Oxidative stress might be a mechanism connected with the decreased α7 nicotinic receptor influenced by high-concentration of fluoride in SH-SY5Y neuroblastoma cells

The possible mechanism concerning decreased α7 nicotinic acetylcholine receptor (nAChR) influenced by fluorosis was investigated. SH-SY5Y cells were exposed to fluoride within the range of 0.05-5 μM, or ferrous iron (1-100 μM), a free radical inducer. The levels of α7 nAChR expression, lipid peroxidation and protein oxidation were detected. The results showed that both high-concentrations of fluoride and ferrous iron induced increased levels of lipid peroxidation and protein oxidation in SH-SY5Y cells with concentration-dependent manners. In addition, inhibition of α7 nAChR at protein level was observed in the cells exposed to high amounts of fluoride or ferrous iron. Furthermore, a declined value of Bmax in [125I]α-bungarotoxin binding sites was found in the cells treated with the high-concentration of fluoride. Interestingly, antioxidants (vitamin E and glutathione) can attenuate the inhibition of the receptor induced by fluoride. These findings suggest that oxidative stress resulted from fluorosis might directly induce the deficit of α7 nAChR.