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 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.

scholarly journals Detection of new epitopes formed upon oxidation of low-density lipoprotein, lipoprotein (a) and very-low-density lipoprotein. Use of an antiserum against 4-hydroxynonenal-modified low-density lipoprotein

1990 ◽  
Vol 265 (2) ◽  
pp. 605-608 ◽  
Author(s):  
G Jürgens ◽  
A Ashy ◽  
H Esterbauer
Keyword(s):  
Unsaturated Fatty Acids ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Lipid Hydroperoxides ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Dependent Manner ◽  
Lipoprotein A

4-Hydroxynonenal (HNE) is a major aldehydic propagation product formed during peroxidation of unsaturated fatty acids. The aldehyde was used to modify freshly prepared human low-density lipoprotein (LDL). A polyclonal antiserum was raised in the rabbit and absorbed with freshly prepared LDL. The antiserum did not react with human LDL, but reacted with CuCl2-oxidized LDL and in a dose-dependent manner with LDL, modified with 1, 2 and 3 mM-HNE, in the double-diffusion analysis. LDL treated with 4 mM of hexanal or hepta-2,4-dienal or 4-hydroxyhexenal or malonaldehyde (4 or 20 mM) did not react with the antiserum. However, LDL modified with 4 mM-4-hydroxyoctenal showed a very weak reaction. Lipoprotein (a) and very-low-density lipoprotein were revealed for the first time to undergo oxidative modification initiated by CuCl2. This was evidenced by the generation of lipid hydroperoxides and thiobarbituric acid-reactive substances, as well as by a marked increase in the electrophoretic mobility. After oxidation these two lipoproteins also reacted positively with the antiserum against HNE-modified LDL.

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.

Scavenging of Reactive Oxygen Species and Inhibition of the Oxidation of Low Density Lipoprotein by the Aqueous Extraction ofAnoectochilus formosanus

2003 ◽  
Vol 31 (01) ◽  
pp. 25-36 ◽  
Author(s):  
Chun-Ching Shih ◽  
Yueh-Wern Wu ◽  
Wen-Chuan Lin
Keyword(s):  
Reactive Oxygen Species ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Reactive Oxygen ◽  
In Vivo Studies ◽  
Ldl Oxidation ◽  
Low Density ◽  
Dependent Manner ◽  
Oxygen Species

The ability of Anoectochilus formosanus extract (AFE) to react with relevant biological oxidants was evaluated in this study. In addition, its effect on oxidation of low density lipoprotein (LDL) was investigated in vitro and in vivo. AFE could scavenge reactive oxygen species, such as superoxide anion and hydroxyl radical. The study of human LDL oxidation showed that AFE delayed oxidation in a concentration-dependent manner. In vivo studies also showed that oral administration of AFE delayed the oxidation of LDL from hyperlipidemic hamsters. The ability of AFE to scavenge free radicals suggests that it may be a promising anti-atherogenic agent.

scholarly journals The effects of ascorbate and dehydroascorbate on the oxidation of low-density lipoprotein

1996 ◽  
Vol 320 (2) ◽  
pp. 373-381 ◽  
Author(s):  
Suzanne E. STAIT ◽  
David S. LEAKE
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Conjugated Dienes ◽  
Ldl Oxidation ◽  
Lag Phase ◽  
Prolonged Storage ◽  
Low Density ◽  
Dependent Manner ◽  
Conjugated Diene

Ascorbate at concentrations of 60–100 µM inhibits the modification of freshly prepared low-density lipoprotein (LDL) by macrophages. With ‘moderately oxidized’ LDL (produced by prolonged storage in a refrigerator), however, ascorbate does not inhibit LDL modification by macrophages and actually modifies the LDL itself in the absence of macrophages [Stait and Leake (1994) FEBS Lett. 341, 263–267]. We have now shown that dehydroascorbate can modify both ‘fresh’ LDL and moderately oxidized LDL in a dose-dependent manner to increase its uptake by macrophages. The modification of moderately oxidized LDL by ascorbate and dehydroascorbate or of ‘fresh’ LDL by dehydroascorbate is dependent on the presence of iron or copper. In ‘fresh’ LDL, ascorbate inhibited conjugated-diene formation by copper. In moderately oxidized LDL, the number of conjugated dienes present was decreased rapidly in the presence of copper and ascorbate. Dehydroascorbate decreased the lag phase and increased the rate of copper-induced conjugated-diene formation in ‘fresh’ LDL (although in some experiments it inhibited the formation of conjugated dienes). The ascorbate-modified moderately oxidized LDL was taken up by macrophages by their scavenger receptors, as the uptake was inhibited by polyinosinic acid or fucoidan. Ascorbate and dehydroascorbate therefore have the potential to increase LDL oxidation under certain conditions, but whether or not they do so in vivo is unknown.

