Sulfur Dioxide Derivative Prevents Left Ventricular Hypertrophy and Electrophysiological Alterations

SO 2 and derivatives generally accepted as toxic gasseous molecules and inhalation of itdrives biological systems severe conditions. On the other hand, they are used as safepreservative in foods. Recently, SO 2 was discovered to be produced in thecardiovascular system and to influence important biological processes. It was reported by Liang Y. et al that endogenous SO 2 progressively inhibit hypertrophycaused by isoproterenol application to rats via increasing antioxidation capacity. In this study we aimed to investigate underlying molecular and electro physiological mechanisms of this inhibition of ventricular hypertrophy. Wistar rats were administrated 20 mg/kg isoproterenolfor seven days subcutaneuosly to drive hypertropic cardiomyopathy and some animals was taken SO 2 donor sodium metabisulfite together with isoproterenol through i.p. at a dose of 85 mg/kg. At the end of the experiment, animals were sacrified by heart exicition and followed by enzimatic dissociation of single left ventricular myocytes. Iso admistrated animal heart (6.69±0.41 mg/kg bodyweight) were hypertrofied compared to control animals hearts(3.94±0.12 mg/kg). On the other hand, metabisulfite inhibits hypertrothy of the rats hearts (4.27±0.32 mg/kg).Single cardiomyocytes were examined electrophysiologicaly by voltage clamp in order to examine effect of SO 2 on potassium currents (I K1 , I to and I ss ), action potential (AP) and L‐type calcium current (I CaL ). While metabisulfite had no effect on potassium currents, prolonged AP and reduced I CaL ameliorate to the control level. In conclusion, SO 2 derivative sodium metabisulfite prevent cardiac hypertrophy generated by adrenergicstimulation both electrophysiologicaly and histologicaly. This work supported by Akdeniz University Scientific Research Unit.