Phytochemicals And Cardiovascular Disease

Oxidative reactions have been linked to atherosclerosis through several different mechanisms. The most widely studied hypothesis of lipid oxidation and atherosclerosis involves the formation of oxidized, cytotoxic lipoproteins, particularly low-density lipoprotein (LDL) (37). During the oxidation of LDL, the lipoproteins become modified through either direct free-radical attack or formation of adducts between proteins and lipid oxidation products. The oxidized LDL can then be recognized and engulfed by macrophages, leading to the formation of foam cells that accumulate in arterial walls and form plaques (Fig. 2). Oxidized LDL has also been postulated to cause vascular inflammation and stimulate autoimmune reactions. Evidence supporting the relationship between LDL oxidation and cardiovascular disease is increasing; however, the importance of this mechanism to the development of cardiovascular disease has yet to be fully understood.

A second proposed mechanism for the link between oxidative reactions and atherosclerosis involves endothe-lium-derived relaxation factor (EDRF) (38). The endothelium, the cells that line the vascular lumenal surface, is a physiologically active organ that regulates vascular tone. The predominant regulator of vasodilation is EDRF, which

Q Native LDL I Endothelial cells tDOOCD^

oxidation ^^^H Macrophage

Metal-induced^v. /


0x,dtzed LDL hSEcell

Smooth muscle

Figure 2. The proposed mechanism for promotion of coronary heart disease by oxidized LDL.

is thought to be identical to or similar to the free radical nitric oxide. Superoxide anion, another type of free radical, is believed to be vasoconstrictive owing to its ability to inactivate nitric oxide by converting it to peroxynitrite. Because peroxynitrite is a strong oxidizing agent, this can cause modification of proteins and DNA and thus damage endothelium function (Fig. 3). Therefore, the interaction of superoxide anion with nitric oxide leads to restriction in vascular dilation, which in turn can cause damage to the endothelium and lead to the development of atherosclerotic plaque formation. Theoretically, the introduction of antioxidants into the vasculature at suitable levels would negate the loss of dilation by inactivating superoxide anions and thus protect the vasodilatory activity of nitric oxide.


Carotenoids, including /^-carotene, are incorporated into LDL, but they only weakly inhibit LDL oxidation. Clinical and epidemiological studies have been largely inconclusive about the ability of carotenoids to inhibit atherosclerosis. These observations could be due to the weak antioxidant or even pro-oxidative activity of carotenoids (7). Recent research has suggested that foods high in carotenoids have been linked with decreased occurrence of atherosclerotic plaques, suggesting that carotenoids exert their protective effect later in the atherosclerotic process (39). However, this study was not able to specifically link dietary carotenoids with an antiatherogenic activity because the observed protective effects could be the result of other phy-tochemicals found in carotenoid-rich foods.

Ascorbic Acid

Vitamin C is an effective scavenger of superoxide anions and other free radicals, suggesting that it may protect endothelial function and inhibit the development of atherosclerosis. Ascorbate can inhibit the oxidation of LDL (40), and in studies on hypocholesterolemic individuals, ascorbic acid has been shown to improve vasodilation in subjects with chronic heart failure (41). However, epidemiological studies linking dietary vitamin C with prevention of ath-

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