Vitamin C intake attenuates the degree of experimental atherosclerosis induced by periodontitis in the rat by decreasing oxidative stress.
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.
Ekuni
Daisuke
D
Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8525, Japan.
Tomofuji
Takaaki
T
Sanbe
Toshihiro
T
Irie
Koichiro
K
Azuma
Tetsuji
T
Maruyama
Takayuki
T
Tamaki
Naofumi
N
Murakami
Jun
J
Kokeguchi
Susumu
S
Yamamoto
Tatsuo
T
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*
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