scholarly journals Non-oxidative modification of native low-density lipoprotein by oxidized low-density lipoprotein

1996 ◽  
Vol 316 (2) ◽  
pp. 377-380 ◽  
Author(s):  
Min YANG ◽  
David S. LEAKE ◽  
Catherine A. RICE-EVANS
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Low Density ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Process Studies

The oxidative modification of low-density lipoprotein (LDL) has been implicated in the pathogenesis of atherosclerosis, although little is known as yet about the precise mechanism of oxidation in vivo. The studies presented here demonstrate that, in the absence of cells or transition metals, oxidized LDL can modify native LDL through co-incubation in vitro such as to increase its net negative charge, in a concentration-dependent manner. The interaction is not inhibited by peroxyl radical scavengers or metal chelators, precluding the possibility that the modification of native LDL by oxidized LDL is through an oxidative process. Studies with radioiodinated oxidized LDL showed no transfer of radioactivity to the native LDL, demonstrating that fragmentation of protein and the transfer of some of the fragments does not account for the modified charge on the native LDL particle. The adjacency of native to oxidized LDL in the arterial wall may be a potential mechanism by which the altered recognition properties of the apolipoprotein B-100 may arise rapidly without oxidation or extensive modification of the native LDL lipid itself.

scholarly journals Prediabetic and diabetic in vivo modification of circulating low-density lipoprotein attenuates its stimulatory effect on adrenal aldosterone and cortisol secretion

2008 ◽  
Vol 200 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Steffi Kopprasch ◽  
Jens Pietzsch ◽  
Ishrath Ansurudeen ◽  
Juergen Graessler ◽  
Alexander W Krug ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mass Spectrometry Analysis ◽  
Ldl Oxidation ◽  
Low Density ◽  
Cortisol Secretion ◽  
Adrenocortical Cells ◽  
Cortisol Metabolism ◽  
Cortisol Release

Modification of low-density lipoprotein (LDL) and abnormal aldosterone and cortisol metabolism have been implicated in the pathogenesis of type 2 diabetes (DM2) and diabetic vascular disease. Since LDL serves as a major cholesterol source for adrenal steroidogenesis, we investigated whether LDL modification in prediabetic and diabetic subjects influences adrenocortical aldosterone and cortisol release. LDL was isolated from 30 subjects with normal glucose tolerance (NGT-LDL), 30 subjects with impaired glucose tolerance (IGT-LDL), and 26 patients with DM2 (DM2-LDL). Oxidation and glycoxidation characteristics of LDL apolipoprotein B100 of each individual was assessed by gas chromatography–mass spectrometry analysis. Human adrenocortical cells (NCI-H295R) were incubated for 24 h with 100 μg/ml LDL and after removal of supernatants stimulated for a further 24 h with angiotensin II (AngII). In supernatants, aldosterone and cortisol secretion was measured. IGT-LDL and DM2-LDL were substantially more modified than NGT-LDL. Each of the five measured oxidation/glycoxidation markers was significantly positively associated with glycemic control, measured as HbA1c. LDL from all subjects stimulated both the basal and AngII-induced aldosterone and cortisol release from adrenocortical cells. However, hormone secretion was significantly inversely related to the degree of LDL oxidation/glycoxidation. We conclude that LDL modifications in IGT and DM2 subjects may have significant clinical benefits by counteracting prediabetic and diabetic overactivity of the renin–angiotensin–aldosterone system and enhanced cortisol generation.

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.

Effects of lactic acid bacteria on low-density lipoprotein susceptibility to oxidation and aortic fatty lesion formation in hyperlipidemic hamsters

2015 ◽  
Vol 6 (3) ◽  
pp. 287-293 ◽  
Author(s):  
M. Ito ◽  
K. Oishi ◽  
Y. Yoshida ◽  
T. Okumura ◽  
T. Sato ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Streptococcus Thermophilus ◽  
Ldl Oxidation ◽  
Low Density ◽  
Lag Times

We investigated the effects of Streptococcus thermophilus YIT 2001, a strain of lactic acid bacteria, on the susceptibility of low-density lipoprotein (LDL) to oxidation and the formation of aortic fatty lesions in hyperlipidemic hamsters. S. thermophilus YIT 2001 had the highest in vitro antioxidative activity against LDL oxidation among the 79 strains of lactic acid bacteria and bifidobacteria tested, which was about twice that of S. thermophilus YIT 2084. The lag time of LDL oxidation in the YIT 2001 feeding group was significantly longer than in controls, but was unchanged in the YIT 2084 group. After the feeding of YIT 2001, lag times were prolonged and areas of aortic fatty lesions were dose-dependently attenuated, although there were no effects on plasma lipid levels. These results suggest that YIT 2001 has the potential to prevent the formation of aortic fatty lesions by inhibiting LDL oxidation.

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