scholarly journals A Rapid Method for Measurement of the Susceptibility to Oxidation of Low-Density Lipoprotein

1995 ◽  
Vol 32 (2) ◽  
pp. 167-174 ◽  
Author(s):  
Ian F W McDowell ◽  
Jane McEneny ◽  
Elisabeth R Trimble
Keyword(s):  
Protein Concentration ◽  
Low Density Lipoprotein ◽  
Gel Filtration ◽  
Density Lipoprotein ◽  
Normal Subjects ◽  
Total Sample ◽  
Lag Time ◽  
Ldl Oxidation ◽  
Low Density ◽  
Frozen Plasma

Oxidation of low-density lipoprotein (LDL) may be important in the pathogenesis of atherosclerosis. We describe a method which measures the oxidation resistance of LDL isolated by a rapid procedure without added antioxidants. LDL was isolated from heparinized plasma by density gradient ultracentrifugation and desalted by gel filtration. The protein concentration was standardized to 50 mg/L and oxidation was promoted by copper (2 μmol/L) at 37°C. The total sample preparation time was 2·5 h. Conjugated diene production was monitored at λ = 234 nm with computation of the lag time. LDL oxidation was inhibited by EDTA but not heparin. Albumin inhibited LDL oxidation but only in concentrations greater than 50 mg/L. LDL was stable in frozen plasma (–70°C) for 10 weeks, but unstable in the isolated and desalted state. The lag time for LDL from patients treated with the antioxidant probucol was markedly prolonged compared to normal subjects.

scholarly journals The Effect of Quail Egg and Hen Egg Consumption on Low-Density Lipoprotein Oxidation and Small Dense Low-Density Lipoprotein

2020 ◽  
Author(s):  
Raveenan Mingpakanee ◽  
Chatchanok Chaisitthichai ◽  
Nattaporn Wichitamporn ◽  
Paradee Sappittayakorn ◽  
Suparnnikar Phongphanwatana
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lag Time ◽  
Plasma Triglyceride ◽  
Ldl Oxidation ◽  
Low Density ◽  
Egg Consumption ◽  
Hen Egg ◽  
Lipoprotein Profiles

Objective: The aim of the study was to investigate the effect of quail egg and hen egg supplements on lipoprotein profiles, low-density lipoprotein (LDL) oxidation and small dense LDL cholesterol (sd-LDL-C) in young healthy people, compared with hen eggs. Material and Methods: Twenty-three healthy volunteers (11 men and 12 women) were randomly assigned to consume 3 whole hen eggs per day (hen group, n=11) (total cholesterol 633 mg) or 9 quail eggs per day (quail group, n=12) (total cholesterol 459 mg) for 30 days. The plasma cholesterol and plasma triglyceride concentrations and lipoprotein fractions (Triglyceride-rich lipoprotein; TRL, LDL and high-density lipoprotein; HDL) were determined at baseline and after the 30-day period of egg consumption. The LDL oxidation (lag time) was measured by the increase of conjugated diene production. Sd-LDL-C was calculated from the major lipid and lipoprotein parameters. Results: In the quail group, plasma triglyceride (TG) and LDL-TG were significantly decreased, whereas the plasma cholesterol and HDL-C were unchanged. There was no alteration in lipoprotein profiles in the hen group. The LDL lag time of the quail group was longer than at baseline. There were no significant changes in sd-LDL-C levels in both groups during the study.Conclusion: Quail egg and hen egg consumptions for 30 days did not change the lipoprotein profiles, sd-LDL as well as the LDL-oxidation, which not modified the cardiovascular disease risk factor.

Improved Measurement of Low-Density-Lipoprotein Susceptibility to Copper-Induced Oxidation: Application of a Short Procedure for Isolating Low-Density Lipoprotein

1992 ◽  
Vol 38 (10) ◽  
pp. 2066-2072 ◽  
Author(s):  
H A Kleinveld ◽  
H L Hak-Lemmers ◽  
A F Stalenhoef ◽  
P N Demacker
Keyword(s):  
Low Density Lipoprotein ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
Thiobarbituric Acid ◽  
Lag Time ◽  
Butylated Hydroxytoluene ◽  
Ldl Oxidation ◽  
Low Density ◽  
Short Run

