3-Hydroxyanthranilic Acid Is an Efficient, Cell-derived Co-antioxidant for α-Tocopherol, Inhibiting Human Low Density Lipoprotein and Plasma Lipid Peroxidation

Abstract Purpose Dyslipidemia is a major health concern associated with an increased risk of cardiovascular mortality. Long-term fasting (LF) has been shown to improve plasma lipid profile. We performed an in-depth investigation of lipoprotein composition. Methods This observational study included 40 volunteers (50% men, aged 32–65 years), who underwent a medically supervised fast of 14 days (250 kcal/day). Changes in lipid and lipoprotein levels, as well as in lipoprotein subclasses and particles, were measured by ultracentrifugation and nuclear magnetic resonance (NMR) at baseline, and after 7 and 14 fasting days. Results The largest changes were found after 14 fasting days. There were significant reductions in triglycerides (TG, − 0.35 ± 0.1 mmol/L), very low-density lipoprotein (VLDL)-TG (− 0.46 ± 0.08 mmol/L), VLDL-cholesterol (VLDL-C, − 0.16 ± 0.03 mmol/L) and low-density lipoprotein (LDL)-C (− 0.72 ± 0.14 mmol/L). Analysis of LDL subclasses showed a significant decrease in LDL1-C (− 0.16 ± 0.05 mmol/L), LDL2-C (− 0.30 ± 0.06 mmol/L) and LDL3-C (− 0.27 ± 0.05 mmol/L). NMR spectroscopy showed a significant reduction in large VLDL particles (− 5.18 ± 1.26 nmol/L), as well as large (− 244.13 ± 39.45 nmol/L) and small LDL particles (− 38.45 ± 44.04 nmol/L). A significant decrease in high-density lipoprotein (HDL)-C (− 0.16 ± 0.04 mmol/L) was observed. By contrast, the concentration in large HDL particles was significantly raised. Apolipoprotein A1 decreased significantly whereas apolipoprotein B, lipoprotein(a), fibrinogen and high-sensitivity C-reactive protein were unchanged. Conclusion Our results suggest that LF improves lipoprotein levels and lipoprotein subclasses and ameliorates the lipoprotein-associated atherogenic risk profile, suggesting a reduction in the cardiovascular risk linked to dyslipidemia. Trial Registration Study registration number: DRKS-ID: DRKS00010111 Date of registration: 03/06/2016 “retrospectively registered”.

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Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation

Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism ◽

10.1016/0005-2760(92)90237-p ◽

1992 ◽

Vol 1126 (3) ◽

pp. 247-254 ◽

Cited By ~ 215

Author(s):

Detlef Mohr ◽

Vincent W. Bowry ◽

Roland Stocker

Keyword(s):

Lipid Peroxidation ◽

Coenzyme Q10 ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Dietary Supplementation ◽

Low Density

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Derivatization of Apo-Low-Density Lipoprotein Lysine Residues by Lipid Peroxidation Products during Low-Density Lipoprotein Oxidation

Cardiovascular Disease ◽

10.1007/978-1-4684-5296-9_14 ◽

1987 ◽

pp. 133-138

Author(s):

Urs Peter Steinbrecher

Keyword(s):

Lipid Peroxidation ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Low Density ◽

Lipoprotein Oxidation ◽

Lipid Peroxidation Products ◽

Lysine Residues ◽

Low Density Lipoprotein Oxidation

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Electronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative Biomarkers

Circulation Research ◽

10.1161/circresaha.120.317828 ◽

2021 ◽

Author(s):

Rajat Gupta ◽

Yan Lin ◽

Karla Luna ◽

Anjali Logue ◽

Alexander J Yoon ◽

...

Keyword(s):

Lipid Peroxidation ◽

Fatty Acids ◽

Cardiovascular Risk ◽

Polyunsaturated Fatty Acids ◽

Low Density Lipoprotein ◽

Plasma Concentrations ◽

Multivariable Analysis ◽

Plasma Lipid ◽

Density Lipoprotein ◽

Heme Oxygenase 1

Rationale: Chronic electronic cigarette (EC) users exhibit a higher susceptibility of low-density lipoprotein (LDL) to undergo oxidation as compared to non-user controls. However, there is a paucity of data regarding EC effects on lipid peroxidation in the blood and their relationship to cardiovascular risk. Objective: To test the hypothesis that chronic (≥1 year) EC use exerts intermediate effects on plasma lipid peroxidation and/or antioxidant defense compared to chronic tobacco cigarette (TC) smoking. Methods and Results: We enrolled EC-users (n=32), TC-smokers (n=29) and non-users (n=45), with mean ages of 28.3, 27.8 and 27.4 years, respectively. Plasma concentrations of free polyunsaturated fatty acids and oxidized metabolites were assessed by mass spectrometry. Total antioxidant capacity (TAC), concentrations of glutathione, bilirubin, heme oxygenase-1 (HO-1), and functional activity of paraoxonase1 (PON1) were determined by colorimetric and enzymatic assays. Multivariable analysis was performed using classification models for segregating participants based on biomarker profiles. Plasma arachidonic acid (AA) concentration was higher in TC-smokers but lower in EC-users, together with linoleic acid (LA) concentration, as compared to TC-smokers and non-users (p<0.05). Oxidized LA metabolites (9- and 13-hydroxyoctadecadienoic acid (HODE)) were lower in EC-users and TC-smokers as compared to non-users (p<0.001). Consistently, TAC and bilirubin were elevated in EC-users and TC-smokers as compared to non-users (p<0.05). Of interest, plasma HO-1 concentration was higher in TC-smokers as compared to non-users (p=0.01) with intermediate levels in EC-users. Multivariable analysis identified 5 biomarkers (13-HODE, LA, 9-HODE, 12-hydroxyeicosatetraenoic acid (HETE), AA) that discriminated EC-users from TC-smokers and non-users with an accuracy of 73.4%. Conclusions: Chronic use of EC induces common (i.e. lower 9- and/or 13-HODEs and higher TAC and bilirubin) as well as differential effects (i.e. altered AA and LA concentrations) to those induced by TC, along with intermediate plasma HO-1 concentration, suggesting that EC, likewise TC smoke, could impact cardiovascular risk.

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