General Description

Sulfur dioxide is a colorless gas with a pungent odor commonly released through the combustion of coal and oil in power plants. It has distinct properties, including solubility in water, toxic effects when inhaled, and plays an essential role in various industries. Research suggests that endogenous sulfur dioxide exhibits vasorelaxation effects and regulates vascular structure by suppressing vascular smooth muscle cell proliferation and collagen remodeling. The HDX treatment affects the production of endogenous sulfur dioxide and its vasorelaxation response, mediated by the sGC/cGMP/PKG signaling pathway. Overall, these findings highlight the importance of handling and controlling sulfur dioxide with caution in industrial applications while also recognizing its potential physiological benefits.

Figure 1. Sulfur dioxide

Properties and Applications of Sulfur Dioxide

Sulfur dioxide is a colorless gas with a pungent odor. It can also exist as a liquid under pressure and readily dissolves in water. Common sources of atmospheric sulfur dioxide include the combustion of coal and oil in power plants, as well as copper smelting. Additionally, volcanic eruptions can release sulfur dioxide into the air. Physically, sulfur dioxide appears as a colorless gas with a choking or suffocating odor. It has a boiling point of -10 °C and is heavier than air. Inhalation of sulfur dioxide can be very toxic and may cause irritation to the eyes and mucous membranes. Furthermore, in the presence of fire or heat, prolonged exposure to sulfur dioxide can lead to violent container rupture and even a rocket-like effect. Sulfur dioxide finds application in various industries. It is used in the manufacturing of chemicals, paper pulping, metal processing, and food processing. Overall, sulfur dioxide possesses distinct properties, including its colorless gaseous form, pungent odor, solubility in water, and toxic effects when inhaled. These properties make it essential to handle and control sulfur dioxide with caution in industrial applications. ¹

Physiologic effects

Vasorelaxation

Sulfur dioxide has been found to exhibit vasorelaxation effects. HDX treatment, ranging from 40-160 μM, has been shown to reduce the production of endogenous Sulfur dioxide. This reduction inhibits the vasorelaxation response of Sulfur dioxide to acetylcholine and sodium nitroprusside, but enhances the vasoconstriction response to norepinephrine. Additionally, HDX treatment in concentrations of 10-6–10-3 M induces the concentration-dependent contraction of the aortic ring. Research suggests that HDX attenuates disulfide bond-dependent soluble guanylyl cyclase (sGC) dimerization. This attenuation may inactivate sGC and reduce cyclic guanosine-3￠,5￠-monophosphate (cGMP) production, leading to a decrease in intracellular cGMP content and the inactivation of protein kinase G (PKG). These findings suggest that the activation of the sGC/cGMP/PKG signaling pathway, mediated by sulfhydryl-dependent dimerization, is one of the important mechanisms for Sulfur dioxide -induced vasorelaxation. In summary, research indicates that endogenous Sulfur dioxide relaxes blood vessels and plays a role in the regulation of vascular tension. HDX treatment affects the production of endogenous Sulfur dioxide and its vasorelaxation response by influencing the sGC/cGMP/PKG signaling pathway. ²

Maintenance of normal vascular structure

Sulfur dioxide plays a crucial role in maintaining the normal vascular structure. Research conducted on WKY rats treated with HDX (3.7 mg/kg) revealed significant remodeling of vascular structure, increased proliferation of vascular smooth muscle cells (VSMCs), and elevated levels of phosphorylated ERK. Cell experiments further confirmed that knockdown of angiotensinogen (AAT) facilitated VSMC proliferation, while AAT overexpression inhibited it. In VSMC-AAT1 knockout mice, reduced plasma and aortic Sulfur dioxide levels were observed, along with significantly elevated expression of type I/III collagen in the aorta. Additionally, AAT overexpression was found to inhibit the activation of the TGF-b1/type I TGF-b receptor/Smad2/3 pathway, leading to decreased collagen synthesis and increased collagen degradation. This suppresses collagen remodeling in VSMCs. Conversely, AAT knockdown promotes collagen remodeling. These findings suggest that endogenous Sulfur dioxide suppresses VSMC proliferation and collagen remodeling, thereby maintaining the vascular structure under physiological conditions. In summary, Sulfur dioxide plays a vital role in regulating VSMC behavior and collagen synthesis, contributing to the overall maintenance of a healthy vascular structure. ³

Reference

1. Sulfur Dioxide. National Center for Biotechnology Information, 2023, PubChem Compound Summary for CID 1119.

2. Yao Q, Huang Y, Liu AD, Zhu M, Liu J, Yan H, Zhang Q, Geng B, Gao Y, Du S, Huang P, Tang C, Du J, Jin H. The vasodilatory effect of sulfur dioxide via SGC/cGMP/PKG pathway in association with sulfhydryl-dependent dimerization. Am J Physiol Regul Integr Comp Physiol. 2016 Jun 1;310(11):R1073-1080.

3. Huang Y, Zhang H, Lv B, Tang C, Du J, Jin H. Sulfur Dioxide: Endogenous Generation, Biological Effects, Detection, and Therapeutic Potential. Antioxid Redox Signal. 2022 Feb;36(4-6):256-274.