Endogenous sulfur dioxide protects against isoproterenol-induced myocardial injury and increases myocardial antioxidant capacity in rats.

Recently, sulfur dioxide (SO(2)) was discovered to be produced in the cardiovascular system and to influence important biological processes. Here, we investigated changes in endogenous SO(2)/glutamic oxaloacetic transaminase (GOT) pathway in the development of isoproterenol (ISO)-induced myocardial injury in rats and the regulatory effect of SO(2) on cardiac function, myocardial micro- and ultrastructure, and oxidative stress. Wistar male rats were divided into control, ISO-treated, ISO+SO(2), and SO(2) groups. At the termination of the experiment, parameters of cardiac function and hemodynamics were measured and the micro- and ultrastructure of myocardium and stereological ultrastructure of mitochondria were analyzed. Myocardial SO(2) content was detected by high-performance liquid chromatography. GOT (key enzyme for endogenous SO(2) production) activity and gene (GOT1 and GOT2) expressions were measured, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), hydrogen peroxide, and superoxide radical levels were assayed. SOD (SOD1 and SOD2) and GSH-Px (GSH-Px1) gene expressions were also detected. The results showed that SO(2) donor at a dose of 85 mg/(kg day) did not impact the cardiac function and structure of rats, but exerted a subtle influence on myocardial redox status. ISO-treated rats exhibited decreased cardiac function, damaged myocardial structures, and downregulated endogenous SO(2)/GOT pathway. Meanwhile, myocardial oxidative stress increased, whereas antioxidative capacity downregulated. Administration of SO(2) markedly improved cardiac function and ISO-induced myocardial damage by ameliorating the pathological structure of the myocardium and the mitochondria. At the same time, myocardial products of oxidative stress decreased, whereas antioxidative capacity increased. These results suggest that downregulation of the endogenous SO(2)/GOT pathway is likely involved in the pathogenesis of ISO-induced myocardial injury. SO(2) protects against ISO-induced myocardial injury associated with increased myocardial antioxidant capacity in rats.