Inhibit LDL oxidation

Antioxidants that inhibit LDL oxidation in vitro prevent fetty streak formation in animal models (Carew etal., 1987 Kita etal., 1987 Bjorkhem etal., 1991) and others are associated with protection against coronary artery disease in population studies (Gey et al., 1991 Stampfer etal., 1993 Rimm etal., 1993). 

Jialal, L, Norkus, E.P., Cristot, L. and Grundy, S.M. (1991). i8-Carotene inhibits LDL oxidation. Biochim. Biophys. Acta 1086, 134-138. 

This method is also used to measure ex vivo low-density lipoprotein (LDL) oxidation. LDL is isolated fresh from blood samples, oxidation is initiated by Cu(II) or AAPH, and peroxidation of the lipid components is followed at 234 nm for conjugated dienes (Prior and others 2005). In this specific case the procedure can be used to assess the interaction of certain antioxidant compounds, such as vitamin E, carotenoids, and retinyl stearate, exerting a protective effect on LDL (Esterbauer and others 1989). Hence, Viana and others (1996) studied the in vitro antioxidative effects of an extract rich in flavonoids. Similarly, Pearson and others (1999) assessed the ability of compounds in apple juices and extracts from fresh apple to protect LDL. Wang and Goodman (1999) examined the antioxidant properties of 26 common dietary phenolic agents in an ex vivo LDL oxidation model. Salleh and others (2002) screened 12 edible plant extracts rich in polyphenols for their potential to inhibit oxidation of LDL in vitro. Gongalves and others (2004) observed that phenolic extracts from cherry inhibited LDL oxidation in vitro in a dose-dependent manner. Yildirin and others (2007) demonstrated that grapes inhibited oxidation of human LDL at a level comparable to wine. Coinu and others (2007) studied the antioxidant properties of extracts obtained from artichoke leaves and outer bracts measured on human oxidized LDL. Milde and others (2007) showed that many phenolics, as well as carotenoids, enhance resistance to LDL oxidation. 

In the recent review Carr et al. [54] considered potential antiatherogenic mechanisms of a-tocopherol and ascorbic acid. These authors concluded that these antioxidants are able to inhibit LDL oxidation, leukocyte adhesion to the endothelium, and vascular endothelial dysfunction. They also believe that ascorbic acid is more effective than a-tocopherol in the inhibition of these pathophysiological processes due to its capacity of reacting with a wide spectrum of oxygen and nitrogen free radicals and its ability to regenerate a-tocopherol. 

Flavonoids exhibit protective action against LDL oxidation. It has been shown [145] that the pretreatment of macrophages and endothelial cells with tea flavonoids such as theaflavin digallate diminished cell-mediated LDL oxidation probably due to the interaction with superoxide and the chelation of iron ions. Quercetin and epicatechin inhibited LDL oxidation catalyzed by mammalian 15-lipoxygenase, and are much more effective antioxidants than ascorbic acid and a-tocopherol [146], Luteolin, rutin, quercetin, and catechin suppressed copper-stimulated LDL oxidation and protected endogenous urate from oxidative degradation [147]. Quercetin was also able to suppress peroxynitrite-induced oxidative modification of LDL [148],... 

In 1998, Schlotte et al. [259] showed that uric acid inhibited LDL oxidation. However, subsequent studies showed that in the case of copper-initiated LDL oxidation uric acid behaves itself as prooxidant [260,261]. It has been suggested that in this case uric acid enhances LDL oxidation by the reduction of cupric into cuprous ions and that the prooxidant effect of uric acid may be prevented by ascorbate. On the other hand, urate radicals formed during the interaction of uric acid with peroxyl radicals are able to react with other compounds, for example, flavonoids [262], and by that participate in the propagation of free radical damaging reactions. In addition to the inhibition of oxygen radical-mediated processes, uric acid is an effective scavenger of peroxynitrite [263]. 

Fuhrman, B., M. Rosenblat, T. Hayek, R. Coleman, and M. Aviram. Ginger extract consumption reduces plasma cholesterol, inhibits LDL oxidation and attenuates development of atherosclerosis in atherosclerotic, apolipo-protein E-deficient mice. J Nutr 2000 130(5) 1124-1131. 

In conclusion, phenolic-rich fractions of oats possess an antioxidant capacity that can be assessed quantitatively through their ability to inhibit LDL oxidation and protein oxidation. The greatest degree of antioxidant capacity was associated with compounds extracted with methanol from the aleurone. The identification of the oat constituents from these fractions should be investigated, although candidate compounds include caffeic acid, ferulic acid, and avenanthramides. These compounds may be bioavailable and contribute to the health effects associated with dietary antioxidants and oats. 

AO/FRS — inhibits LDL oxidation [anti-ageing, antiatherosclerotic, membrane stabilizer, nutriceutical]... 

AO/FRS - inhibit LDL oxidation [I HMGCoAR, antiproliferative, antiatherosclerotic, neuroprotective]... 

Jin and collaborators reported the antioxidant activity of cleomiscosins A (9) and C (7), isolated from the leaves and twigs of Acer okamotoatum (19). Compound 7 inhibited LDL oxidation mediated by either catalytic copper ions or free radicals generated with 2,2 -azobis(2-amidinopropane) dihydrochloride, in a dose-dependent manner. By means of electrophoretic analysis it was also observed that 7 protected apolipoprotein B-lOO against Cu fragmentation. Also, fluorescence analysis clearly indicated that both 7 and 9 protect against the oxidative modification of apoB-100, induced by either Cu + or HOCl. Compounds 7 and 9 could, therefore, be beneficial in preventing LDL oxidation in atherosclerotic lesions. 

While the positive health benefits associated with the consumption of a flavonoid-rich diet cannot be attributed to any one factor, the antioxidant properties of certain flavonoids have been the focus of considerable attention [8]. The antioxidant actions of chocolate flavonoids were first studied inhibiting LDL-oxidation [9,10]. As a consequence of the availability of purified procyanidins from cocoa (dimer-decamer), this particular family of... 

A corollary of the oxidation hypothesis of atherogenesis is that antioxidants may reduce the progression of the disease (114). Antioxidants present in LDL, including alpha-tocopherol, and antioxidants present in the extracellular fluid of the arterial wall, including ascorbic acid (vitamin C), inhibit LDL oxidation (132), and this action is extended to multiple oxLDL-mediated signaling pathways (133). Vitamin C may potentiate NO activity and normalize vascular function in patients with CHD and classical risk factors (132). Thus, NO may restore endothelial dysfunction and ameliorate vascular remodeling in several clinical correlates to experimental... 

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