INCREASED LIPID-PEROXIDATION AS A MECHANISM OF METHIONINE-INDUCED ATHEROSCLEROSIS IN RABBITS

Citation
M. Toborek et al., INCREASED LIPID-PEROXIDATION AS A MECHANISM OF METHIONINE-INDUCED ATHEROSCLEROSIS IN RABBITS, Atherosclerosis, 115(2), 1995, pp. 217-224
Citations number
42
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas
Journal title
ISSN journal
00219150
Volume
115
Issue
2
Year of publication
1995
Pages
217 - 224
Database
ISI
SICI code
0021-9150(1995)115:2<217:ILAAMO>2.0.ZU;2-K
Abstract
Methionine is converted by the transmethylation/transsulfuration pathw ay to homocysteine which may exert atherogenic effects by several mech anisms, including lipid peroxidation. Therefore, the excessive dietary methionine may induce the development of atherosclerosis. To test thi s hypothesis, plasma and aortic thiobarbituric acid reactive substance s (TEARS), as well as activities of aortic and erythrocyte superoxide dismutase (SOD), catalase and selenium-dependent glutathione peroxidas e (GPX) were measured in rabbits fed a diet enriched with 0.3% methion ine for 6 or 9 months. Histological examinations of aortas also were p erformed. Feeding rabbits a methionine-enriched diet for 6 or 9 months resulted in significant increases in plasma and aortic TEARS levels a nd aortic antioxidant enzyme activities. However, a decrease in plasma antioxidant activity (AOA) was observed. In erythrocytes, SOD activit y increased, catalase remained normal and GPX decreased in the treated animals. Histological examination of aortas showed typical atheroscle rotic changes, such as intimal thickening, deposition of cholesterol, and calcification in methionine-fed rabbits. These results confirm tha t high-methionine diet may induce atherosclerosis in rabbits and indic ate disturbances in lipid peroxidation and antioxidant processes as po ssible mechanisms of its atherogenic influence.