Evaluation of multi-endpoint assay to detect genotoxicity and oxidative stress in mice exposed to sodium fluoride

Fluoride compounds are naturally present in soil, water and food. The objective of this study was to investigate the genotoxic and oxidative damage induced by chronic fluoride exposure on mammalian cells in vivo. For this purpose, the genotoxic potential was investigated in bone marrow cells by the micronucleus test, chromosome aberration assay and comet assay (DNA strand breaks). In addition, DNA damage was evaluated in soft tissues and organs like spleen, liver and kidney cells. The oxidative damage was assessed by selective biochemical parameters by the measurement of lipid peroxidation, reduced glutathione (GSH), glutathione S-transferase (GST) and catalase (CAT) activity in liver. Adult Swiss albino male mice were exposed to sodium fluoride in drinking water at the concentrations of 4, 12 and 20mg/L for 30 consecutive days. Control groups (vehicle and positive) were also included. Animals were sacrificed; bone marrow and soft tissue samples were collected and subjected to series of assays respectively. We observed that NaF exposure, at the various concentrations tested caused a significant increase in the frequency of micronucleus (MN) in polychromatic erythrocytes (PCEs), structural chromosome aberrations in bone marrow cells. With the exception of the spleen cells, DNA damage was observed in bone marrow cells as well as in kidney and liver cells. We found an increase in lipid peroxidation, and catalase activity as well as decrease in glutathione activity (GSH and GST) in liver of mice respectively which were exposed to sodium fluoride. In conclusion, the data obtained clearly documents that NaF exhibits genotoxic activity and enhanced oxidative damage in mouse model.