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

IN VITRO STUDY OF A NOVEL LOW-DENSITY LIPOPROTEIN ADSORBENT

2002 ◽  
Vol 30 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Ning-Ning Cao ◽  
Yao-Ting Yu ◽  
Man-Yan Wang ◽  
Chang-Zhi Chen
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
In Vitro Study ◽  
Vitro Study ◽  
Low Density

scholarly journals In-Vitro Study of the Properties of Components for the Synthesis of Sorbent for Low-Density Lipoprotein Apheresis

Pharmacophore ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 37-41
Author(s):  
Anna Andreevna Bazhenova ◽  
Natalia Igorevna Guryanova ◽  
Gleb Sergeevich Guryanov ◽  
Heda Abdul Vahidovna Alieva ◽  
Diana Tamerlanovna Kachmazova ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
In Vitro Study ◽  
Vitro Study ◽  
Low Density ◽  
Lipoprotein Apheresis

Antioxidant properties of aged garlic extract: an in vitro study incorporating human low density lipoprotein

Life Sciences ◽  
2003 ◽  
Vol 72 (14) ◽  
pp. 1583-1594 ◽  
Author(s):  
Stephanie A Dillon ◽  
Rajpal S Burmi ◽  
Gordon M Lowe ◽  
David Billington ◽  
Khalid Rahman
Keyword(s):  
Low Density Lipoprotein ◽  
Antioxidant Properties ◽  
Density Lipoprotein ◽  
In Vitro Study ◽  
Garlic Extract ◽  
Vitro Study ◽  
Low Density ◽  
Aged Garlic Extract ◽  
Aged Garlic

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 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.

In vitro study of LDL transport under pressurized (convective) conditions

2007 ◽  
Vol 293 (1) ◽  
pp. H126-H132 ◽  
Author(s):  
Limary M. Cancel ◽  
Andrew Fitting ◽  
John M. Tarbell
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
In Vitro Study ◽  
Vitro Study ◽  
Bovine Aortic Endothelial Cell ◽  
Convective Conditions ◽  
Transport Pathways ◽  
Ldl Transport

It is difficult to assess the transport pathways that carry low-density lipoprotein (LDL) into the artery wall in vivo, and there has been no previous in vitro study that has examined transendothelial transport under physiologically relevant pressurized (convective) conditions. Therefore, we measured water, albumin, and LDL fluxes across bovine aortic endothelial cell (BAEC) monolayers in vitro and determined the relative contributions of vesicles, paracellular transport through “breaks” in the tight junction, and “leaky” junctions associated with dying or dividing cells. Our results show that leaky junctions are the dominant pathway for LDL transport (>90%) under convective conditions and that albumin also has a significant component of transport through leaky junctions (44%). Transcellular transport of LDL by receptor-mediated processes makes a minor contribution (<10%) to overall transport under convective conditions.

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.

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