A moderate in vivo vitamin E supplement counteracts the fish-oil-induced increase in in vitro oxidation of human low-density lipoproteins

1993 ◽  
Vol 57 (5) ◽  
pp. 827S-827S ◽  
Author(s):  
Gerard S Oostenbrug ◽  
Ronald P Mensink ◽  
Gerard Hornstra
Keyword(s):  
Vitamin E ◽  
Fish Oil ◽  
Low Density Lipoproteins ◽  
Low Density

scholarly journals Aggregation and fusion of low-density lipoproteins in vivo and in vitro

2013 ◽  
Vol 4 (5) ◽  
pp. 501-518 ◽  
Author(s):  
Mengxiao Lu ◽  
Olga Gursky
Keyword(s):  
Lipid Droplet ◽  
Current Knowledge ◽  
Single Copy ◽  
Droplet Formation ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Atherosclerotic Lesions ◽  
Lipid Droplet Formation

AbstractLow-density lipoproteins (LDLs, also known as ‘bad cholesterol’) are the major carriers of circulating cholesterol and the main causative risk factor of atherosclerosis. Plasma LDLs are 20- to 25-nm nanoparticles containing a core of cholesterol esters surrounded by a phospholipid monolayer and a single copy of apolipoprotein B (550 kDa). An early sign of atherosclerosis is the accumulation of LDL-derived lipid droplets in the arterial wall. According to the widely accepted ‘response-to-retention hypothesis’, LDL binding to the extracellular matrix proteoglycans in the arterial intima induces hydrolytic and oxidative modifications that promote LDL aggregation and fusion. This enhances LDL uptake by the arterial macrophages and triggers a cascade of pathogenic responses that culminate in the development of atherosclerotic lesions. Hence, LDL aggregation, fusion, and lipid droplet formation are important early steps in atherogenesis. In vitro, a variety of enzymatic and nonenzymatic modifications of LDL can induce these reactions and thereby provide useful models for their detailed analysis. Here, we summarize current knowledge of the in vivo and in vitro modifications of LDLs leading to their aggregation, fusion, and lipid droplet formation; outline the techniques used to study these reactions; and propose a molecular mechanism that underlies these pro-atherogenic processes. Such knowledge is essential in identifying endogenous and exogenous factors that can promote or prevent LDL aggregation and fusion in vivo and to help establish new potential therapeutic targets to decelerate or even block these pathogenic reactions.

Mécanisme moléculaire de l'effet protecteur de la vitamine E dans l'athérosclérose

2002 ◽  
Vol 80 (7) ◽  
pp. 662-669 ◽  
Author(s):  
Abdelouahed Khalil
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Vascular Diseases ◽  
Epidemiologic Studies ◽  
Low Density Lipoproteins ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Prooxidant Effect

Oxidation of low-density lipoproteins constitutes the first step of a very complex process leading to atherosclerosis. Vitamin E, and principally alpha-tocopherol, is considered as the principal inhibitor of lipid peroxidation. Some studies showed the beneficial role of vitamin E in the prevention and reduction of atherosclerosis and its associated pathologies. However, other in vitro studies advance a prooxidant role of vitamin E. The results of the epidemiologic studies are difficult to generalize without taking account of the clinical randomized tests. In this work, we reviewed the principal studies devoted to the role of vitamin E and discussed the assumption of a prooxidant effect of this molecule.Key words: vitamin E, low-density lipoproteins (LDL), lipid peroxidation, cardio-vascular diseases.

Probucol protects low-density lipoproteins from in vitro and in vivo oxidation

1994 ◽  
Vol 29 (4) ◽  
pp. 337-344 ◽  
Author(s):  
Gabriele Bittolo-Bon ◽  
Giuseppe Cazzolato ◽  
Pietro Avogaro
Keyword(s):  
Low Density Lipoproteins ◽  
Low Density

scholarly journals Uptake of chemically modified low density lipoproteins in vivo is mediated by specific endothelial cells.

