title: Vitamin C intake attenuates the degree of experimental atherosclerosis induced by periodontitis in the rat by decreasing oxidative stress.
abstract: OBJECTIVE
  Periodontitis has been causally linked to cardiovascular disease, which is mediated through the oxidative stress induced by periodontitis. Since vitamin C has been suggested to limit oxidative damage, we hypothesized that vitamin C intake may reduce endothelial oxidative stress induced by periodontitis in the aorta. The aim of this study was to investigate the effects of vitamin C intake on the initiation of atherosclerosis in a ligature-induced rat periodontitis model.
  
  
  METHODS
  Eighteen 8-week-old-male Wistar rats were divided into three groups of six rats and all rats received daily fresh water and powdered food through out the 6-week study. In the vitamin C and periodontitis groups, periodontitis was ligature-induced for the first 4 weeks. In the vitamin C group, rats were given distilled water containing 1 g/L vitamin C for the 2 weeks after removing the ligature.
  
  
  RESULTS
  In the periodontitis group, there was lipid deposition in the descending aorta and significant increases of serum level of hexanoyl-lysine (HEL), and aortic levels of nitrotyrosine expression, HEL expression and 8-hydroxydeoxyguanosine (8-OHdG) compared to the control group. Vitamin C intake significantly increased plasma vitamin C level and GSH:GSSG ratio (178% and 123%, respectively), and decreased level of serum HEL and aortic levels of nitrotyrosine, HEL and 8-OHdG (23%, 87%, 84%, and 38%, respectively).
  
  
  CONCLUSIONS
  These results suggest that vitamin C intake attenuates the degree of experimental atherosclerosis induced by periodontitis in the rat by decreasing oxidative stress.
authors.affiliation: Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8525, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Ekuni
authors.forename: Takaaki
authors.initials: T
authors.lastname: Tomofuji
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Sanbe
authors.forename: Koichiro
authors.initials: K
authors.lastname: Irie
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Azuma
authors.forename: Takayuki
authors.initials: T
authors.lastname: Maruyama
authors.forename: Naofumi
authors.initials: N
authors.lastname: Tamaki
authors.forename: Jun
authors.initials: J
authors.lastname: Murakami
authors.forename: Susumu
authors.initials: S
authors.lastname: Kokeguchi
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Yamamoto
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000975:Antioxidants / Q000032:analysis / Q000627:therapeutic use*; D001013:Aorta, Thoracic / Q000187:drug effects / Q000473:pathology; D001018:Aortic Diseases / Q000473:pathology / Q000517:prevention & control; D001205:Ascorbic Acid / Q000097:blood / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000473:pathology / Q000517:prevention & control*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000032:analysis; D004730:Endothelium, Vascular / Q000187:drug effects; D005978:Glutathione / Q000097:blood; D008239:Lysine / Q000032:analysis / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010518:Periodontitis / Q000097:blood / Q000150:complications*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014443:Tyrosine / Q000031:analogs & derivatives / Q000032:analysis; D014815:Vitamins / Q000097:blood / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; C120589:N(epsilon)-hexanoyllysine; D014815:Vitamins; C002744:3-nitrotyrosine; D014443:Tyrosine; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; D005978:Glutathione; D008239:Lysine; D001205:Ascorbic Acid