Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Kaschin-Beck Disease Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, 150081, Heilongjiang Province, China.
Biol Trace Elem Res. 2021 Jun;199(6):2238-2246. doi: 10.1007/s12011-020-02336-z. Epub 2020 Aug 13.
Endemic fluorosis is a systemic chronic disease caused by excessive intake of fluoride. It is widely accepted that oxidative stress is closely related to fluorosis; however, molecular mechanism of oxidative stress in fluorosis remains unclear. This study investigated the effects of fluoride (F) on oxidative stress markers of lipid, gene, and protein in rats for revealing molecular mechanism of oxidative stress in fluorosis. The results showed concentration and exposure time of fluoride both had a significant effect on MDA and 8-OHdG. Fluoride concentration significantly impacted AGEs level, but exposure time did not. AOPP was not statistically different among the groups. AGEs decreased with the increase of fluoride in the rats with 3 months of fluoride treatment. The correlation analysis showed the degree of dental fluorosis was significantly negatively correlated with 8-OHdG at 1 month and 3 months, and negatively correlated with AGEs at 3 months. In the rats with 100 mg/L of fluoride treatment, MDA was significant positively correlated with 8-OHdG, and negatively correlated with AGEs. 8-OHdG was significantly negatively correlated with AGEs in the control group and 100 mg/L fluoride group. Taken together, fluoride had different effects on oxidative stress markers of lipid, gene, and protein. Excessive fluoride could increase MDA content, and decrease 8-OHdG and AGEs. These findings suggest that oxidative stress involved in molecular pathogenesis of fluorosis is complicated, and needs to furtherly study in the future.
地方性氟中毒是一种由氟化物过量摄入引起的全身性慢性疾病。氧化应激与氟中毒密切相关，这已被广泛接受；然而，氟中毒中氧化应激的分子机制仍不清楚。本研究探讨了氟化物（F）对大鼠脂质、基因和蛋白质氧化应激标志物的影响，以揭示氟中毒中氧化应激的分子机制。结果表明，氟化物的浓度和暴露时间对 MDA 和 8-OHdG 均有显著影响。氟化物浓度对 AGEs 水平有显著影响，但暴露时间没有影响。AOPP 在各组之间无统计学差异。在氟处理 3 个月的大鼠中，随着氟化物浓度的增加，AGEs 水平降低。相关性分析表明，在 1 个月和 3 个月时，氟斑牙程度与 8-OHdG 显著负相关，与 3 个月时的 AGEs 显著负相关。在 100mg/L 氟化物处理的大鼠中，MDA 与 8-OHdG 呈显著正相关，与 AGEs 呈显著负相关。在对照组和 100mg/L 氟化物组中，8-OHdG 与 AGEs 呈显著负相关。总之，氟化物对脂质、基因和蛋白质的氧化应激标志物有不同的影响。过量的氟化物会增加 MDA 含量，降低 8-OHdG 和 AGEs。这些发现表明，氟中毒中涉及的氧化应激的分子发病机制很复杂，需要进一步研究。
