Effect of Antioxidants Alone and in Combination With Monounsaturated Fatty Acid–Enriched Diets on Lipoprotein Oxidation

Reaven, Peter D.; Grasse, Barbara J.; Barnett, Joellen

doi:10.1161/01.atv.16.12.1465

Cited by 24 publications

(15 citation statements)

References 54 publications

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“…Similarly, although studies in nonsmokers have noted a salutary effect of vitamin E on LDL kinetic parameters, 38,41 we noted no effect of vitamin E on the mean LDL oxidation rate. Again, these disparities may be a function of the specific conditions of each study.…”

Section: Discussionsupporting

confidence: 45%

“…7,[37][38][39][40][41][42] However, given the presence of potent aqueous phase antioxidants such as urate and ascorbate, 55 it seems unlikely that LDL oxidation could occur in the plasma or interstitial compartments. Moreover, the radical flux rate in vivo is likely orders of magnitude smaller than that generated by chemical catalysis in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…To this end, we have investigated the effects of a high PUFA diet and vitamin E supplementation on oxidation stress in cigarette smokers by using 2 informative measures: the kinetics of in vitro copper-catalyzed LDL peroxidation, the most frequently used method to assess the effects of diet and antioxidants on lipid oxidation, 27,[37][38][39][40][41][42] and the plasma concentration of F 2 -isoprostanes, which are biologically active prostanoids formed by free radial-initiated rearrangement of arachidonic acid, 43 and which may be a much better indicator of global in vivo oxygen-derived free radical stress. 44 …”

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confidence: 99%

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Pro-Oxidant Effect of Vitamin E in Cigarette Smokers Consuming a High Polyunsaturated Fat Diet

Weinberg

VanDerWerken

Anderson

et al. 2001

ATVB

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Abstract-Dietary polyunsaturated fats and vitamin E are associated with reduced risk for atherosclerosis, but in smokers, they could promote lipid oxidation. Therefore, we examined the effects of a high polyunsaturated fat diet and vitamin E supplementation on measures of lipid oxidation in cigarette smokers. Ten subjects who smoked Ͼ1 pack of cigarettes per day were sequentially fed the following: a baseline diet in which the major fat source was olive oil, a diet in which the major fat source was high-linoleic safflower oil, and finally, the safflower oil diet plus 800 IU vitamin E per day. LDL oxidation lag time and rate and plasma total F 2 -isoprostanes and prostaglandin F 2␣ (PGF 2␣ ) were determined after 3 weeks on each diet. is the leading cause of morbidity and mortality in the developed world. Peroxidation of plasma LDLs by oxygen-derived free radicals has been ascribed a central role in the etiology of ASCVD. 1 The corollary to this theory is that agents that can protect LDL from peroxidation should decrease the risk of developing ASCVD, attenuate its progression, or even reverse established disease. 2 Indeed, epidemiological studies have suggested that antioxidants, such as ␣-tocopherol, confer dose-dependant protection against ASCVD, 3-5 yet prospective intervention trials 6 -8 have failed to observe a protective effect.Tobacco use is one of the most potent risk factors for ASCVD. The high concentration of free radical oxidants in tobacco smoke 9 and the fact that the impact of smoking on the incidence ASCVD correlates with plasma LDL levels 10,11 are consistent with the concept that LDL peroxidation by cigarette smoke promotes atherogenesis. 12 Indeed, measures of lipid oxidation, such as thiobarbituric acid-reactive substances (TBARS) in plasma, 13 LDL, 14 -16 and red blood cells 17 ; breath alkane excretion 18 -20 ; and F 2 -isoprostanes in urine 21 and plasma, 22 are increased in cigarette smokers. Conversely, plasma levels of antioxidant vitamins in smokers, which could protect LDL against the damaging effects of free radicals, are depressed. 23 Cigarette smokers thus constitute a high-risk population in which intervention could reduce the risk of ASCVD. Diets high in monounsaturated fatty acid (MUFA) or polyunsaturated fatty acid (PUFA) effectively lower plasma LDL, 24 but high PUFA diets constitute a theoretical risk, because PUFAs are excellent substrates for lipid peroxidation. 25 Indeed, studies in cigarette smokers 15 and in nonsmokers 26,27 have found that PUFAs increase LDL oxidation rate and also breath pentane excretion. 28 The deleterious impact of dietary PUFA on lipid oxidation, in theory, could be mitigated by concomitant supplementation with antioxidant vitamins. However, although antioxidant vitamins are generally considered to be nontoxic, 29 vitamin E is a redox reagent that can function as a pro-oxidant under certain conditions. 30 -32 This has led some to voice concerns that antioxidant vitamins could function as pro-oxidants in vivo. 33,34 The fact that prospective studi...

