Metformin Impedes Oxidation of LDL In Vitro.

Metformin is the most commonly prescribed glucose-lowering drug for the treatment of type 2 diabetes. The aim of this study was to investigate whether metformin is capable of impeding the oxidation of LDL, a crucial step in the development of endothelial dysfunction and atherosclerosis. LDL was oxidized by addition of CuCl in the presence of increasing concentrations of metformin.

Superparamagnetic iron oxide nanoparticles for their application in the human body: Influence of the surface.

Iron oxide nanoparticles (IONs) are of great interest in nanomedicine for imaging, drug delivery, or for hyperthermia treatment. Although many research groups have focused on the synthesis and application of IONs in nanomedicine, little is known about the influence of the surface properties on the particles' behavior in the human body. This study analyzes the impact of surface coatings (dextran, polyvinyl alcohol, polylactide-co-glycolide) on the nanoparticles' cytocompatibility, agglomeration, degradation, and the resulting oxidative stress induced by the particle degradation.

Endothelial lipase increases antioxidative capacity of high-density lipoprotein.

Endothelial lipase (EL) is a strong determinant of structural and functional properties of high-density lipoprotein (HDL). We examined whether the antioxidative capacity of HDL is affected by EL. EL-modified HDL (EL-HDL) and control EV-HDL were generated by incubation of HDL with EL- overexpressing or control HepG2 cells.

Ethyl pyruvate inhibits oxidation of LDL in vitro and attenuates oxLDL toxicity in EA.hy926 cells.

Background: Ethyl pyruvate (EP) exerts anti-inflammatory and anti-oxidative properties. The aim of our study was to investigate whether EP is capable of inhibiting the oxidation of LDL, a crucial step in atherogenesis. Additionally, we examined whether EP attenuates the cytotoxic effects of highly oxidized LDL in the human vascular endothelial cell line EA.

Simvastatin Efficiently Lowers Small LDL-IgG Immune Complex Levels: A Therapeutic Quality beyond the Lipid-Lowering Effect.

We investigated a polyethylene glycol non-precipitable low-density lipoprotein (LDL) subfraction targeted by IgG and the influence of statin therapy on plasma levels of these small LDL-IgG-immune complexes (LDL-IgG-IC). LDL-subfractions were isolated from 6 atherosclerotic subjects and 3 healthy individuals utilizing iodixanol density gradient ultracentrifugation. Cholesterol, apoB and malondialdehyde (MDA) levels were determined in each fraction by enzymatic testing, dissociation-enhanced lanthanide fluorescence immunoassay and high-performance liquid chromatography, respectively.

Bed rest does not induce hypercoagulability.

Background: Although there is no direct evidence, it is generally believed that bed rest shifts the haemostatic system towards hypercoagulability; thus, immobilized patients are commonly treated with anticoagulants. We therefore aimed to investigate whether long-term bed rest actually leads to an elevated risk for thromboembolic events.

Materials And Methods: Eleven healthy men were enrolled in our study (bed rest campaign in MEDES Clinique d'Investigation, Toulouse, France).

Virtually same oxidizability of LDL but higher Lp(a) levels in arterial compared to venous plasma.

Plaque formation is confined to the arterial trunk. We assumed that due to the higher aeration of arterial compared to venous blood, higher levels of the atherogenic agent oxidized LDL might be present in arteries, contributing to plaque formation. We aimed to compare (i) the basal oxidative status of LDL in arterial and venous blood and (ii) the susceptibility of arterial and venous LDL to oxidation.

In vitro oxidation of LDL by ozone.

Recent studies suggest that ozone is present in atherosclerotic lesions. Since these lesions are characterized by a dramatic accumulation of low-density lipoprotein (LDL), we aimed to investigate whether ozone is capable of oxidizing LDL, thereby rendering this lipoprotein atherogenic. Lipid hydroperoxide (LPO) concentrations and thiobarbituric acid reactive substances (TBARS) were measured to assess the oxidative status of the lipid part of LDL.

Effects of a single bout of walking exercise on blood coagulation parameters in obese women.

Obesity is associated with increased prevalence of thromboembolic events. We aimed to investigate whether obese women might benefit from vigorous aerobic exercise. Forty-two overweight and obese women performed a 30-min walking exercise test (treadmill ergometer) at an intensity of 70% of individual peak oxygen uptake.

Supplementation with a juice powder concentrate and exercise decrease oxidation and inflammation, and improve the microcirculation in obese women: randomised controlled trial data.

