Fluorosis caused cellular apoptosis and oxidative stress of rat kidneys

Abstract

As the strongest electronegative element, fluorine can stimulate the production of superoxide radicals in cells. In view of the important roles of kidneys in bone metabolism, the authors analyzed the quantitative pathomorphological characteristics of renal damage and the potential cellular apoptosis and oxidative stress mechanisms in rats treated with excessive fluoride. Wistar rats were exposed to 50 mg F−(110.5 mg NaF)/L, 100 mg F−(221.0 mg NaF)/L and 150 mg F−(331.5 mg NaF)/L in drinking water for 70 and 140 d, respectively. Microscope with image analysis was used to quantitate pathomorphological changes in renal tissues of the rats. Reactive oxygen species(ROS), the cell cycle and apoptosis of renal cells were measured by flow cytometry and TUNEL technique(terminal deoxynucleotidyl transferase dUTP nick end labeling), respectively. The ion concentrations in serum and renal functional parameters were detected by automatic biochemical analyzer. Quantitative analysis results demonstrate the expanded Bowman’s space of glomerulus and obvious dilatation of renal tubule. TUNEL technique revealed that NBT/BCIP (nitro blue tetrazolium/5-bromo-4-chloro-3′-indolylphosphate, p-toluidine salt)-staining positive apoptotic cells selectively located in medullocortical junction areas. The data suggest that renal damage in chronic fluorostic rats is associated with the cellular apoptosis and oxidative stress.