Vitamin E does not slow the progression of hypercholesterolemic atherosclerosis

Abstract

Background: Vitamin E suppresses the development of atherosclerosis but does not regress established hypercholesterolemic atherosclerosis.

Objectives: To investigate whether vitamin E slows the progression of established atherosclerosis, and whether this effect is associated with reductions in serum lipids and oxidative stress.

Methods: THE PRESENT STUDY WAS PERFORMED IN FOUR GROUPS OF RABBITS: group I, regular diet (control); group II, 0.25% cholesterol diet (two months); group III, 0.25% cholesterol diet (four months); and group IV, 0.25% cholesterol diet (two months) followed by 0.25% cholesterol and vitamin E (two months). Serum lipids and the chemiluminescent activity of white blood cells (WBC-CL), a measure of oxygen radical production by white blood cells, were measured before and at monthly intervals for the duration of the study. Aortas were removed at the end of the protocol for assessment of atherosclerosis and the chemiluminescent activity of aortic tissue (aortic-CL), a measure of antioxidant reserve.

Results: Atherosclerosis was associated with hyperlipidemia and increased oxidative stress, indicated by increased nonactivated WBC-CL and alteration of the aortic-CL. Significant areas of the intimal surfaces of the aortas from group II (26.54%±4.11%), group III (69.37%±5.34%) and group IV (65.96%±7.86%) were covered with atherosclerotic lesions. Vitamin E did not alter serum lipids, aortic antioxidant reserve or WBC-CL. Vitamin E was ineffective in slowing the progression of hypercholesterolemic atherosclerosis.

Conclusion: Vitamin E did not slow the progression of hypercholesterolemic atherosclerosis, and this effect was associated with its ineffectiveness in reducing serum lipids and oxidative stress.

Figure 1)

Sequential changes in the serum triglycerides and total cholesterol of the four experimental groups. Results are expressed as mean ± SE. *P<0.05, month 0 versus other months in the respective groups; ^†P<0.05, month 1 versus other months in the respective groups; ^‡P<0.05, group I versus other groups

Figure 2)

Changes in the levels of serum low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) of the four experimental groups. Results are expressed as mean ± SE. *P<0.05, month 0 versus other months in the respective groups; ^†P<0.05, month 1 versus other months in the respective groups

Figure 3)

Representative photographs of the intimal surfaces of aortas of the four groups stained with Sudan IV. The lipid deposits on the intimal surfaces of the aortas are brick red in colour. Lipid deposits are absent on the intimal surface of the aorta from group I. I, control; II, 0.25% cholesterol (2 months); III, 0.25% cholesterol (4 months); and IV, 0.25% cholesterol (2 months) plus 0.25% cholesterol and vitamin E (2 months)

Figure 4)

Extent of atherosclerotic lesions in the aortas of the four experimental groups. Results are expressed as mean ± SE. Note that the control group has a value for atherosclerotic lesions to demonstrate the location of this group only; there were no atherosclerotic lesions in this group. *P<0.05, group I versus other groups; ^†P<0.05, group II versus other groups

Figure 5)

Chemiluminescent activity of aortic tissue (aortic-CL) of the four experimental groups. Results are expressed as mean ± SE. *P<0.05, group I versus other groups; ^†P<0.05, group II versus other groups. RLU Relative light unit