title: Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats.
abstract: OBJECTIVE
  The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO2) 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-beta- hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO2 group receiving MCT plus SO2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO2 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 SO2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDXtreated rats, lung tissues and plasma SO2 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 MCT-treated rats (P<0.01). In contrast, with the use of a SO2 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.
  
  
  CONCLUSIONS
  Endogenous SO2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
authors.forename: Hong-fang
authors.initials: HF
authors.lastname: Jin
authors.forename: Shu-xu
authors.initials: SX
authors.lastname: Du
authors.forename: Xia
authors.initials: X
authors.lastname: Zhao
authors.forename: Hong-ling
authors.initials: HL
authors.lastname: Wei
authors.forename: Yan-fei
authors.initials: YF
authors.lastname: Wang
authors.forename: Yin-fang
authors.initials: YF
authors.lastname: Liang
authors.forename: Chao-shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Jun-bao
authors.initials: JB
authors.lastname: Du
mesh_terms: D000410:Alanine Transaminase / Q000096:biosynthesis; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001219:Aspartate Aminotransferases / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D016686:Monocrotaline / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D013458:Sulfur Dioxide / Q000097:blood / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D013458:Sulfur Dioxide; D016686:Monocrotaline; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase