The role of pulmonary ORCC and CLC-2 channels in the response to oxidative stress

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. To identify the channel related to O3 induced current changes. 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. 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.