1985 ◽  
Vol 100 (1) ◽  
pp. 103-117 ◽  
Author(s):  
R E Pitas ◽  
J Boyles ◽  
R W Mahley ◽  
D M Bissell
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Kupffer Cells ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Coated Pits ◽  
Sinusoidal Endothelial Cells ◽  
Modified Lipoproteins

Acetoacetylated (AcAc) and acetylated (Ac) low density lipoproteins (LDL) are rapidly cleared from the plasma (t1/2 approximately equal to 1 min). Because macrophages, Kupffer cells, and to a lesser extent, endothelial cells metabolize these modified lipoproteins in vitro, it was of interest to determine whether endothelial cells or macrophages could be responsible for the in vivo uptake of these lipoproteins. As previously reported, the liver is the predominant site of the uptake of AcAc LDL; however, we have found that the spleen, bone marrow, adrenal, and ovary also participate in this rapid clearance. A histological examination of tissue sections, undertaken after the administration of AcAc LDL or Ac LDL (labeled with either 125I or a fluorescent probe) to rats, dogs, or guinea pigs, was used to identify the specific cells binding and internalizing these lipoproteins in vivo. With both techniques, the sinusoidal endothelial cells of the liver, spleen, bone marrow, and adrenal were labeled. Less labeling was noted in the ovarian endothelia. Uptake of AcAc LDL by endothelial cells of the liver, spleen, and bone marrow was confirmed by transmission electron microscopy. These data suggest uptake through coated pits. Uptake of AcAc LDL was not observed in the endothelia of arteries (including the coronaries and aorta), veins, or capillaries of the heart, testes, kidney, brain, adipose tissue, and duodenum. Kupffer cells accounted for a maximum of 14% of the 125I-labeled AcAc LDL taken up by the liver. Isolated sinusoidal endothelial cells from the rat liver displayed saturable, high affinity binding of AcAc LDL (Kd = 2.5 X 10(-9) M at 4 degrees C), and were shown to degrade AcAc LDL 10 times more effectively than aortic endothelial cells. These data indicate that specific sinusoidal endothelial cells, not the macrophages of the reticuloendothelial system, are primarily responsible for the removal of these modified lipoproteins from the circulation in vivo.

scholarly journals Plasma metabolites of quercetin and their antioxidant properties

1998 ◽  
Vol 275 (1) ◽  
pp. R212-R219 ◽  
Author(s):  
Christine Morand ◽  
Vanessa Crespy ◽  
Claudine Manach ◽  
Catherine Besson ◽  
Christian Demigné ◽  
...  
Keyword(s):  
Fruits And Vegetables ◽  
Antioxidant Properties ◽  
Total Antioxidant Status ◽  
Low Density Lipoproteins ◽  
Ldl Oxidation ◽  
Plasma Metabolites ◽  
Low Density ◽  
Very Low Density Lipoproteins

Quercetin is one of the most widely distributed flavonoids present in fruits and vegetables. The present experiments were performed on rats adapted for 3 wk to a semipurified diet supplemented with 0.2% quercetin. The major part of the circulating metabolites of quercetin (91.5%) are glucurono-sulfo conjugates of isorhamnetin (3′-O-methyl quercetin; 89.1 ± 2.1 μM) and of quercetin (14.7 ± 1.7 μM); the minor part (8.5%) is constituted by glucuronides of quercetin and its methoxylated forms (9.6 ± 2.3 μM). Conjugated dienes formation, resulting from Cu2+-catalyzed oxidation of rat very low density lipoproteins + low density lipoproteins (LDL), was effectively inhibited in vitro by conjugated metabolites of quercetin. These metabolites appeared to be four times more potent than trolox in inhibiting LDL oxidation. Moreover, the plasma from rats adapted to a diet containing 0.2% quercetin exhibited a total antioxidant status markedly higher than that of control rats (+60%). This study shows that ubiquitous quercetin is conjugated in vivo, yielding metabolites that exhibit antioxidant properties. Thus the health benefits of flavonoids in foods can be due to the antioxidant properties of their metabolites.

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