Background

Exposure of human lung epithelial cells to the oxidant pollutant ozone (O₃) alters cell Cl⁻ currents inducing an outward rectifier effect. Among the various Cl⁻ channels, ClC-2 and ORCC seemed to be involved in this response.

Objectives

To identify the channel related to O₃ induced current changes.

Results

Down regulating the expression of ORCC and ClC-2 genes and analyzing the membrane current show that the enhancement of the current disappeared when ORCC was silenced. The contribution of ORCC and ClC-2 channels in control and O₃ treated cells was obtained by a mathematical approach.

Conclusion

We suggest that O₃ activates ORCC channels and slightly inhibited ClC-2 channels in the negative voltage range. These findings open the possibility of identifying the biomolecular changes induced by O₃ allowing a possible pharmacological intervention towards chloride current due to oxidative stress.

中文翻译：

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肺ORCC和CLC-2通道在氧化应激反应中的作用

背景

人肺上皮细胞暴露于氧化剂污染物臭氧（O ₃）涂改小区C1 ^-电流诱导向外整流器效应。在各种氯^-信道，CLC-2和ORCC似乎参与这种反应。

目标

以确定与O ₃感应电流变化有关的通道。

结果

下调ORCC和ClC-2基因的表达并分析膜电流表明，沉默ORCC后，电流的增强消失了。通过数学方法获得了在对照细胞和O ₃处理细胞中ORCC和ClC-2通道的贡献。

结论

我们建议O ₃在负电压范围内激活ORCC通道并略微抑制ClC-2通道。这些发现打开了鉴定由O ₃诱导的生物分子变化的可能性，从而允许由于氧化应激而可能对氯离子电流进行药理干预。