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There are a number of ways in which beta-carotene may act to protect against cardiovascular disease. Free radical scavenging may prevent cellular transformations leading to atherosclerosis and protection of LDL oxidation may further act to protect against atheroma formation (Halliwell 1993). Other mechanisms proposed for the possible favourable effect of antioxidants include an increase of HDL cholesterol and the preservation of endothelial functions (Tavani & La Vecchia 1999). Patients with acute myocardial infarction (AMI) have also been shown to have reduced plasma antioxidant vitamins and enhanced lipid peroxidation upon thrombolysis, suggesting that antioxidants may reduce free radical generation processes in reperfusion injury in AMI (Levy et al 1998).

In an animal study, atherosclerosis was inhibited in rabbits fed a high-cholesterol diet supplemented with all-trans beta-carotene. In that study all-trans beta-carotene © 2007 Elsevier Australia

was undetectable In LDL, although tissue levels of retlnyl palmltate were Increased, suggesting that any antiatherogenic effect Is separate from the resistance of LDL to oxidation and that metabolites of beta-carotene may inhibit atherosclerosis in hypercholesterolaemic rabbits, possibly via stereospecific interactions with retinoic acid receptors in the artery wall (Shaish et a I 1995). A randomised, placebo-controlled trial in 149 male smokers taking 20 mg/day of beta-carotene for 14 weeks, however, found no influence on haemostatic measures, suggesting that it is unlikely that cardiovascular protection from beta-carotene is via an effect on haemostasis (Van Poppel et al 1995).

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