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Atherosclerosis antioxidants

Rueckschloss U, Duerrschmidt N, Mtnawietz H. NADPH oxidase in endothelial cells impact on atherosclerosis. Antioxid Redox Signal 2003 5 171-180. [Pg.172]

Probucol. Probucol is an antioxidant that is effective in lowering LDL cholesterol. Whereas probucol was known to lower cholesterol after relatively simple clinical trials (160), its mechanism of action as an antioxidant in the treatment of atherosclerosis is quite novel. Probucol has been shown to have the abiUty to produce regression of atherosclerotic lesions in animal models (161). Probucol therefore represents a novel class of pharmaceutical agent for the treatment of atherosclerosis. This effect occurs mechanistically, in part, by preventing oxidation of LDL, a necessary step in foam cell formation. This antioxidant activity has been shown in laboratory experiments and its activity in lowering LDL cholesterol in human studies is well documented (162). [Pg.131]

CHOPRA M, MCLOONE u L, o neill m, WILLIAMS N and THURNHAM DI (1996) Fruit and vegetable supplementation - effect on ex vivo LDL oxidation in hiunans , in Kumpulainen, J T and Saonen, J T (eds), Natural Antioxidants and Food Quality in Atherosclerosis and Cancer Prevention, Cambridge, Royal Society of Chemistry, 150-55. [Pg.40]

In addition to the effects on blood lipids, it has been suggested that soy consumption has a beneficial action on arterial function and improves antioxidant status (Lichtenstein, 1998 and refs therein). Genistein and daidzein were shown to have antioxidant properties in vitro (Kerry and Abbey, 1998), to enhance endothelium-dependent vasodilation and to reduce the development of atherosclerosis in monkeys (Honore et al, 1997 Wagner et al, 1997). [Pg.199]

Convincing evidence indicates that ROS generated both endogenously and also in response to diet and lifestyle factors may play a significant role in the etiology of atherosclerosis and CHD. Indeed, free radicals are responsible for LDL oxidation, which is involved in the initiation and promotion of atherosclerosis. Thus, protection from LDL oxidation by antioxidants such as carotenoids may lead to protection against human CHD. [Pg.135]

LDL when oxidized is recognized to play a crucial role in the development of atherosclerosis. It was thought that flavonoids could also protect LDL against oxidation, especially by limiting the degradation of vitamin E, the main antioxidant in LDL. Other beneficial effects of flavonoids have been reported inhibition of platelet... [Pg.137]

Some metabolites of curcumin (particularly tetrahydrocurcumin) may also participate in producing the observed effects of curcumin in different models because these metabolites display greater stabilities than the parent curcumin molecule at physiological pH. Recent data show similar modes of action of curcumin metabolites regarding antioxidant enzyme induction and inhibition of multidrug-resistant proteins. " Additional data indicate that curcumin may even act against other types of diseases such as atherosclerosis " " and Alzheimer s disease. " - " ... [Pg.139]

Bonithon-Kopp, C. et al.. Combined effects of lipid peroxidation and antioxidant status on carotid atherosclerosis in a population aged 59-71 years The EVA (Etude sur le Vieillisement Arteriel) study. Am. J. Clin. Nutr, 65, 121, 1997. [Pg.142]

Cyanidin is the most common anthocyanin in foods. In addition, anthocyanins are stabilized by the formation of complexes with other flavonoids (co-pigmentation). In the United States, the daily anthocyanin consumption is estimated at about 200 mg. Several promising studies have reported that consumption of anthocyanin-rich foods is associated with reductions of the risks of cancers - and atherosclerosis and with preventive effects against age-related neuronal and behavioral declines. These beneficial effects of anthocyanins might be related to their reported biological actions such as modulators of immune response and as antioxidants. Knowledge of anthocyanin bioavailability and metabolism is thus essential to better understand their positive health effects. [Pg.165]

Experimental evidence in humans is based upon intervention studies with diets enriched in carotenoids or carotenoid-contaiifing foods. Oxidative stress biomarkers are measured in plasma or urine. The inhibition of low density lipoprotein (LDL) oxidation has been posmlated as one mechanism by which antioxidants may prevent the development of atherosclerosis. Since carotenoids are transported mainly via LDL in blood, testing the susceptibility of carotenoid-loaded LDL to oxidation is a common method of evaluating the antioxidant activities of carotenoids in vivo. This type of smdy is more precisely of the ex vivo type because LDLs are extracted from plasma in order to be tested in vitro for oxidative sensitivity after the subjects are given a special diet. [Pg.179]

In atherosclerosis and other heart diseases, the role of carotenoids as antioxidants is probable, but for these types of diseases and also for other degenerative diseases such as cancers, non-antioxidant activities constitute other possible prevention mechanisms. These activities are, for example, stimulation of gap junction communications between cells, and the induction of detoxifying enzymes. The... [Pg.179]

Kim, H.S. and Lee, B.M., Protective effects of antioxidant supplementation on plasma lipid peroxidation in smokers, J. Toxicol. Environ. Health A, 63, 583, 2001. Gaziano, J.M. et al.. Supplementation with beta-carotene in vivo and in vitro does not inhibit low density lipoprotein oxidation. Atherosclerosis, 112, 187, 1995. Sutherland, W.H.F. et al.. Supplementation with tomato juice increases plasma lycopene but does not alter susceptibility to oxidation of low-density lipoproteins from renal transplant recipients, Clin. Nephrol, 52, 30, 1999. [Pg.189]

