Fluoride Action Network



  • NaF enhances intracellular generation of ROS and RNS in human RBC.
  • It increases oxidation of proteins, thiols and lipids.
  • NaF inhibits antioxidant enzymes and lowers antioxidant power of RBC.
  • Antioxidant 3,4-dihydroxybenzaldehyde mitigates NaF-induced oxidative damage in RBC.


Fluoride is an essential micronutrient that is needed for mineralization of bones and formation of dental enamel. It is a widely dispersed environmental pollutant and chronic exposure to it is toxic, resulting in malignancies and hematological damage in humans. Blood is a major and early target of environmental pollutants and toxicants like fluoride. Fluoride generates reactive oxygen species and free radicals which induce oxidative stress in target cells and mediate its toxic effects. The aim of this study was to determine the mitigating effect of plant antioxidant 3,4-dihydroxybenzaldehyde (DHB) on sodium fluoride (NaF) induced oxidative damage and cytotoxicity in isolated human red blood cells (RBC)


Isolated human RBC were treated with 0.5 mM NaF, in absence or presence of different concentrations of DHB (0.1–2.5 mM). Several biochemical parameters were analyzed in cell lysates and whole cells.


Treatment of RBC with NaF increased the formation of reactive oxygen and nitrogen species. It oxidized thiols, proteins and lipids and generated their peroxidative products. Methemoglobin level, heme degradation and lipid peroxidation were increased but cellular antioxidant status declined significantly in NaF alone treated RBC, compared to the control. NaF inhibited antioxidant, membrane bound and glycolytic enzymes in RBC. However, prior incubation of RBC with DHB significantly attenuated the NaF-induced alterations in all these parameters in a DHB concentration-dependent manner.


These results show that DHB mitigates NaF-induced oxidative damage in human RBC, probably because of its antioxidant character.