Aim: The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO 2 ) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. Methods: Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-β-hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO 2 group receiving MCT plus SO 2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO 2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed. Results: In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P<0.01), pulmonary vascular structural remodeling developed, and SOD, GSHPx, CAT, GSH, and MDA levels of lung homogenates significantly increased (P<0.01) in association with the elevated SO 2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDX-treated rats, lung tissues and plasma SO 2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCTtreated rats (P<0.01). In contrast, with the use of a SO 2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels. Conclusion: Endogenous SO 2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.