However, peroxidation can also occur in extracellular lipid transport proteins, such as low-density lipoprotein (LDL), that are protected from oxidation only by antioxidants present in the lipoprotein itself or the exttacellular environment of the artery wall. It appeats that these antioxidants are not always adequate to protect LDL from oxidation in vivo, and extensive lipid peroxidation can occur in the artery wall and contribute to the pathogenesis of atherosclerosis (Palinski et al., 1989 Ester-bauer et al., 1990, 1993 Yla-Herttuala et al., 1990 Salonen et al., 1992). Once initiation occurs the formation of the peroxyl radical results in a chain reaction, which, in effect, greatly amplifies the severity of the initial oxidative insult. In this situation it is likely that the peroxidation reaction can proceed unchecked resulting in the formation of toxic lipid decomposition products such as aldehydes and the F2 isoprostanes (Esterbauer et al., 1991 Morrow et al., 1990). In support of this hypothesis, cytotoxic aldehydes such as 4-... [Pg.24]

It appears then that both intracellular and extracellular antioxidants may be important in the prevention of atherosclerosis. The progression of a lesion may signify that these protective pathways are overwhelmed. [Pg.33]

Del Boccio, C., Laprenna, D., Porreca, E., Pennilli, A., Savini, F., Feliciani, P., Ricci, G. and CuccuruUo, F. (1990). Aortic antioxidant defence mechanisms time-related changes in cholesterol fed rabbits. Atherosclerosis 81, 127-135. [Pg.34]

Bjorkhem, L, Henriksson-Frayschuss, A., Breuer, O., Dieztalusy, V., Beiglund, L. and Henriksson, P. (1991). The antioxidant butylated hydroxytoluene protects against atherosclerosis. Arterioscler. Thromb. 11, 15-22. [Pg.49]

Carew, T.E., Schwenke, D.C. and Steinberg, O. (1987). Antiatherogenic effect of probucol unrelated to its hyper-cholesterolaemic effect evidence that antioxidants in vim can selectively inhibit low density lipoprotein degradation in macroph -rich fatty streaks slowing the progression of atherosclerosis in the WHHL rabbit. Proc. Natl Acad. Sci. USA 84, 7725-7729. [Pg.49]

Depletion of the antioxidant capacity of LDL is an early event in the oxidation process. The main antioxidant in LDL is a-tocopherol, with smaller quantities of 0-carotene and 7-tocopherol also present. The importance of antioxidants in inhibiting the oxidative modification of LDL is su ested by human and animal studies on the prevention of atherosclerosis. Preliminary reports... [Pg.105]

There have been more than 20 studies relating to the prevention of atherosclerosis by antioxidants. In vitro, several studies have shown that antioxidant treatment (e.g. vitamin E) inhibits both oxidation and the formation of cytotoxic LDL (Steinbrecher etal., 1984 Par-thasarathy etal., 1986 Esterbauer etal., 1987). In vivo, vitamin E supplementation prevents LDL oxidation in... [Pg.192]

Flavonoids protect LDL from oxidation, delaying the onset of lipid peroxidation, however, the prevention of atherosclerosis by flavonoids occurs not only by the inhibition of LDL oxidation, but also by the increase of cellular resistance to harmful effects of the oxidized LDL (de Luis and Aller, 2008). The antioxidant activity of anthocyanidins, as well as their protective role against LDL oxidation, has been well demonstrated in different in vitro systems (Aviram and Fuhrman, 2002 Satue-Gracia and others 1997 Teissedre and others 1996). [Pg.160]

Murr C, Winklhofer-Roob BM, Schroecksnadel K, Maritschnegg M, Mangge H, Bohm BO, Winkelmann BR, Marz M and Fuchs D. 2009. Inverse association between serum concentrations of neopterin and antioxidants in patients with and without angiographic coronary artery disease. Atherosclerosis. In press. [Pg.217]

Antioxidizability and its control are relevant for various areas in medicine and industry. Atherosclerosis, cardiac infarction, malignant growth, and aging are consequences of uncontrolled oxidation. Currently, oxidizability and antioxidants are also actual problems for alternative and complementary therapies like phyto-, helio-, and aero-ion therapy. [Pg.498]


See other pages where Atherosclerosis antioxidants is mentioned: [Pg.977]    [Pg.977]    [Pg.162]    [Pg.224]    [Pg.481]    [Pg.486]    [Pg.139]    [Pg.287]    [Pg.288]    [Pg.296]    [Pg.33]    [Pg.33]    [Pg.34]    [Pg.42]    [Pg.47]    [Pg.106]    [Pg.243]    [Pg.162]    [Pg.163]    [Pg.246]   
See also in sourсe #XX -- [ Pg.33 , Pg.39 , Pg.40 , Pg.41 , Pg.42 , Pg.43 , Pg.44 , Pg.45 , Pg.46 , Pg.47 , Pg.48 , Pg.49 , Pg.50 , Pg.51 ]




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