Delayed rectifier potassium channels are involved in SO2 derivative-induced hippocampal neuronal injury

Recent studies implicate the possible neurotoxicity of SO2, however, its mechanisms remain unclear. In the present study, we investigated SO2 derivative-induced effect on delayed rectifier potassium channels (IK) and cellular death/apoptosis in primary cultured hippocampal neurons. The results demonstrate that SO2 derivatives (NaHSO3 and Na2SO3, 3:1 M/M) effectively augmented IK and promoted the activation of delayed rectifier potassium channels. Also, SO2 derivatives increased neuronal death percentage and contributed to the formation of DNA ladder in concentration-dependent manners. Interestingly, the neuronal death and DNA ladder formation, caused by SO2 derivatives, could be attenuated by the delayed rectifier potassium channel blocker (tetraethylammonium, TEA), but not by the transient outward potassium channel blocker (4-aminopyridine, 4-AP). It implies that stimulating delayed rectifier potassium channels were involved in SO2 derivative-caused hippocampal neuronal insults, and blocking these channels might be one of the possibly clinical treatment for SO2-caused neuronal dysfunction.