Research: KARTAL and colleagues,

Listed in Issue 101

Abstract

KARTAL and colleagues, Department of Biochemistry, Faculty of Medicine, Marmara University, 81326 Haydarpasa, Istanbul, Turkey, nkozer@escortnet.com, have investigated the role of vitamin E in the molecular mechanisms involved with the development of atherosclerosis.

Background

The development of atherosclerosis ('hardening of arteries') is a multi-factor process in which both elevated plasma cholesterol levels and the proliferation of smooth muscle cells play a central role. Numerous studies have emphasized the role of oxidative processes and especially the role of oxidized low-density lipoprotein. In addition, homocysteine turns out to be an extra risk factor, and it has been suggested that this may be due to the hydrogen peroxide that is generated in homocysteine metabolism. It is now known that high levels of vitamin E are associated with lower levels of atherosclerosis.

Methodology

Biochemical study using vascular smooth muscle cells in culture.

Results

It was shown that vitamin E inhibits smooth muscle cell proliferation and thus protects tissue against atherosclerosis. However it was also shown that homocysteine induces smooth muscle cell proliferation even in the presence of a free radical-scavenging enzyme (catalase).

Conclusion

The results indicate a possible molecular mechanism by which vitamin E protects against atherosclerosis, as well as showing that homocysteine acts to promote smooth muscle proliferation in a manner independent of hydrogen peroxide.

References

Kartal ON Negis Y, Aytan N. Molecular mechanisms of cholesterol or homocysteine effect in the development of atherosclerosis: role of vitamin E. BioFactors 19 (1-2): 63-70, 2003.

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