scholarly journals Investigation of Lipoproteins Oxidation Mechanisms by the Analysis of Lipid Hydroperoxide Isomers

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1598
Author(s):  
Shunji Kato ◽  
Yusuke Osuka ◽  
Saoussane Khalifa ◽  
Takashi Obama ◽  
Hiroyuki Itabe ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Healthy Subjects ◽  
Lipid Hydroperoxide ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Enzymatic Oxidation ◽  
Human Organism ◽  
Lipid Hydroperoxides ◽  
Radical Oxidation ◽  
Oxidation Mechanisms

The continuous formation and accumulation of oxidized lipids (e.g., lipid hydroperoxides (LOOH)) which are present even in plasma lipoproteins of healthy subjects, are ultimately considered to be linked to various diseases. Because lipid peroxidation mechanisms (i.e., radical, singlet oxygen, and enzymatic oxidation) can be suppressed by certain proper antioxidants (e.g., radical oxidation is efficiently suppressed by tocopherol), in order to suppress lipid peroxidation successfully, the determination of the peroxidation mechanism involved in the formation of LOOH is deemed crucial. In this study, to determine the peroxidation mechanisms of plasma lipoproteins of healthy subjects, we develop novel analytical methods using liquid chromatography-tandem mass spectrometry (LC-MS/MS) for 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine hydroperoxide (PC 16:0/18:2;OOH) and cholesteryl linoleate hydroperoxide (CE 18:2;OOH) isomers. Using the newly developed methods, these PC 16:0/18:2;OOH and CE 18:2;OOH isomers in the low-density lipoprotein (LDL) and high-density lipoprotein (HDL) of healthy subjects are analyzed. Consequently, it is found that predominant PC 16:0/18:2;OOH and CE 18:2;OOH isomers in LDL and HDL are PC 16:0/18:2;9OOH, PC 16:0/18:2;13OOH, CE 18:2;9OOH, and CE 18:2;13OOH, which means that PC and CE in LDL and HDL are mainly oxidized by radical and/or enzymatic oxidation. In conclusion, the insights about the oxidation mechanisms shown in this study would be useful for a more effective suppression of oxidative stress in the human organism.

scholarly journals Low-density lipoprotein is the major carrier of lipid hydroperoxides in plasma. Relevance to determination of total plasma lipid hydroperoxide concentrations

1996 ◽  
Vol 313 (3) ◽  
pp. 781-786 ◽  
Author(s):  
Jaffar NOUROOZ-ZADEH ◽  
Jarad TAJADDINI-SARMADI ◽  
K. L. Eddie LING ◽  
Simon P. WOLFF
Keyword(s):  
Total Lipid ◽  
Xylenol Orange ◽  
Low Density Lipoprotein ◽  
Lipid Hydroperoxide ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Lipid Hydroperoxides ◽  
Very Low Density Lipoprotein ◽  
Low Density

High-density lipoprotein (HDL) has been proposed as the principal carrier of hydroperoxides in plasma, based upon data gathered with an HPLC-chemiluminescence technique. To test this hypothesis we have measured total lipid hydroperoxides in native plasma using the ferrous oxidation in Xylenol Orange (FOX) assay and then fractionated plasma into very-low-density lipoprotein, low-density lipoprotein (LDL) and HDL fractions. Hydroperoxides were found to accumulate principally (more than 65%) in LDL, as judged by hydroperoxide content per amount of protein or cholesterol, or expressed as a proportion of total hydroperoxide in plasma. Plasma was also incubated at 37 °C in the presence and absence of 2,2´-azo-bis-(2-amidinopropane) hydrochloride (AAPH), an azo-initiator of lipid peroxidation. The majority of hydroperoxides generated in plasma were recovered in the LDL fraction. Furthermore, when isolated lipoproteins were subject to oxidation initiated by AAPH, very-low-density lipoprotein and LDL showed the greatest propensity for hydroperoxide accumulation, whereas HDL seemed relatively resistant. Estimates for plasma and LDL peroxidation based upon techniques which measure total lipid hydroperoxides suggest that levels of hydroperoxides in plasma and LDL are far higher than that those estimates generated by ostensibly more selective techniques. Higher levels of hydroperoxides in LDL than those reported by HPLC-chemiluminescence also seem in greater accordance with other available data concerning LDL oxidation.

scholarly journals Decomposition of lipid hydroperoxides enhances the uptake of low density lipoprotein by macrophages.

