Progress in sulfur dioxide biology: from toxicology to physiology / 生理学报

Based on our studies for more than 20 years, we review the recent advances in sulfur dioxide (SO2) biology. Three sections are involved: (1) The studies on SO2 toxicological effects and its underlying mechanisms; (2) The new investigations on SO2 donor and physiological role of SO2 as a new type-gas transmitter; (3) The observations on pathophysiologic roles of SO2.

Effects of sodium metabisulfite on potassium currents in acutely isolated rat hippocampal CA1 neurons / 中国应用生理学杂志

<p><b>AIM</b>To 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.</p><p><b>METHODS</b>By using whole-cell patch-clamp technique, the effects of SMB on transient outward K+ (I(A)) and delayed rectifier K+ currents(IK) were observed.</p><p><b>RESULTS</b>(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).</p><p><b>CONCLUSION</b>SMB, 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.</p>

Sulfur dioxide-induced liver pathology / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate effects of short-term sulfur dioxide inhalation to the liver.</p><p><b>METHODS</b>Haematoxylin and eosin staining (HE) and transmission electron microscopy (TEM) were used to study the pathologic changes in mice liver after sulfur dioxide (SO(2)) inhalation.</p><p><b>RESULTS</b>Exposure to 56 mg/m(3), 112 mg/m(3) 168 mg/m(3) SO(2) caused increasingly severe liver injuries, as detected by HE staining and TEM. The morphologic changes included spotty necrosis with lymphocyte, monocyte, and neutrophil infiltration, fatty degeneration of hepatocytes with dilatation of rough endoplasmic reticulum and dissociation of ribosomes, as well as degeneration of mitochondria and karyorrhexis.</p><p><b>CONCLUSION</b>SO(2) inhalation can cause marked liver injury in experimental settings.</p>

Effects of AlCl3 on transient outward K+ current and delayed rectifier K(+) current in acutely isolated rat hippocampal CA1 neurons / 生理学报

The effects of aluminum chloride (AlCl3) on the transient outward potassium and delayed rectifier K(+) current in hippocampal CA1 neurons of rats were studied by the whole-cell patch clamp technique. It was found that AlCl3 reduced the transient outward potassium current and delayed rectifier K(+) current in a dose-dependent manner. 1000 micromol/L AlCl3 resulted in change in voltage and slope of the half-activation and the half-inactivation of I(A) and I(K). These results imply that AlCl3 may damage potassium channel of the hippocampal CA1 neurons from rats and this may be related to the mechanism of the damage to the central nervous system by aluminum.

Inhibition of sodium currents in acutely isolated hippocampal CA1 neurons of rats by magnesium sulfate / 生理学报

The effects of magnesium sulfate (MgSO4) on sodium currents (Na(+) currents) were studied in freshly dissociated hippocampal CA(1) neurons of rat using the whole-cell patch-clamp technique. The results indicated that MgSO4 caused a concentration-dependent and voltage-dependent decrease in Na(+) currents. The half-inhibitory concentration (IC(50)) was 4.05 mmol/L. This action was frequency-independent. The results also showed that 4 mmol/L MgSO4 shifted the steady state activation curve of Na(+) currents towards positive potential (control V(h)=-55.8+/-6.8 mV, MgSO4 V(h)=-34.2+/-6.2 mV, n=8, P<0.01) without changing the slope factor. However, the steady state inactivation curve was not affected. These results suggest that blockade of Na(+) currents by MgSO4 might be an interpretation for its neuroprotection against damages induced by ischemia and oxygen deprivation.

Blockade of magnesium sulfate on transient outward K+ current and delayed rectifier K+ current in acutely isolated rat hippocampal neurons / 药学学报

<p><b>AIM</b>To study the effect of magnesium sulfate on transient outward K+ current (IA) and delayed rectifier K+ current (IK) in freshly dissociated hippocampal neurons of rats.</p><p><b>METHODS</b>The whole-cell patch clamp techniques were used.</p><p><b>RESULTS</b>Magnesium sulfate reversibly reduced the amplitudes of IA and IK in a concentration-dependent and voltage-dependent, but not frequency-dependent manner. Half-blocking concentration (IC50) on IA and IK were 6.30 mmol.L-1 and 7.60 mmol.L-1, respectively. Magnesium sulfate (6 mmol.L-1) affected the activation process of IA and IK. Before and after application of the drug, the half-activation voltages of IA were (7 +/- 6) mV and (-7 +/- 11) mV (n = 10, P < 0.01), and the half-activation voltages of IK were (20 +/- 6) mV and (28 +/- 4) mV (n = 10, P < 0.01), but the slope factors were not changed. In addition, magnesium sulfate (6 mmol.L-1) also affected the inactivation process of IA. Before and after application of the drug, the half-inactivation voltages of IA were (-65 +/- 5) mV and (-89 +/- 6) mV (n = 10, P < 0.01).</p><p><b>CONCLUSION</b>Magnesium sulfate inhibited IA and IK in freshly dissociated hippocampal neurons of rats, which might contribute to protect the central neuronal system (CNS) against damages induced by ischemia and oxygen deprivation.</p>

Effect of SO2 derivatives on sodium currents in acutely isolated rat hippocampal CA1 neurons / 生理学报

The effect of SO2 derivatives on Na(+) currents was studied in freshly dissociated hippocampal CA1 neurons of rat using the whole-cell patch-clamp technique. The results indicated that SO2 derivatives caused a dose-dependent and voltage-dependent increase in the voltage-activated Na+ currents. The amplitudes of Na(+) currents were increased by 50.59 19.08% and 82.06 18.51% (n=15)by SO2 derivatives at 10 and 100 micromol/L, respectively. The action was frequency-independent. The results also showed that SO2 derivatives did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 micromol/L SO2 derivatives, the half-inactivation voltage was -69.71+/-4.67 and -53.27+/-4.95 mV (n=10, P<0.01), respectively, but the slope factor was not changed. These results imply that SO2 derivatives have neurotoxic effects and that SO2 pollution is probably related to some diseases of central neuronal system.