Abstract：
OBJECTIVE: Although there is growing evidence linking the exposure to sulphur dioxide (SO2) and fluoride to human diseases, there is little data on the co-exposure of SO2 and fluoride. Moreover, literature on SO2 and fluoride co-exposure to enamel damage is insufficient. In this work, we concentrate on the concurrent environmental issues of excessive SO2 and fluoride in several coal-consuming regions.
METHODS: To identify the toxicity of SO2 and fluoride exposure either separately or together, we used both ICR mice and LS8 cells, and factorial design was employed to assess the type of potential combined action.
RESULTS: In this study, co-exposure to SO2 and fluoride exacerbated enamel damage, resulting in more severe enamel defects of incisor and the damage occurred earlier. Cl-/HCO3- exchanger expression is increased by SO2 and fluoride in mouse incisor. Consistent with in vivo results, co-exposure of SO2 and fluoride decreased pHi and increased [Cl-]i level by increasing the expression of the Cl-/HCO3- exchanger in LS8 cells. Furthermore, SO2 and F may increase merlin protein expression, and merlin deficiency causes AE2 expression to decrease in vitro.
CONCLUSIONS: Overall, these results indicate that co-exposure to SO2 and fluoride may result in more toxicity both in vitro and in vivo than a single exposure to SO2 and fluoride, suggesting that residents in areas contaminated with SO2 and fluoride may be more likely to suffer enamel damage.
METHODS: To identify the toxicity of SO2 and fluoride exposure either separately or together, we used both ICR mice and LS8 cells, and factorial design was employed to assess the type of potential combined action.
RESULTS: In this study, co-exposure to SO2 and fluoride exacerbated enamel damage, resulting in more severe enamel defects of incisor and the damage occurred earlier. Cl-/HCO3- exchanger expression is increased by SO2 and fluoride in mouse incisor. Consistent with in vivo results, co-exposure of SO2 and fluoride decreased pHi and increased [Cl-]i level by increasing the expression of the Cl-/HCO3- exchanger in LS8 cells. Furthermore, SO2 and F may increase merlin protein expression, and merlin deficiency causes AE2 expression to decrease in vitro.
CONCLUSIONS: Overall, these results indicate that co-exposure to SO2 and fluoride may result in more toxicity both in vitro and in vivo than a single exposure to SO2 and fluoride, suggesting that residents in areas contaminated with SO2 and fluoride may be more likely to suffer enamel damage.
摘要：
目标：尽管越来越多的证据表明二氧化硫(SO2)和氟化物与人类疾病有关，关于SO2和氟化物共同暴露的数据很少。此外，关于SO2和氟化物共同暴露于牙釉质损伤的文献不足。在这项工作中,我们专注于几个煤炭消耗地区同时存在的过量SO2和氟化物的环境问题。
方法：为了单独或共同确定SO2和氟化物暴露的毒性，我们使用了ICR小鼠和LS8细胞，和析因设计用于评估潜在的联合作用的类型。
结果：在这项研究中，共同暴露于SO2和氟化物会加剧牙釉质损伤，导致门牙牙釉质缺损较严重，损伤发生较早。小鼠切牙中的SO2和氟化物会增加Cl-/HCO3-交换剂的表达。与体内结果一致，SO2和氟化物的共同暴露通过增加LS8细胞中Cl-/HCO3-交换剂的表达来降低pHi并增加[Cl-]i水平。此外，SO2和F可能会增加Merlin蛋白的表达，和merlin缺乏导致AE2表达在体外降低。
结论：总体而言，这些结果表明，与单一暴露于SO2和氟化物相比，共同暴露于SO2和氟化物可能在体外和体内产生更大的毒性，这表明，受SO2和氟化物污染地区的居民更有可能遭受牙釉质损害。
方法：为了单独或共同确定SO2和氟化物暴露的毒性，我们使用了ICR小鼠和LS8细胞，和析因设计用于评估潜在的联合作用的类型。
结果：在这项研究中，共同暴露于SO2和氟化物会加剧牙釉质损伤，导致门牙牙釉质缺损较严重，损伤发生较早。小鼠切牙中的SO2和氟化物会增加Cl-/HCO3-交换剂的表达。与体内结果一致，SO2和氟化物的共同暴露通过增加LS8细胞中Cl-/HCO3-交换剂的表达来降低pHi并增加[Cl-]i水平。此外，SO2和F可能会增加Merlin蛋白的表达，和merlin缺乏导致AE2表达在体外降低。
结论：总体而言，这些结果表明，与单一暴露于SO2和氟化物相比，共同暴露于SO2和氟化物可能在体外和体内产生更大的毒性，这表明，受SO2和氟化物污染地区的居民更有可能遭受牙釉质损害。
