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J Cardiovasc Pharmacol Ther. 2009 Sep;14(3):231-41. doi: 10.1177/1074248409337003. Epub 2009 Jun 4.

Vitamin E does not regress hypercholesterolemic atherosclerosis.

Author information

  • Department of Physiology, University of Saskatchewan, Saskatoon, Canada. k.prasad@usask.ca

Abstract

BACKGROUND:

Suppression of hypercholesterolemic atherosclerosis with vitamin E is associated with reductions in oxidative stress without reductions in serum lipids. The objectives of this study were to determine if (1) vitamin E regresses hypercholesterolemic atherosclerosis; and (2) regression is associated with reductions in serum lipids and aortic oxidative stress.

METHODS AND RESULTS:

The studies were conducted in 4 groups of rabbits: group I, control, regular diet (2 months); group II, 0.25% cholesterol diet (2 months); group III, 0.25% cholesterol diet (2 months) followed by regular diet (2 months); and group IV, 0.25% cholesterol diet (2 months) followed by regular diet with vitamin E (40 mg/kg body weight/day) (2 months). Blood samples were collected monthly for the measurement of serum lipids and oxidative stress (chemiluminescent activity of white blood cells [WBC-CL]). Aortas were removed at the end of the protocol for assessment of atherosclerotic lesions, and oxidative stress (malondialdehyde [MDA] and CL). Increases in serum lipids in group II were associated with an increase in oxidative stress and development of atherosclerosis. Serum lipids decreased to a similar extent in groups III and IV but the atherosclerotic lesions increased by 63% and 141% compared to group II. Acceleration of atherosclerosis in the rabbits on regular diet with or without vitamin E was associated with practically no change in the oxidative stress.

CONCLUSION:

These results suggest that (1) regular diet following a high-cholesterol diet decreased oxidative stress but did not induce regression of atherosclerosis; (2) vitamin E did not produce regression; and (3) regular diet with vitamin E following a high-cholesterol diet was not associated with an increase in oxidative stress but produced acceleration of atherosclerosis.

PMID:
19498106
[PubMed - indexed for MEDLINE]
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