Abstract Low-density-lipoprotein (LDL) oxidation may provide the crucial link between plasma LDL and atherosclerotic-lesion formation. Oxidation can be induced in vitro by incubating LDL with cells or metal ions and can be measured by continuously monitoring conjugated-diene absorbance at 234 nm. Measurement of LDL oxidizability was improved by performing the assay with 0.05 g of LDL-protein per liter of phosphate buffer containing 1 mumol of EDTA, by initiating oxidation by adding CuCl2 (5 mumol/L) at 30 degrees C, and by using a short-run ultracentrifugation method for isolating LDL, which reduced the time needed for obtaining purified LDL and thus reduced in vitro oxidation. LDL apolipoprotein analysis and oxidizability determination showed that this method is better than the longer sequential-isolation procedure. Adding butylated hydroxytoluene (BHT) to plasma as an antioxidant unpredictably increased the LDL oxidation lag time, making BHT unsuitable as an antioxidant. Adding EDTA appeared to be sufficient to prevent in vitro oxidation. Additionally, the diene production correlated highly with the concentration of thiobarbituric acid-reactive substances (r = 0.97). No relation between the vitamin E content of LDL and the oxidation lag time was found.

Folate: In Vitro and in Vivo Effects on VLDL and LDL Oxidation

2007 ◽  
Vol 77 (1) ◽  
pp. 66-72 ◽  
Author(s):  
McEneny ◽  
Couston ◽  
McKibben ◽  
Young ◽  
Woodside
Keyword(s):  
Folic Acid ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Folic Acid Supplementation ◽  
Serum Folate ◽  
Ldl Oxidation ◽  
Low Density ◽  
Acid Supplementation

Raised total homocysteine (tHcy) levels may be involved in the etiology of cardiovascular disease and can lead to damage of vascular endothelial cells and arterial wall matrix. Folic acid supplementation can help negate these detrimental effects by reducing tHcy. Recent evidence has suggested an additional anti-atherogenic property of folate in protecting lipoproteins against oxidation. This study utilized both an in vitro and in vivo approach. In vitro: Very-low-density lipoprotein (VLDL) and low density lipoprotein (LDL) were isolated by rapid ultracentrifugation and then oxidized in the presence of increasing concentrations (0→ μmol/L) of either folic acid or 5-methyltetrahydrofolate (5-MTHF). In vivo: Twelve female subjects were supplemented with folic acid (1 mg/day), and the pre- and post-VLDL and LDL isolates subjected to oxidation. In vitro: 5-MTHF, but not folic acid, significantly increased the resistance of VLDL and LDL to oxidation. In vivo: Following folic acid supplementation, tHcy decreased, serum folate increased, and both VLDL and LDL displayed a significant increase in their resistance to oxidation. These results indicated that in vitro, only the active form of folate, 5-MTHF, had antioxidant properties. In vivo results demonstrated that folic acid supplementation reduced tHcy and protected both VLDL and LDL against oxidation. These findings provide further support for the use of folic acid supplements to aid in the prevention of atherosclerosis.

Protective Effects of Berberine against Low-Density Lipoprotein (LDL) Oxidation and Oxidized LDL-Induced Cytotoxicity on Endothelial Cells

2007 ◽  
Vol 55 (25) ◽  
pp. 10437-10445 ◽  
Author(s):  
Yih-Shou Hsieh ◽  
Wu-Hsien Kuo ◽  
Ta-Wei Lin ◽  
Horng-Rong Chang ◽  
Teseng-His Lin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Low Density ◽  
Protective Effects

scholarly journals The role of high-density lipoprotein and lipid-soluble antioxidant vitamins in inhibiting low-density lipoprotein oxidation

1993 ◽  
Vol 294 (3) ◽  
pp. 829-834 ◽  
Author(s):  
M I Mackness ◽  
C Abbott ◽  
S Arrol ◽  
P N Durrington
Keyword(s):  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Antioxidant Vitamins ◽  
Ldl Oxidation ◽  
Low Density ◽  
Conjugated Diene ◽  
Peroxide Formation

1. The oxidation of low-density lipoprotein (LDL) is believed to play a central role in atherogenesis. We have compared the effect of antioxidant vitamins and high-density lipoprotein (HDL) on the Cu(2+)-catalysed oxidation of LDL. 2. Antioxidant vitamin supplementation significantly reduced conjugated diene formation but did not affect the formation of lipid peroxides. 3. Conversely, HDL did not affect conjugated diene formation but inhibited the formation of lipid peroxides by up to 90%. 4. The inhibition by HDL of lipid peroxide formation in oxidized LDL was dependent on the concentration of HDL and was not due to HDL chelating Cu2+. 5. Large interindividual variations in the inhibition of lipid peroxide formation by autologous HDL were evident, which were related to the rate of lipid peroxide generation in the LDL. 6. We conclude that HDL is a powerful antioxidant or more probably inhibitor of LDL oxidation in vitro and may play an important role in vivo in preventing atherosclerosis by inhibiting LDL oxidation in the artery wall.

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