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.

Uptake of cholesterol from the very low density lipoprotein or its remnants by the perfused rat liver

1981 ◽  
Vol 59 (6) ◽  
pp. 447-453 ◽  
Author(s):  
Simon-Pierre Noël ◽  
David Rubinstein
Keyword(s):  
Rat Liver ◽  
Lipid Composition ◽  
Low Density Lipoprotein ◽  
Liver Perfusion ◽  
Density Lipoprotein ◽  
Hepatic Uptake ◽  
Low Density ◽  
Perfused Liver ◽  
Very Low Density Lipoproteins

[3H]Cholesterol labelled very low density lipoproteins ([3H]chol-VLDL) were prepared to study the hepatic uptake of cholesterol associated with VLDL and its remnants in the perfused liver system. [3H]Chol-VLDL was incubated with rat postheparin plasma to produce labelled remnants in vitro. The degree of lipolysis of [3H]chol-VLDL depended on the ratio of triacylglycerols to lipase in the incubation medium. Therefore, the produced remnant of d < 1.019 g∙mL−1 had a variable lipid composition depending on the degree of lipolysis. [3H]Chol-VLDL or its remnants were added to liver perfusate and the radioactivity remaining in the perfusate was measured. The kinetic disappearance of [3H]chol-VLDL and its remnants in the perfused liver system indicated that remnant of d < 1.019 g∙mL−1 was taken up by the liver faster than the original VLDL preparation (t1/2 of 8 min vs. 51 min). Appearance of the label in bile during the perfusion was significantly faster when livers were perfused with [3H]chol-VLDL remnants as opposed to uncatabolized [3H]chol-VLDL.The results indicate that first of all, VLDL remnants produced in vitro and reisolated at density less than 1.019 g∙mL−1 do not have a fixed lipid composition but a rather variable one depending on the degree of lipolysis. Secondly, the rat liver may preferentially recognize this VLDL remnant of d < 1.019 g∙mL−1 and take it up more readily than uncatabolized VLDL. Finally when equimolar amount of cholesterol from VLDL or VLDL remnants are circulated in the liver perfusion, the VLDL remnants convey a significantly greater mass of cholesterol to the bile.

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

NMR analysis of low-density lipoprotein oxidatively modified in vitro

1990 ◽  
Vol 9 ◽  
pp. 68
Author(s):  
S. Bradamante ◽  
L. Barenghi ◽  
G. Giudici ◽  
C. Vergani
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Nmr Analysis ◽  
Oxidatively Modified

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

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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