Effects Of Sulfur Dioxide And SO₂-Diviravitives On The Membrane Ion Channels And Its Lipid Peroxidation

Abstract In this article, we study the effect of sulfur dioxide (SO?) inhalation on lipid peroxidation (LPO) in different organs of mice and the effects of aluminum chloride (A1Cl3) on the ion channels of isolated rat hippocampal CAl neurons. The levels of MDA were measured in the organs after the mice were exposed to SO2 at various concentrations for 6h/day x 7 days, using fluorescence spectrophotometer. Our results show that: (1) LPO levels in all organs tested of mice increased with SOi inhalation concentrations in dose-dependent manner; (2) Under SO2 inhalation at low concentration (22 2mg/m3), LPO degrees in different organs tested are different. It was shown that there were differences among the different organs; however, these differences among the organs tested would be lowered with SO2 concentrations; (3) There were sexual differences for levels of oxidation damage by SO2 in various organs from male and female mice. The results suggest: (1) SO2 could cause oxidation damage in multiple organs of mice, it is a systemic toxin; (2) Oxidation damages caused by SO2-producing reactive oxygen species, might be one of the primary mechanisms of toxicological role of SO2 on mammalian cells. The effects of aluminum chloride (AlCl3) on the ion channel of isolated rat hippocampal CAl neurons were studied by the whole-cell patch clamp technique. It was found that AlCl3 could reduce the transient outward potassium current and delayed rectifier current in a dose-dependent manner. 1000 mol/L AlCl3 changed the voltage and slope of the half-activation and the half-inactivation of IA and IK. It was also found that AlCl3 could reduce the sodium current in a dose-dependent manner, but it didn' t change the voltage and slope of the half-activation and the half-inactivation of sodium current. These results imply that AlCl3 may damage potassium channel and sodium channel of the hippocampal CAl neurons from rats and it is suggested that this may be related to mechanism of damage of aluminum on central neuronal system. Based on the results of SO2 derivative and AlCL on the potassium current and sodium current associately, it was found that the activation and inactivation courses of potassium current and sodium current were shifted little but not insignificantly statistically. It is suggested that the effects of SO2 derivative and AlCL on ion channel were antagonistic joint action.