scholarly journals α-tocopherol consumption during low-density-lipoprotein oxidation

1990 ◽  
Vol 265 (2) ◽  
pp. 399-405 ◽  
Author(s):  
W Jessup ◽  
S M Rankin ◽  
C V De Whalley ◽  
J R S Hoult ◽  
J Scott ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Tocopherol Content ◽  
Oxidative Modification ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Resistance To Oxidation ◽  
Endogenous Antioxidants ◽  
Oxidatively Modified

1. The kinetics of the depletion of alpha-tocopherol in human low-density lipoprotein (LDL) were measured during macrophage-mediated and cell-free oxidation. The formation of oxidatively modified, high-uptake species of LDL in these systems was not detectable until all of the endogenous alpha-tocopherol had been consumed. 2. Supplementation of the alpha-tocopherol content of LDL by loading in vivo extended the duration of the lag period during which no detectable oxidative modification occurred. 3. The addition of a flavonoid (morin) prevented both alpha-tocopherol consumption and oxidative modification of LDL. 4. The alpha-tocopherol contents of LDLs from a range of individual donors could not be used to predict their relative resistance to oxidation, indicating that other endogenous antioxidants may also be present, and quantitatively significant, in human LDL.

scholarly journals Low-density lipoprotein oxidation, antioxidants, and atherosclerosis: a clinical biochemistry perspective

1996 ◽  
Vol 42 (4) ◽  
pp. 498-506 ◽  
Author(s):  
I Jialal ◽  
S Devaraj
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
Direct Methods ◽  
Ldl Oxidation ◽  
Low Density ◽  
Indirect Measures ◽  
Oxidatively Modified

Abstract Cardiovascular disease is the leading cause of mortality in westernized populations. An increased concentration of plasma low-density lipoprotein (LDL) cholesterol constitutes a major risk factor for atherosclerosis. Several lines of evidence support a role for oxidatively modified LDL in atherosclerosis and for its in vivo existence. Antioxidants have been shown to decrease atherosclerotic lesion formation in animal models and decrease LDL oxidation; the evaluation of LDL oxidation in vivo is therefore very important. However, there is a paucity of methods for direct measurement of LDL oxidation. Of the direct methods currently available, the preferred ones seem to be the measurement of F2-isoprostanes, autoantibodies to epitopes on oxidized LDL, and the assessment of antioxidant status. Of the indirect measures, the most uniformly accepted procedure is examining the oxidative susceptibility of isolated LDL by monitoring conjugated diene formation.

scholarly journals The action of defined oxygen-centred free radicals on human low-density lipoprotein

1989 ◽  
Vol 262 (3) ◽  
pp. 707-712 ◽  
Author(s):  
S Bedwell ◽  
R T Dean ◽  
W Jessup
Keyword(s):  
Free Radicals ◽  
Negative Charge ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Apo B ◽  
Mouse Macrophages ◽  
Radical Attack

The effects of defined oxygen-centred free radicals on human low-density lipoprotein (LDL) structure and receptor affinity are discussed in relation to the mechanisms of cell-mediated oxidative modification of LDL. Both hydroxyl (OH.) and hydroperoxyl (HO2.) radicals caused depletion of endogenous alpha-tocopherol and formation of hydroperoxides. Superoxide (O2-.) radicals produced only very limited oxidation, but could potentiate oxidation stimulated by the addition of Cu2+. All these radicals enhanced the net negative charge of intact LDL and induced fragmentation of apolipoprotein B-100 (apo B). OH. also caused cross-linking of apo B. Radical attack decreased the affinity of LDL for the fibroblast apo B/E receptor, but did not enhance its endocytosis by mouse macrophages.

scholarly journals Oxidative modification of low density lipoprotein by cigarette smoke extract in vivo

1997 ◽  
Vol 73 ◽  
pp. 184
Author(s):  
Sachiko Matsuno ◽  
Yu Yamaguchi ◽  
Satomi Kagota ◽  
Young Mi Kwon ◽  
Kazumasa Shinozuka ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cigarette Smoke Extract ◽  
Oxidative Modification ◽  
Low Density

scholarly journals Non-oxidative modification of native low-density lipoprotein by oxidized low-density lipoprotein

1996 ◽  
Vol 316 (2) ◽  
pp. 377-380 ◽  
Author(s):  
Min YANG ◽  
David S. LEAKE ◽  
Catherine A. RICE-EVANS
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Low Density ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Process Studies

The oxidative modification of low-density lipoprotein (LDL) has been implicated in the pathogenesis of atherosclerosis, although little is known as yet about the precise mechanism of oxidation in vivo. The studies presented here demonstrate that, in the absence of cells or transition metals, oxidized LDL can modify native LDL through co-incubation in vitro such as to increase its net negative charge, in a concentration-dependent manner. The interaction is not inhibited by peroxyl radical scavengers or metal chelators, precluding the possibility that the modification of native LDL by oxidized LDL is through an oxidative process. Studies with radioiodinated oxidized LDL showed no transfer of radioactivity to the native LDL, demonstrating that fragmentation of protein and the transfer of some of the fragments does not account for the modified charge on the native LDL particle. The adjacency of native to oxidized LDL in the arterial wall may be a potential mechanism by which the altered recognition properties of the apolipoprotein B-100 may arise rapidly without oxidation or extensive modification of the native LDL lipid itself.

scholarly journals Plasma clearance and net uptake of α-tocopherol and low-density lipoprotein by tissues in WHHL and control rabbits

1992 ◽  
Vol 287 (1) ◽  
pp. 247-254 ◽  
Author(s):  
W Cohn ◽  
M A Goss-Sampson ◽  
H Grun ◽  
D P R Muller
Keyword(s):  
Plasma Clearance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Apo B ◽  
Net Uptake ◽  
Lipoprotein Composition

The mechanism(s) of uptake of vitamin E (alpha-tocopherol) by tissues is poorly understood. It has, however, been suggested from studies in vitro that the apolipoprotein B/E (apo B/E) receptor pathway for low-density lipoprotein (LDL) may be involved. To investigate the role of the apo B/E receptor pathway in vivo, we have studied the transport and uptake of alpha-tocopherol by tissues in Watanabe Heritable Hyperlipidaemic (WHHL) rabbits, which lack functional LDL (apo B/E) receptors, and controls. [3H]alpha-Tocopherol incorporated within LDL labelled with [14C]sucrose was used in these studies, as this enabled the uptake of both alpha-tocopherol and LDL to be studied independently. The principal findings were as follows. (1) Concentrations of the circulating lipids (including alpha-tocopherol) and LDL were increased and the plasma fractional disappearance rates of alpha-tocopherol and LDL decreased in the WHHL rabbits. (2) The WHHL rabbits clear more LDL and alpha-tocopherol from the circulation than controls do, because of their increased pool sizes of alpha-tocopherol and LDL. (3) The lipoprotein composition of the WHHL rabbits differed from that of the controls, and there was exchange of alpha-tocopherol between the lipoprotein fractions in vivo and in vitro. (4) High-affinity apo B/E receptors were not essential for the uptake of alpha-tocopherol by tissues. (5) Evidence from the plasma-clearance and tissue data suggest that alpha-tocopherol can be taken up by tissues in association with, and also independent of, LDL. We conclude that there are several different mechanisms for the uptake of alpha-tocopherol by tissues, which include receptor-dependent and receptor-independent pathways, independent transport and co-transport of alpha-tocopherol and LDL, and uptake from a number of different lipoproteins.

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