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Pro-Oxidant Effect of Vitamin E in Cigarette Smokers Consuming a High Polyunsaturated Fat Diet

Weinberg

VanDerWerken

Anderson

et al. 2001

ATVB

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“…22 In the other trial, increased consumption of monounsaturated fatty acids was associated with a lower susceptibility of LDL cholesterol to in vitro peroxidation. 23 In a clinical trial of fruit and vegetable consumption, a diet high in fruits and vegetables increased serum antioxidants, including carotenoids and flavenoids 24 ; however, the effects on lipid peroxidation were not examined. To our knowledge, no trial has examined the impact of healthy dietary patterns with several desirable factors (rich in fruits and vegetables and reduced in saturated fat, total fat, and cholesterol) on lipid peroxidation.…”

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confidence: 99%

Effect of Dietary Patterns on Measures of Lipid Peroxidation

1998

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Background-Free radical-mediated oxidative damage to lipids is thought to be an important process in the pathogenesis of atherosclerosis. Although previous studies have demonstrated a beneficial impact of antioxidant vitamin supplements on lipid peroxidation, the effect of dietary patterns on lipid peroxidation is unknown. Methods and Results-During the 3-week run-in period of a randomized trial, 123 healthy individuals were fed a control diet, low in fruits, vegetables, and dairy products, with 37% of calories from fat. Participants were then randomized to consume for 8 weeks: (1) the control diet, (2) a diet rich in fruits and vegetables but otherwise similar to the control diet, and (3) a combination diet rich in fruits, vegetables, and low-fat dairy products and reduced in fat. Serum oxygen radical-absorbing capacity, malondialdehyde (an in vitro measure of lipid peroxidation), and breath ethane (an in vivo measure of lipid peroxidation) were measured at the end of run-in and intervention periods. Between run-in and intervention, mean (95% CI) change in oxygen radical-absorbing capacity (U/mL) was Ϫ35 (Ϫ93, 13) in the control diet, 26 (Ϫ15, 67) in the fruits and vegetables diet (Pϭ0.06 compared with control), and 19 (Ϫ22, 54) in the combination diet (Pϭ0.10 compared with control

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“…The formation of conjugated dienes was measured as previously described, 21 by incubating lipoproteins at 150 g ApoB100/mL with 5 mol/L copper sulfate in 1 mL of PBS at 30°C. The absorbance at 234 nm was measured continuously in a Uvikon 951 spectrophotometer.…”

Section: Lipoprotein Oxidationmentioning

confidence: 99%

All ApoB-Containing Lipoproteins Induce Monocyte Chemotaxis and Adhesion When Minimally Modified

Lee

Sigari

Segrado

et al. 1999

ATVB

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Abstract-Mildly oxidized LDL has many proinflammatory properties, including the stimulation of monocyte chemotaxis and adhesion, that are important in the development of atherosclerosis. Although ApoB-containing lipoproteins other than LDL may enter the artery wall and undergo oxidation, very little is known regarding their proinflammatory potential. LDL, IDL, VLDL, postprandial remnant particles, and chylomicrons were mildly oxidized by fibroblasts overexpressing 15-lipoxygenase (15-LO) and tested for their ability to stimulate monocyte chemotaxis and adhesion to endothelial cells. When conditioned on 15-LO cells, LDL, IDL, but not VLDL increased monocyte chemotaxis and adhesion Ϸ4-fold. Chylomicrons and postprandial remnant particles were also bioactive. Although chylomicrons had a high 18:1/18:2 ratio, similar to that of VLDL, and should presumably be less susceptible to oxidation, they contained (in contrast to VLDL) essentially no platelet-activating factor acetylhydrolase (PAF-AH) activity. Because PAF-AH activity of lipoproteins may be reduced in vivo by oxidation or glycation, LDL, IDL, and VLDL were treated in vitro to reduce PAF-AH activity and then conditioned on 15-lipoxygenase cells. All 3 PAF-AH-depleted lipoproteins, including VLDL, exhibited increased stimulation of monocyte chemotaxis and adhesion. In a similar manner, lipoproteins from Japanese subjects with a deficiency of plasma PAF-AH activity were also markedly more bioactive, and stimulated monocyte adhesion nearly 2-fold compared with lipoproteins from Japanese control subjects with normal plasma PAF-AH. For each lipoprotein, bioactivity resided in the lipid fraction and monocyte adhesion could be blocked by PAF-receptor antagonists. These data suggest that the susceptibility of plasma lipoproteins to develop proinflammatory activity is in part related to their 18:1/18:2 ratio and PAF-AH activity, and that bioactive phospholipids similar to PAF are generated during oxidation of each lipoprotein. Moreover, LDL, IDL, postprandial remnant particles, and chylomicrons and PAF-AH-depleted VLDL all give rise to proinflammatory lipids when mildly oxidized. Key Words: atherosclerosis Ⅲ lipid peroxidation Ⅲ platelet-activating factor acetylhydrolase Ⅲ autoantibodies Ⅲ LDL oxidation E vidence from both in vitro and in vivo studies suggests that oxidation of LDL may contribute to early atherosclerotic lesion formation. 1,2 The extent of LDL oxidation appears to influence which of a variety of potential atherogenic properties of oxidized LDLs predominate at a given point in time. 3 When LDL is less oxidized, ie, minimally modified LDL (mm-LDL), it stimulates monocyte chemotaxis, adherence to and transmigration through endothelial cells, [3][4][5][6] as well as expression of several growth factors such as macrophage colony-stimulating factor. 3 These and other "bioactive" properties of mm-LDL very likely contribute to the development of atherosclerosis. Many of the proinflammatory properties of mm-LDL may result from the formation of oxidized phospholi...

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Effect of Antioxidants Alone and in Combination With Monounsaturated Fatty Acid–Enriched Diets on Lipoprotein Oxidation

Cited by 24 publications

References 54 publications

Pro-Oxidant Effect of Vitamin E in Cigarette Smokers Consuming a High Polyunsaturated Fat Diet

Pro-Oxidant Effect of Vitamin E in Cigarette Smokers Consuming a High Polyunsaturated Fat Diet

Effect of Dietary Patterns on Measures of Lipid Peroxidation

All ApoB-Containing Lipoproteins Induce Monocyte Chemotaxis and Adhesion When Minimally Modified

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