AIMTo investigate the effects of sodium metabisulfite (SMB), sulfur dioxide (SO2) and its derivatives in vivo, sodium bisulfite and sulfite on K+ channels of the central neurons and its mechanisms.

METHODSBy using whole-cell patch-clamp technique, the effects of SMB on transient outward K+ (I(A)) and delayed rectifier K+ currents(IK) were observed.

RESULTS(1) SMB can increase the amplitudes of I(A) and I(K) in a dose-dependent and voltage-dependent manner. Their half-increase doses were 15.8 micromol/L and 11.5 micromol/L respectively. (2) SMB (10 micromol/L) significantly shifted the activation curves of I(A) and I(K) to more positive potentials. Before and after application of 10 micromol/L SMB, the half-activation voltages of I(A) and I(K) were (- 12.6 +/- 1.6) mV and (- 7.0 +/- 1.3) mV, (10.8 +/- 0.9) mV and (21.6 +/- 0.7) mV (P < 0.01, n = 8), respectively, but the slope factors were not changed. (3) The inactivation curve of I(A) was shifted to positive potentials, the half-inactivation voltage of I(A) were (- 97.0 +/- 1.1) mV and (- 84.4 +/- 3.3) mV (P < 0.01, n = 8) before and after application of SMB (10 micromol/L), without changing the slope factors. (4) SOD, CAT and GPx could partly inhibit the incremental effect of SMB on I(A) and I(K).

CONCLUSIONSMB, SO2 and its derivatives in vivo, sodium bisulfite and sulfite have the damage effects on the central nervous system, and they can cause extracellular K+ increase and induce the disturbance of the central neuronal functions. Its mechanism may involve oxidation damage in the rat hippocampal CA1 neurons, caused by sulfur- and oxygen-centered free radicals formed in the process of sulfite or bisulfite oxidation.