membrane potential, cell cycle and immunoblot analysis indicated that NaF disrupted the intracellular antioxidant potential of the renal cells. Pre-treatment with both mangiferin and genistein, however, exclusively prevented the induction of cytotoxicity induced by NaF at a dose of 5 and 10 μM respectively.
Conclusion: This study is expected to help in understanding the molecular toxicity induced by NaF and the protective role of mangiferin and genistein. The antioxidative and gene modulatory role of mangiferin and genistein were found to be effective in NaF induced oxidative stress in renal cells.