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Sulfur dioxide (SO 2 ) is a colorless and irritating gas. Recent studies indicate that SO 2  acts as the gas signal molecule and inhibits vascular smooth muscle cell (VSMC) proliferation. Cell proliferation depends on intracellular pH (pH i ). Transmembrane cystein mutation of Na + - independent Cl - /HCO 3  -  exchanger (anion exchanger, AE) affects pH i . However, whether SO 2  inhibits VSMC proliferation by reducing pH i  is still unknown. Here, we investigated whether SO 2  reduced pH i  to inhibit the proliferation of VSMCs and explore its molecular mechanisms. Within a range of 50–200 μM, SO 2  was found to lower the pH i  in VSMCs. Concurrently, NH 4 Cl pre-perfusion showed that SO 2  significantly activated AE, whereas the AE inhibitor 4,4′-diisothiocyanatostilbene- 2,20-disulfonic acid (DIDS) significantly attenuated the effect of SO 2  on pH i  in VSMCs. While 200 μM SO 2  sulphenylated AE2, while dithiothreitol (DTT) blocked the sulphenylation of AE2 and subsequent AE activation by SO 2 , thereby restoring the pH i  in VSMCs. Furthermore, DIDS pretreatment eliminated SO 2 -induced inhibition of PDGF-BB-stimulated VSMC proliferation. We report for the first time that SO 2  inhibits VSMC proliferation in part by direct activation of the AE via posttranslational sulphenylation and induction of intracellular acidification.

Sulfur Dioxide Activates Cl-/HCO3- Exchanger via Sulphenylating AE2 to Reduce Intracellular pH in Vascular Smooth Muscle Cells