Do antioxidants and polyunsaturated fatty acids have a combined association with coronary atherosclerosis?

Kok, F.J.; Poppel, G. van; Melse, J.; Verheul, E.H.M.; Schouten, E.G.; Kruyssen, D.H.C.M.; Hofman, Albert

doi:10.1016/0021-9150(91)90101-8

Cited by 88 publications

(28 citation statements)

References 21 publications

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“…For instance, in HAEC cultures, the saturated FAs palmitate and stearate have been found to be pro-apoptotic, whereas unsaturated FAs are antiapoptotic (42). However, high levels of serum PUFAs, when insufficiently protected from peroxidation, may increase the risk of atherosclerotic complications (43). Other studies have demonstrated that exposure to oleic acid and LA increased human LDL transfer across cultured endothelial monolayers, whereas equivalent doses of palmitic, linolenic, arachidonic, and eicosapentaenoic acids did not (13).…”

Section: Discussionmentioning

confidence: 99%

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation

Wang

Gill

Pedersen

et al. 2009

Journal of Lipid Research

242

181

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Triglyceride-rich lipoprotein (TGRL) lipolysis products provide a pro-inflammatory stimulus that can alter endothelial barrier function. To probe the mechanism of this lipolysis-induced event, we evaluated the pro-inflammatory potential of lipid classes derived from human postprandial TGRL by lipoprotein lipase (LpL). Incubation of TGRL with LpL for 30 min increased the saturated and unsaturated FFA content of the incubation solutions significantly. Furthermore, concentrations of the hydroxylated linoleates 9-hydroxy ocatadecadienoic acid (9-HODE) and 13-HODE were elevated by LpL lipolysis, more than other measured oxylipids. The FFA fractions elicited pro-inflammatory responses inducing TNFa and intracellular adhesion molecule expression and reactive oxygen species (ROS) production in human aortic endothelial cells (HAECs). The FFA-mediated increase in ROS was blocked by both the cytochrome P450 2C9 inhibitor sulfaphenazole and NADPH oxidase inhibitors. Compared with linoleate, 13-HODE was found to be a more potent inducer of ROS production in HAECs, an activity that was insensitive to both NADPH oxidase and cytochrome P450 inhibitors. Therefore, although the oxidative metabolism of FFA in endothelial cells can produce inflammatory responses, TGRL lipolysis can also release preformed mediators of oxidative stress (e.g., HODEs) that may influence endothelial cell function in vivo by stimulating intracellular ROS production.-Wang, L., R. Gill, T. L. Pedersen, L. J. Higgins, J. W. Newman, and J. C. Rutledge. Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation. J. Lipid Res. 2009. 50: 204-213.

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Section: Discussionmentioning

confidence: 99%

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation

Wang

Gill

Pedersen

et al. 2009

Journal of Lipid Research

242

181

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“…In a prospective study, Kok et al (8) reported no interaction between serum selenium and serum vitamin E and risk of cardiovascular death. However, in another study (19), patients with severe atherosclerosis had significantly lower plasma selenium levels (relative to polyunsaturated fatty acids) than patients with mild atherosclerosis, but only in the subgroup with low plasma vitamin E status.…”

mentioning

confidence: 86%

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

Kardinaal

Kok

Kohlmeier

et al. 1997

American Journal of Epidemiology

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The association between selenium status and risk of acute myocardial infarction was examined in a multicenter case-control study in 10 centers from Europe and Israel in 1991-1992. Selenium in toenails was assessed for 683 nonfatal male cases with first acute myocardial infarction and 729 controls less than 70 years of age. Median toenail selenium content was 0.553 /xg/g for cases and 0.590 jxg/g for controls. After adjustment for age, center, and smoking, the odds ratio for myocardial infarction in the highest quintile of selenium as compared with the lowest was 0.63 (95 percent confidence interval 0.37-1.07, p for trend = 0.08). The observed inverse trend was somewhat stronger when the authors adjusted for vitamin E status (p = 0.05). Analysis stratified for smoking habits showed an inverse association in former smokers (odds ratio for the 75th-25th percentile contrast = 0.63 (95 percent confidence interval 0.43-0.94)), but not in current smokers (odds ratio = 0.97 ( 0.71-1.32)) or in those who had never smoked (odds ratio = 1.55 (0.87-2.76)). Analysis stratified by center showed a significant inverse association between selenium levels and risk of myocardial infarction for Germany (Berlin) only (75th to 25th percentile odds ratio = 0.62 (95 percent confidence interval 0.42-0.91)), which was the center with the lowest selenium levels. It appears that the increased risk of acute myocardial infarction at low levels of selenium intake is largely explained by cigarette smoking; selenium status does not appear to be an important determinant of risk of myocardial infarction at the levels observed in a large part of Europe. Am J Epidemiol 1997;145:373-9. antioxidants; case-control studies; myocardial infarction; selenium Evidence is accumulating that oxidation of low density lipoprotein particles and cytotoxic effects of lipid peroxides enhance the formation of foam cells and atherosclerotic lesions (1, 2). Selenium is part of the enzyme glutathione peroxidase, which plays an important role in the antioxidant defense of the body against the deleterious actions of free radicals and lipid per-

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“…In hypercholesterolemia, the cholesterol content of erythrocytes, platelets, polymorphonuclear leucocytes and endothelial cells increases. This increase is reported to activate these cells and cause the enhanced production of oxygen free radicals (Kok et al, 1991;Prasad and Kalra, 1989). Erythrocytes, because of their intrinsic potential for free radical generation, might be a very suitable environment for cholesterol to exert its prooxidant action (Kay, 1991).…”

Section: Introductionmentioning

confidence: 99%

Role of lupeol and lupeol linoleate on lipemic–oxidative stress in experimental hypercholesterolemia

2006

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Do antioxidants and polyunsaturated fatty acids have a combined association with coronary atherosclerosis?

Cited by 88 publications

References 21 publications

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

Role of lupeol and lupeol linoleate on lipemic–oxidative stress in experimental hypercholesterolemia

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