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      Correlation of trans fatty acids with the severity of coronary artery disease lesions

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          Abstract

          Background

          Nutritional choices, which include the source of dietary fatty acids (FA), have an important significant impact on coronary artery disease (CAD). We aimed to determine on patients with CAD the relationships between Trans fatty acids (Trans FA) and different CAD associated parameters such as inflammatory and oxidative stress parameters in addition to Gensini score as a vascular severity index.

          Methods

          Fatty acid profiles were established by gas chromatography from 111 CAD patients compared to 120 age-matched control group. Lipid peroxidation biomarkers, oxidative stress, inflammatory parameters and Gensini score were studied.

          Results

          Our study showed a significant decrease of the antioxidant parameters levels such as erythrocyte glutathione peroxydase (GPx) and superoxide dismutase (SOD) activities, plasma antioxidant status (FRAP) and thiol (SH) groups in CAD patients. On the other hand, catalase activity, conjugated dienes and malondialdehyde were increased. Plasmatic and erythrocyte Trans FA were also increased in CAD patients compared to controls. Furthermore, divergent associations of these Trans FA accumulations were observed with low-density lipoprotein-cholesterol/ high-density lipoprotein-cholesterol (LDL-C/HDL-C) ratio, Apolipoprotein B (ApoB), lipid peroxidation parameters, high-sensitivity C Reactive Protein (hs-CRP), Interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and Gensini score. Especially, elaidic acid (C18:1 trans 9), trans C18:2 isomers and trans 11 eicosanoic acid are correlated with these parameters. Trans FA are also associated with oxidative stress, confirmed by a positive correlation between C20:1 trans 11 and GPx in erythrocytes.

          Conclusions

          High level of Trans FA was highly associated with the induction of inflammation, oxidative stress and lipoperoxidation which appear to be based on the vascular severity and might be of interest to assess the stage and progression of atherosclerosis. The measurement of these Trans FA would be of great value for the screening of lipid metabolism disorders in CAD patients.

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          Most cited references39

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          Superoxide radical and superoxide dismutases.

          O2- oxidizes the [4Fe-4S] clusters of dehydratases, such as aconitase, causing-inactivation and release of Fe(II), which may then reduce H2O2 to OH- +OH.. SODs inhibit such HO. production by scavengingO2-, but Cu, ZnSODs, by virtue of a nonspecific peroxidase activity, may peroxidize spin trapping agents and thus give the appearance of catalyzing OH. production from H2O2. There is a glycosylated, tetrameric Cu, ZnSOD in the extracellular space that binds to acidic glycosamino-glycans. It minimizes the reaction of O2- with NO. E. coli, and other gram negative microorganisms, contain a periplasmic Cu, ZnSOD that may serve to protect against extracellular O2-. Mn(III) complexes of multidentate macrocyclic nitrogenous ligands catalyze the dismutation of O2- and are being explored as potential pharmaceutical agents. SOD-null mutants have been prepared to reveal the biological effects of O2-. SodA, sodB E. coli exhibit dioxygen-dependent auxotrophies and enhanced mutagenesis, reflecting O2(-)-sensitive biosynthetic pathways and DNA damage. Yeast, lacking either Cu, ZnSOD or MnSOD, are oxygen intolerant, and the double mutant was hypermutable and defective in sporulation and exhibited requirements for methionine and lysine. A Cu, ZnSOD-null Drosophila exhibited a shortened lifespan.
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            CD36 is a receptor for oxidized low density lipoprotein.

            The oxidation of low density lipoprotein (LDL) in the arterial wall is thought to contribute to human atherosclerotic lesion formation, in part by the high affinity uptake of oxidized LDL (OxLDL) by macrophages, resulting in foam cell formation. We have utilized cloning by expression to identify CD36 as a macrophage receptor for OxLDL. Transfection of a CD36 clone into 293 cells results in the specific and high affinity binding of OxLDL, followed by its internalization and degradation. An anti-CD36 antibody blocks 50% of the binding of OxLDL to platelets and to human macrophage-like THP cells. Furthermore, like mouse macrophages, 293 cells expressing CD36 recognize LDL which has been oxidized only 4 h, whereas more extensive oxidation of the LDL is required for recognition by the other known OxLDL receptors, the acetylated LDL (AcLDL) receptor and Fc gamma RII-B2. CD36 may play a role in scavenging LDL modified by oxidation and may mediate effects of OxLDL on monocytes and platelets in atherosclerotic lesions.
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              Lipid peroxidation in maternal and cord blood and protective mechanism against activated-oxygen toxicity in the blood.

              Concentrations of a peroxidation product (malondialdehyde), fluorescent chromophores, lipofuscin-like fluorescent products, superoxide dismutase, catalase, glutathione peroxidase, and vitamin E in the maternal blood and the cord blood were determined and the results obtained were related to the estimation of lipid peroxidation and protective mechanism against uncontrolled oxidative processes in late pregnancy. Serum levels of fluorescent products were higher in the maternal blood than in the cord blood, indicating less frequent lipid peroxidation in the fetus than in the mother. In support of this assumption, the three protective enzymes and vitamin E were present in relatively lower concentrations in the cord blood. Sudden exposure of the newborn infant to a normobaric atmosphere after beginning breathing seems, therefore, to cause oxidation of red blood cell membrane, denaturation of the membrane, inducing hemoglobin breakdown, and consequently hemolysis.
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                Author and article information

                Contributors
                +21655 277 704 , hjsamia@yahoo.fr
                wafa.kharroubi@hotmail.com
                nba_ko@yahoo.fr
                zarroukamira@gmail.com
                fethi.batbout@rns.tn
                hgamra@rns.tn
                najjar.fadhel@rns.tn
                gerard.lizard@u-bourgogne.fr
                Isabelle.Hininger@univ-grenoble-alpes.fr
                mohamed.hammami@fmm.rnu.tn
                Journal
                Lipids Health Dis
                Lipids Health Dis
                Lipids in Health and Disease
                BioMed Central (London )
                1476-511X
                15 March 2018
                15 March 2018
                2018
                : 17
                : 52
                Affiliations
                [1 ]ISNI 0000 0004 0593 5040, GRID grid.411838.7, Research Laboratory LR12ES05 LR-NAFS ‘Nutrition - Functional Food & Vascular Health’ Faculty of Medicine, , University of Monastir, ; Avicene st, 5019 Monastir, Tunisia
                [2 ]GRID grid.420157.5, Department of Cardiology, , CHU Fattouma Bourguiba, ; Monastir, Tunisia
                [3 ]GRID grid.420157.5, Department of Biochemistry, , CHU Fattouma Bourguiba, ; Monastir, Tunisia
                [4 ]ISNI 0000 0001 2298 9313, GRID grid.5613.1, Team ‘Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism’ EA 7270 / INSERM, , University of Bourgogne Franche-Comté, ; Dijon, France
                [5 ]GRID grid.450307.5, Laboratory of Fundamental and Applied Bioenergetic, INSERM, , Grenoble Alpes University, ; F-38041 Grenoble, France
                Article
                699
                10.1186/s12944-018-0699-3
                5856295
                29544473
                414ba69c-1e40-4d9a-8151-27a5e3f60fe2
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 15 November 2017
                : 7 March 2018
                Categories
                Research
                Custom metadata
                © The Author(s) 2018

                Biochemistry
                elaidic acid,trans c18:2 isomers,oxidative stress,lipid peroxidation,coronary artery disease

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