1999 ◽  
Vol 46 (1) ◽  
pp. 31-42 ◽  
Author(s):  
A V Babiy ◽  
J M Gebicki
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Lipid Hydroperoxide ◽  
Significant Proportion ◽  
Density Lipoprotein ◽  
Scavenger Receptors ◽  
Lipid Hydroperoxides ◽  
Strictly Anaerobic ◽  
Low Density ◽  
Apo B

This study examined the roles of low-density lipoprotein (LDL) lipid oxidation and peroxide breakdown in its conversion to a form rapidly taken up by mouse peritoneal macrophages. Oxidation of the LDL without decomposition of the hydroperoxide groups was performed by exposure to gamma radiation in air-saturated solutions. Virtually complete decomposition of the hydroperoxides was achieved by treatment of the irradiated LDL with Cu2+ under strictly anaerobic conditions. No uncontrolled LDL uptake by macrophages occurred when the lipoprotein contained less than 150 hydroperoxide groups per particle. More extensively oxidized LDL was taken up and degraded by mouse macrophages significantly faster than the native lipoprotein. The uptake was greatly enhanced by treatment of the oxidized LDL with Cu2+. A significant proportion of the LDL containing intact or copper-decomposed LDL hydroperoxide groups accumulated within the macrophages without further degradation. Treatment of the radiation-oxidized LDL with Cu2+ was accompanied by aggregation of the particles. Competition studies showed that the oxidized LDL was taken up by macrophages via both the LDL and the scavenger receptors, whereas the copper-treated lipoprotein entered the cells only by the scavenger pathway. Phagocytosis also played an important role in the metabolism of all forms of the extensively modified LDL. Our results suggest that minimally-oxidized LDL is not recognized by the macrophage scavenger receptors unless the lipid hydroperoxide groups are decomposed to products able to derivatize the apo B protein.

scholarly journals Lipid Peroxidation

2021 ◽  
Author(s):  
Suzan Onur Yaman ◽  
Adnan Ayhanci
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Structural Changes ◽  
Lipid Membrane ◽  
Membrane Damage ◽  
Lipid Hydroperoxide ◽  
Electrolyte Balance ◽  
Lipid Hydroperoxides ◽  
Carbon Centered Radical ◽  
Cellular Components

Lipid peroxidation (LPO) is initiated by the attack of free radicals (eg OH ·, O2- and H2O2) on cellular or organelle membranes phospholipids or polyunsaturated fatty acids (PUFA), and with the formation of various types of aldehydes, ketones, alkanes, carboxylic acids and polymerization products. It is an autoxidation process that results. These products are highly reactive with other cellular components and serve as biological markers of LPO. Malondialdehyde (MDA), a toxic aldehyde end product of LPO, causes structural changes that mediate its oxidation, such as fragmentation, modification, and aggregation, especially in DNA and protein. The excessive binding of these reactive aldehydes to cellular proteins alters membrane permeability and electrolyte balance. Degradation of proteins leads to progressive degradation of the biological system mediated by oxidative stress. The chain reaction (CR) of LPO is initiated by the attack of free radicals on the PUFA of the cell membrane to form a carbon centered radical (R*). The O2 · - radical attacks the other lipid molecule to form lipid hydroperoxide (ROOH), thereby spreading the CR and forming the lipid peroxyl radical (ROO). These lipid hydroperoxides severely inhibit membrane functionality by allowing ions such as increased hardness and calcium to leak through the membrane. Damage to the lipid membrane and macromolecule oxidation can result in activation of necrotic or apoptotic tissue death pathways if severe enough.

scholarly journals Oxidation of low-density lipoprotein by hypochlorite causes aggregation that is mediated by modification of lysine residues rather than lipid oxidation

1994 ◽  
Vol 302 (1) ◽  
pp. 297-304 ◽  
Author(s):  
L J Hazell ◽  
J J M van den Berg ◽  
R Stocker
Keyword(s):  
Lipid Peroxidation ◽  
Lipid Oxidation ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Size Exclusion ◽  
Lipid Hydroperoxides ◽  
Low Density ◽  
Lysine Residues

Peroxidation of low-density lipoprotein (LDL) lipid is generally thought to represent the initial step in a series of modification reactions that ultimately transform the protein moiety of the lipoprotein into a form recognized by receptors different from those that bind native LDL. Uptake of LDL via these alternative receptors can lead to the formation of lipid-laden cells, which are typical for the early stages of atherogenesis. We have studied the oxidative modification of LDL by hypochlorite (-OCl), a powerful oxidant produced from H2O2 and chloride via the action of myeloperoxidase which is released from activated neutrophils and monocytes. Exposure of LDL to reagent or enzymically generated -OCl at 4 or 37 degrees C resulted in immediate and preferential oxidation of amino acid residues of apolipoprotein B-100, the single protein associated with LDL. Lysine residues quantitatively represented the major target and, like tryptophan, were oxidized to approximately the same extent with reagent or enzymically generated -OCl. In contrast, LDL lipid oxidation was less favoured than protein oxidation, as judged by the amounts of lipid hydroperoxides, chlorohydrins, cholesterol or fatty acid oxidation products formed. Treatment with -OCl caused aggregation of LDL, as shown by an increased turbidity of the oxidized LDL solution and elution from a size-exclusion h.p.l.c. column of high-molecular-mass LDL complexes. Chemical modification of lysine residues before oxidation with -OCl prevented aggregation, while it enhanced the extent of lipid peroxidation. Treatment of LDL with -OCl also caused the formation of carbonyl groups and release of ammonia; both these modifications were inhibited by lysine-residue modification before oxidation. These results demonstrate that aggregation reactions are dependent on initial lysine oxidation by -OCl, followed by deamination and carbonyl formation, but do not involve lipid (per)oxidation. We propose that the observed -OCl-mediated aggregation of LDL is caused, at least in part, by cross-linking of apoproteins by Schiff-base formation independently of lipid peroxidation.

