scholarly journals Antioxidative Effects and Inhibition of Human Low Density Lipoprotein OxidationIn Vitroof Polyphenolic Compounds inFlammulina velutipes(Golden Needle Mushroom)

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Mohammad Azizur Rahman ◽  
Noorlidah Abdullah ◽  
Norhaniza Aminudin
Keyword(s):  
Low Density Lipoprotein ◽  
Radical Scavenging ◽  
Density Lipoprotein ◽  
Thiobarbituric Acid ◽  
Polyphenolic Compounds ◽  
Oxidative Modification ◽  
Ldl Oxidation ◽  
Total Phenolic ◽  
Low Density ◽  
Antioxidative Effects

Dietary polyphenolic compounds mediate polynomial actions in guarding against multiple diseases. Atherosclerosis is an oxidative stress driven pathophysiological complication where free radical induced oxidative modification of low density lipoprotein (LDL) plays the ground breaking role. Mushrooms have been highly regarded for possessing an antioxidant arsenal. Polyphenolic compounds present in dietary mushrooms seem pertinent in withstanding LDL oxidation en route to controlling atherosclerosis. In this study, the antioxidative effect of five solvent fractions consisting of methanol : dichloromethane (M : DCM), hexane (HEX), dichloromethane (DCM), ethyl acetate (EA), and aqueous residue (AQ) ofFlammulina velutipeswas evaluated. M : DCM fraction showed the most potent 2,2-diphenyl-1-picrylhydrazyl radical scavenging effect with IC50of 0.86 mg/mL and total phenolic content of 56.36 gallic acid equivalent/g fraction. In LDL oxidation inhibitory tests, M : DCM fraction at 1 µg/mL concentration mostly lengthened the lag time (125 mins) of conjugated diene formation and inhibited the formation of thiobarbituric acid reactive substances (48.71%, at 1 mg/mL concentration). LC-MS/MS analyses of M : DCM fraction identified the presence of polyphenolic substances protocatechuic acid,p-coumaric, and ellagic acid. These chain-breaking polyphenolics might impart the antioxidative effects ofF. velutipes. Thus, mushroom-based dietary polyphenolic compounds might be implicated in slowing down the progression of atherosclerosis.

Antioxidants and atherosclerosis

2004 ◽  
Vol 32 (1) ◽  
pp. 156-159 ◽  
Author(s):  
E. Niki
Keyword(s):  
Free Radical ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Radical Scavenging ◽  
Density Lipoprotein ◽  
Active Species ◽  
Oxidative Modification ◽  
Ldl Oxidation ◽  
Low Density ◽  
Mediated Oxidation

The oxidative modification of low-density lipoprotein (LDL) can be induced by various active species by different mechanisms. Vitamin E and other radical-scavenging antioxidants can inhibit the free radical-mediated oxidation of LDL, but they are not effective against LDL oxidation induced by non-radical mechanisms.

scholarly journals 5-Lipoxygenase is not essential in macrophage-mediated oxidation of low-density lipoprotein

1991 ◽  
Vol 278 (1) ◽  
pp. 163-169 ◽  
Author(s):  
W Jessup ◽  
V Darley-Usmar ◽  
V O'Leary ◽  
S Bedwell
Keyword(s):  
Low Density Lipoprotein ◽  
Radical Scavenging ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Ldl Oxidation ◽  
Low Density ◽  
Lipoxygenase Pathway ◽  
Lipoxygenase Inhibitors ◽  
Radical Scavenging Properties ◽  
Mediated Oxidation

The concentration-dependent effects of a series of lipoxygenase inhibitors and antioxidants on the macrophage-mediated oxidative modification of low-density lipoprotein (LDL) were measured. Their influence on macrophage 5-lipoxygenase pathway activity was also studied over the same concentration range. No correlation between inhibition of 5-lipoxygenase and of macrophage-mediated oxidation of LDL was observed. The capacity of the compounds to prevent cell-mediated modification of LDL could be explained in terms of their activity as either aqueous- or lipid-peroxyl radical scavengers. Two potent 5-lipoxygenase inhibitors (MK 886 and Revlon 5901), which had no radical-scavenging properties, were unable to block LDL modification. It is concluded that 5-lipoxygenase is not essential for LDL oxidation by macrophages.

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.

scholarly journals Lipoxygenase treatment render low-density lipoprotein susceptible to Cu2+-catalysed oxidation

1996 ◽  
Vol 314 (2) ◽  
pp. 577-585 ◽  
Author(s):  
Achim LASS ◽  
Jutta BELKNER ◽  
Hermann ESTERBAUER ◽  
Hartmut KÜHN
Keyword(s):  
Low Density Lipoprotein ◽  
Complex Mixture ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Oxidation Products ◽  
Ldl Oxidation ◽  
Foam Cell Formation ◽  
Low Density ◽  
Catalysed Oxidation ◽  
Lag Period