Obesity and sedentary lifestyle are associated with increased oxidative stress, inflammation and vessel dysfunction. Previous research has shown that an encapsulated fruit/berry/vegetable juice powder (FBV) supplement or controlled exercise training improve the markers of redox biology, low-grade inflammation and circulation. The aim of the present study was to assess the effects of 8 weeks of supplementation with FBV or placebo, and a single bout of controlled walking on the markers of oxidation, inflammation and skin capillary microcirculation in forty-two obese pre-menopausal women (41 (SD 5) years, non-smokers and BMI 34·5 (SD 3·8) kg/m(2)) using a randomised, double-blind, placebo-controlled design.

Oxidized LDL induces ventricular myocyte damage and abnormal electrical activity--role of lipid hydroperoxides.

Objective: It was our aim to investigate effects of human LDL, copper-, or AAPH-oxidized over different periods of time to different degrees (ox-LDL), on viability and electrophysiological parameters of isolated ventricular myocytes of guinea pigs.

Methods: Guinea pig ventricular myocytes were incubated with ox-LDL or native LDL (at 0.5 mg/ml) for 12 h, and afterwards myocyte damage, action potentials, and transmembrane ion currents were studied (at 37 degrees C).

Peroxiredoxin 6 deficiency and atherosclerosis susceptibility in mice: significance of genetic background for assessing atherosclerosis.

Peroxiredoxin 6 (Prdx6; also called antioxidant protein 2, or Aop2) is a candidate gene for Ath1, a locus responsible for the respective susceptibility and resistance of mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) to diet-induced atherosclerosis. To evaluate if Prdx6 underlies Ath1, we compared the diet-induced atherosclerotic lesions in Prdx6 targeted mutant (Prdx6-/-) mice of different genetic backgrounds: B6, 129, and B6;129. PRDX6 protein and mRNA were expressed in normal and atherosclerotic aortas.

The hypolipidemic natural product Commiphora mukul and its component guggulsterone inhibit oxidative modification of LDL.

There is accumulating evidence that LDL oxidation is essential for atherogenesis, and that antioxidants that prevent this oxidation may either slow down or prevent atherogenesis. In the present study, we found that Commiphora mukul and its cholesterol-lowering component, guggulsterone, effectively inhibited LDL oxidation mediated by either catalytic copper ions, free radicals generated with the azo compound 2,2'-azobis-(2-amidinopropane)dihydrochloride (AAPH), soybean lipoxygenase enzymatically, or mouse peritoneal macrophages. This inhibition was assessed by the decrease in the following parameters describing LDL oxidation: conjugated dienes, relative electrophoretic mobility (REM), thiobarbituric acid reactive substances, lipid hydroperoxides, oxidation-specific immune epitopes as detected with a monoclonal antibody against oxidized LDL, and the accumulation of LDL derived cholesterol esters in mouse peritoneal macrophages.

Low-density lipoprotein modification by normal, myeloperoxidase-deficient and NADPH oxidase-deficient granulocytes and the impact of redox active transition metal ions.

The modification of low-density lipoprotein (LDL) by normal, myeloperoxidase (MPO)-deficient and NADPH oxidase-deficient granulocytes was investigated using the monoclonal antibody (mAb) OB/04, which was originally generated against copper-oxidized LDL. Incubation of LDL with normal granulocytes increased the reactivity of LDL with mAb OB/04. These effects were even more pronounced using MPO-deficient granulocytes.

Neopterin and 7,8-dihydroneopterin interfere with low density lipoprotein oxidation mediated by peroxynitrite and/or copper.

Low density lipoprotein (LDL) oxidation within the artery wall likely represents a key event in the formation of atherosclerotic lesions. Oxidatively modified LDL particles exert chemotactic properties on macrophages, and the uncontrolled uptake of modified LDL by macrophages leads to the formation of lipid-loaded foam cells, a hallmark of early stage atherosclerosis. Human macrophages stimulated by interferon-gamma generate reactive oxygen species (ROS), neopterin, and 7,8-dihydroneopterin.

Relationship between the sialic acid content of low-density lipoprotein (LDL) and autoantibodies to oxidized LDL in the plasma of healthy subjects and patients with atherosclerosis.

To determine whether the sialic acid (SA) content of the low-density lipoprotein (LDL) is related to the plasma concentration of autoantibodies to oxidized LDL (oxLDL), we measured the SA content of LDL and the concentrations of oxLDL and autoantibodies to oxLDL in plasma of 20 apparently healthy subjects and 20 patients with advanced coronary atherosclerosis. In the healthy subjects the SA content of LDL correlated positively with plasma concentration of autoantibodies to oxLDL. In agreement with the literature the decreased SA content of LDL was associated with an increased fraction of oxLDL; a decreased fraction of oxLDL was associated with an increased plasma concentration of autoantibodies to oxLDL.