scholarly journals Vitamin E in human low-density lipoprotein. When and how this antioxidant becomes a pro-oxidant

1992 ◽  
Vol 288 (2) ◽  
pp. 341-344 ◽  
Author(s):  
V W Bowry ◽  
K U Ingold ◽  
R Stocker
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Peroxyl Radicals ◽  
Careful Examination ◽  
Early Event ◽  
Low Density ◽  
Tocopheroxyl Radical

Uptake of oxidatively modified low-density lipoprotein (LDL) by cells in the arterial wall is believed to be an important early event in the development of atherosclerosis. Because vitamin E is the major antioxidant present in human lipoproteins, it has received much attention as a suppressor of LDL lipid oxidation and as an epidemiological marker for ischaemic heart disease. However, a careful examination of lipid peroxidation in LDL induced by a steady flux of aqueous peroxyl radicals has demonstrated that, following consumption of endogenous ubiquinol-10, the rate of peroxidation (i) declines as vitamin E is consumed, (ii) is faster in the presence of vitamin E than following its complete consumption, (iii) is substantially accelerated by enrichment of the vitamin in LDL, either in vitro or by diet, and (iv) is virtually independent of the applied radical flux. We propose that perodixation is propagated within lipoprotein particles by reaction of the vitamin E radical (i.e. alpha-tocopheroxyl radical) with polyunsaturated fatty acid moieties in the lipid. This lipid peroxidation mechanism, which can readily be rationalized by the known chemistry of the alpha-tocopheroxyl radical and by the radical-isolating properties of fine emulsions such as LDL, explains how reagents which reduce the alpha-tocopheroxyl radical (i.e. vitamin C and ubiquinol-10) strongly inhibit lipid peroxidation in vitamin E-containing LDL.

scholarly journals Lipid peroxidation and susceptibility of low-density lipoprotein to in vitro oxidation in hyperhomocysteinaemia

1995 ◽  
Vol 25 (3) ◽  
pp. 149-154 ◽  
Author(s):  
H. J. BLOM ◽  
H. A. KLEINVELD ◽  
G. H. J. BOERS ◽  
P. N. M. DEMACKER ◽  
H. L. M. HAK-LEMMERS ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density

scholarly journals Resistance of lipoprotein(a) to lipid peroxidation induced by oxygenated free radicals produced by γ radiolysis: a comparison with low-density lipoprotein

1996 ◽  
Vol 314 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Jean-Louis BEAUDEUX ◽  
Monique GARDES-ALBERT ◽  
Jacques DELATTRE ◽  
Alain LEGRAND ◽  
François ROUSSELET ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Peroxyl Radicals ◽  
Low Density ◽  
Lipoprotein A ◽  
Acetylneuraminic Acid ◽  
Paired Samples ◽  
Apolipoprotein A

Lipid peroxidation of lipoprotein(a) [Lp(a)] by defined oxygen-centred free radicals (O2-· /OH·, O2-·, O2-· /HO2·) produced by γ radiolysis was compared with that of paired samples of low-density lipoprotein (LDL). Lp(a) appeared to be more resistant to oxidation than LDL, as indicated by the kinetic study of four markers of lipid peroxidation: decrease in vitamin E, formation of conjugated dienes and aldehydic products, and modification of electrophoretic mobility. In contrast, similar kinetics of lipid peroxidation were obtained for LDL and Lp(a-), which is the lipoparticle issued following the reductive cleavage of apolipoprotein(a) from Lp(a), thus suggesting that the greater resistance of Lp(a) to lipid peroxidation was due to the presence of apolipoprotein(a). Lipid peroxidation of Lp(a) and LDL induced by peroxyl radicals, which were produced by an azo compound [2,2′-azobis-(2-amidinopropane)dihydrochloride], confirmed both the resistance of Lp(a) to lipid peroxidation and the propensity of Lp(a-) to exhibit a greater susceptibility to oxidation than intact Lp(a). Our findings also indicated that the high content of apolipoprotein(a) in N-acetylneuraminic acid residues was only partly responsible for the resistance of Lp(a) to oxidation.

scholarly journals Altered hepatic catabolism of low-density lipoprotein subjected to lipid peroxidation in vitro

1994 ◽  
Vol 297 (3) ◽  
pp. 573-579 ◽  
Author(s):  
W L Stone ◽  
M Heimberg ◽  
R L Scott ◽  
I LeClair ◽  
H G Wilcox
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Low Density Lipoprotein ◽  
Liver Perfusion ◽  
Density Lipoprotein ◽  
Low Density ◽  
Perfusion System ◽  
Oxidatively Modified ◽  
Generating System

Recent evidence suggests that oxidatively modified forms of low-density lipoprotein (LDL) may be particularly atherogenic. In this investigation, the catabolism of human LDL modified by lipid peroxidation in vitro was studied with a recirculating rat liver perfusion system. A dual-labelling technique was used that permitted native LDL and modified LDL to be studied simultaneously in the liver perfusion system. Native human LDL was found to have a fractional catabolic rate (FCR) of 1.00 +/- 0.21%/h, in agreement with other investigators. Subjecting LDL to oxidation for 12 h in the presence of 30 microM FeEDTA did not significantly affect its FCR. LDL treated with a superoxide-generating system (xanthine oxidase, hypoxanthine, O2) in the presence of 30 microM FeEDTA did, however, show a significant increase in FCR (3.23 +/- 0.19%/h). The hepatic uptakes of native LDL and LDL oxidized with FeEDTA+O2 were similar, but both were significantly lower than the hepatic uptake of LDL treated with the superoxide-radical-generating system. The proteolysis of LDL with pancreatin did not influence either its susceptibility to oxidation or its FCR. LDL oxidation resulted in the preferential loss of alpha-tocopherol rather than gamma-tocopherol. These data indicate that the rat liver effectively catabolizes LDL oxidatively modified by treatment with the superoxide-generating system. Furthermore, our results suggest that only very low plasma levels of highly oxidized LDL could be found under conditions in vivo. The liver may therefore play a major role in protecting the arterial vasculature from highly atherogenic forms of LDL.

Does Mercury Promote Lipid Peroxidation?: An In Vitro Study Concerning Mercury, Copper, and Iron in Peroxidation of Low-Density Lipoprotein

2004 ◽  
Vol 101 (2) ◽  
pp. 117-132 ◽  
Author(s):  
Kari Seppänen ◽  
Pasi Soininen ◽  
Jukka T. Salonen ◽  
Simo Lötjönen ◽  
Reino Laatikainen
Keyword(s):  
Lipid Peroxidation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
In Vitro Study ◽  
Vitro Study ◽  
Low Density
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