Oxidative modification of low-density lipoprotein (LDL) has been implicated in foam-cell formation at all stages of atherosclerosis. Since transition metals and mammalian 15-lipoxygenases are capable of oxidizing LDL to its atherogenic form, a concerted action of these two catalysts in atherogenesis has been suggested. Cu2+-catalysed LDL oxidation is characterized by a kinetic lag period in which the lipophilic antioxidants are decomposed and by a complex mixture of unspecific oxidation products. We investigated the kinetics of the 15-lipoxygenase-catalysed oxygenation of LDL and found that the enzyme is capable of oxidizing LDL in the presence of the endogenous lipophilic antioxidants. In contrast with the Cu2+-catalysed reaction, no kinetic lag phase was detected. The pattern of products formed during short-term incubations was highly specific, with cholesterol-esterified (13S)-hydroperoxy-(9Z,11E)-octadecadienoic acid being the major product. However, after long-term incubations the product pattern was less specific. Preincubation with 15-lipoxygenase rendered human LDL more susceptible to Cu2+-catalysed oxidation as indicated by a dramatic shortening of the lag period. Addition of Cu2+ to lipoxygenase-treated LDL led to a steep decline in its antioxidant content and to a greatly reduced lag period. Interestingly, if normalized to a comparable hydroperoxide content, autoxidation and addition of exogenous hydroperoxy fatty acids both failed to overcome the lag period. The local peroxide concentrations in various LDL subcompartments will be discussed as a possible reason for this unexpected behaviour.

Intracellular GSH of Streptococcus thermophilus shows anti-oxidative activity against low-density lipoprotein oxidation in vitro and in a hyperlipidaemic hamster model

2018 ◽  
Vol 9 (1) ◽  
pp. 143-152 ◽  
Author(s):  
S. Kusuhara ◽  
M. Ito ◽  
T. Sato ◽  
W. Yokoi ◽  
Y. Yamamoto ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Streptococcus Thermophilus ◽  
Oxidative Modification ◽  
Mass Spectrometry Analysis ◽  
Oxidative Activity ◽  
Ldl Oxidation ◽  
Low Density ◽  
Dependent Manner ◽  
Hamster Model

Streptococcus thermophilus YIT 2001 (ST-1), a lactic acid bacterial strain, was shown to have inhibitory effects on the oxidation of low-density lipoprotein (LDL) and the development of aortic fatty lesions in an animal model, and lower the serum levels of malondialdehyde-modified LDL, an oxidative modification product of LDL, in a clinical trial. This study aimed to identify the intracellular active component of ST-1 associated with anti-oxidative activity against LDL oxidation. High-performance liquid chromatography-electrospray ionisation mass spectrometry analysis after fractionation of the cellular extract by reversed-phase chromatography demonstrated that the active fraction contained reduced glutathione (GSH). GSH showed anti-oxidative activity in a dose-dependent manner, while this activity disappeared following thiol derivatisation. ST-1 had the strongest anti-oxidative activity against LDL oxidation and the highest level of intracellular GSH among five strains of S. thermophilus. In addition, the anti-oxidative activity of ST-1 after thiol derivatisation decreased by about half, which was similar to that of three other strains containing poor or no intracellular GSH or thiol components. Moreover, anti-oxidative activity against LDL oxidation was observed in hyperlipidaemic hamsters fed with high GSH ST-1 cells but not in those given low GSH cells. These findings suggest that intracellular GSH in ST-1 may provide beneficial effects via anti-oxidative activity against LDL oxidation and excess oxidative stress in the blood.

scholarly journals Human macrophage-mediated oxidation of low-density lipoprotein is delayed and independent of superoxide production

1994 ◽  
Vol 301 (2) ◽  
pp. 421-428 ◽  
Author(s):  
B Garner ◽  
R T Dean ◽  
W Jessup
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Direct Methods ◽  
Thiobarbituric Acid ◽  
Human Monocyte ◽  
Ldl Oxidation ◽  
Human Macrophage ◽  
Low Density ◽  
Oxidatively Modified

There is growing evidence that oxidatively modified low-density lipoprotein (LDL) accumulates in the atherosclerotic intima of arteries. Cells present in the intima (including the monocyte/macrophage) are capable of oxidizing LDL in vitro, but the mechanisms by which this occurs are unknown. Several reports have claimed a crucial role for superoxide as a cell-derived radical species capable of enhancing the rate of LDL oxidation. We have used a sensitive h.p.l.c. system with chemiluminescence detection to measure LDL cholesteryl ester hydroperoxides at early stages of LDL oxidation. During the initial stages of LDL oxidation, there is at least a 2 h delay before human monocyte-derived macrophages enhance this process. Stimulation of these cells to produce large fluxes of superoxide does not increase the rate of LDL oxidation or decrease the delay of its onset. Prior exposure of LDL to a high flux of superoxide does not increase its susceptibility to oxidation by human monocyte-derived macrophages. We also show that the thiobarbituric acid-reactive substances (TBARS) assay does not always correlate with more direct methods of assessing LDL oxidation and confirm recent reports that superoxide dismutase only partially inhibits cell-mediated LDL oxidation. We conclude that superoxide does not play a major role in human monocyte-derived macrophage-mediated LDL oxidation under the conditions that we describe.

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