Abstract
Sulfur dioxide (SO2) was previously regarded as a toxic gas in atmospheric pollutants. But it has been found to be endogenously generated from metabolism of sulfur-containing amino acids in mammals through transamination by aspartate aminotransferase (AAT). SO2 could be produced in cardiovascular tissues catalyzed by its synthase AAT. In recent years, studies revealed that SO2 had physiological effects on the cardiovascular system, including vasorelaxation and cardiac function regulation. In addition, the pathophysiological effects of SO2 were also determined. For example, SO2 ameliorated systemic hypertension and pulmonary hypertension, prevented the development of atherosclerosis, and protected against myocardial ischemia-reperfusion (I/R) injury and isoproterenol-induced myocardial injury. These findings suggested that endogenous SO2 was a novel gasotransmitter in the cardiovascular system and provided a new therapy target for cardiovascular diseases.
Highlights
Sulfur dioxide (SO2) was regarded as a toxic gas and environmental pollutant
Sulfur dioxide aspartate aminotransferase (AAT) (SO2) produced negative inotropic effects through upregulating the activities of protein kinase C (PKC), cyclooxygenase, and cyclic guanosine monophosphate (cGMP), while, at high concentrations, the inotropic effects induced by SO2 were associated with the activation of Adenosine triphosphate-sensitive potassium cAMP (KATP) channel by increasing the expressions of Kir6.2 and SUR2A and the inhibition of calcium influx via the L-type calcium channel by decreasing the expressions of Cav1.2 and Cav1.3 in rat hearts [36, 37]
SO2 could depress L-type calcium channel current in isolated rat cardiomyocytes [38]. These data indicated that SO2 had a negative inotropic effect on myocardial contractility and hemodynamic parameters, which might help to explain some cardiovascular effects induced by SO2
Summary
Sulfur dioxide (SO2) was regarded as a toxic gas and environmental pollutant. It is colorless, transparent, odorous, and water-soluble. SO2 can be endogenously generated from metabolism of the sulfur-containing amino acid L-cysteine in mammals [3]. It has features of low molecular weight, continuous production, and fast diffusion and plays extensive biological action independent of membrane receptors [4, 5]. The objective of this review was to elaborate on the generation and metabolism of endogenous SO2 and give a summary of the physiological and pathophysiological effects of SO2 on the cardiovascular system
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