title: Regulatory effects of sulfur dioxide on the development of atherosclerotic lesions and vascular hydrogen sulfide in atherosclerotic rats.
abstract: OBJECTIVE
  This study was designed to examine the effect of sulfur dioxide (SO(2)) on atherosclerotic progression and endogenous vascular hydrogen sulfide (H(2)S) in rats with atherosclerosis (AS).
  
  
  METHODS
  Twenty-eight male rats were randomly divided into control, AS and AS+SO(2) groups. Rats were given a single dose of vitamin D(3) and fed a high-cholesterol diet for 8 weeks to induce AS. Plasma lipids, aortic ultrastructure, and atherosclerotic lesions were detected at the termination of experiment. Plasma and aortic SO(2) were measured using high-performance liquid chromatography, and aspartate aminotransferase (AAT) 1 and AAT2 mRNAs were detected by real-time PCR. Plasma and aortic H(2)S levels were determined with a sulfide-sensitive electrode. Cystathionine-γ-lyase (CSE) mRNA and protein expression was detected. Plasma glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, malondialdehyde (MDA) and nitric oxide (NO) contents, inducible NO synthase (iNOS) and eNOS activities, and aortic SOD1 and SOD2 expressions were detected.
  
  
  RESULTS
  Marked atherosclerotic lesions with elevated levels of TC and LDL-C were observed in AS rats. While, there were decreased plasma SO(2) levels and aortic SO(2) production, with a reduced aortic AAT activity in atherosclerotic rats. Plasma GSH-Px and SOD activities were decreased but MDA level increased. Plasma NO content and iNOS activity were also increased. SO(2) donor, however, significantly decreased the atherosclerotic lesions with an increased aortic H(2)S/CSE pathway. It elevated plasma GSH-Px and SOD activities, reduced plasma MDA level, and increased NO/NOS pathway.
  
  
  CONCLUSIONS
  SO(2) has a marked anti-atherogenic effect with an increase in endogenous H(2)S production in rats with AS.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Chaoshu
authors.initials: C
authors.lastname: Tang
authors.forename: Hongfang
authors.initials: H
authors.lastname: Jin
authors.forename: Junbao
authors.initials: J
authors.lastname: Du
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D001219:Aspartate Aminotransferases / Q000378:metabolism; D050197:Atherosclerosis / Q000097:blood / Q000473:pathology* / Q000517:prevention & control; D003542:Cystathionine gamma-Lyase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000097:blood; D006862:Hydrogen Sulfide / Q000097:blood*; D008297:Male; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects; D052250:Nitric Oxide Synthase Type III / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013458:Sulfur Dioxide / Q000378:metabolism / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D013458:Sulfur Dioxide; D005979:Glutathione Peroxidase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D003542:Cystathionine gamma-Lyase; D006862:Hydrogen Sulfide