Oxidative Modification of Low-Density Lipoprotein and Atherogenetic Risk in β-Thalassemia

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3936-3942 ◽  
Author(s):  
M.A. Livrea ◽  
L. Tesoriere ◽  
A. Maggio ◽  
D. D’Arpa ◽  
A.M. Pintaudi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Lipid Hydroperoxides ◽  
Low Density ◽  
Healthy Controls ◽  
The Mean ◽  
Β Carotene

We investigated the oxidative state of low-density lipoprotein (LDL) in patients with β-thalassemia to determine whether there was an association with atherogenesis. Conjugated diene lipid hydroperoxides (CD) and the level of major lipid antioxidants in LDL, as well as modified LDL protein, were evaluated in 35 β-thalassemia intermedia patients, aged 10 to 60, and compared with age-matched healthy controls. Vitamin E and β-carotene levels in LDL from patients were 45% and 24% of that observed in healthy controls, respectively. In contrast, the mean amount of LDL-CD was threefold higher and lysil residues of apo B-100 were decreased by 17%. LDL-CD in thalassemia patients showed a strong inverse correlation with LDL vitamin E (r = −0.784; P < .0001), while a negative trend was observed with LDL-β–carotene (r = −0.443; P = .149). In the plasma of thalassemia patients, malondialdehyde (MDA), a byproduct of lipid peroxidation, was increased by about twofold, while vitamin E showed a 52% decrease versus healthy controls. LDL-CD were inversely correlated with plasma vitamin E (r = −0.659; P < .0001) and correlated positively with plasma MDA (r = 0.621; P < .0001). Plasma ferritin was positively correlated with LDL-CD (r = 0.583; P =.0002). No correlation was found between the age of the patients and plasma MDA or LDL-CD. The LDL from thalassemia patients was cytotoxic to cultured human fibroblasts and cytotoxicity increased with the content of lipid peroxidation products. Clinical evidence of mild to severe vascular complications in nine of the patients was then matched with levels of LDL-CD, which were 36% to 118% higher than the mean levels of the patients. Our results could account for the incidence of atherogenic vascular diseases often reported in β-thalassemia patients. We suggest that the level of plasma MDA in β-thalassemia patients may represent a sensitive index of the oxidative status of LDL in vivo and of its potential atherogenicity.

scholarly journals LIPID PEROXIDATION IN MULTIPLE ORGAN FAILURE CAUSED BY ASSOCIATED CHEST AND HIP TRAUMA

2017 ◽  
Author(s):  
M. I. Maruschak ◽  
M. M. Khudobyak ◽  
I. Ya. Krynytska ◽  
I. V. Antonyshyn
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Free Radical Oxidation ◽  
Multiple Organ ◽  
Control Group ◽  
Lipid Hydroperoxides ◽  
Radical Oxidation ◽  
Post Traumatic

Background. The injured with polytrauma are classified as extremely severe patients, as their emergency care and intensive care is followed by significant difficulties, frequent development of complications, high mortality and survivors disability.Objective. This study is aimed to evaluate the effect of lipid peroxidation in heart, lungs, liver and blood of rats in early and late periods of combined traumatic injury of chest and hips and to establish their influence on the development of multiple organ failure.Methods. The study was conducted on 70 adult male white nonlinear rats. It was determined the content of lipid hydroperoxides and concentration of TBA-active products in erythrocyte mass, heart, lungs and liver.Results. The data prove activation of free radical oxidation at the first day of post-traumatic period. Analysis of the data evidences the increase in of lipid hydroperoxides (HPL) rate in liver homogenate in group E1 in 1.5 times, in all subsequent periods of the research the increase in rate fluctuated within 1.9-2.0 times. In blood and heart the HPL rate increased twice in group E1, reached maximum in group E2 and gradually decreased till the end of the experiment, data exceeded the control group. The highest level of HPL was determined in lung tissues (r≤0.01). In the post traumatic period the highest TBA-AP was detected in lungs and liver.Conclusions. In case of simulated trauma (injury of chest with fractures of both hips) hyperactivation processes of free radical oxidation is observed in 1 day, reaching a peak in 7-14 days of post-traumatic period in blood, tissues, liver, heart and lungs if compared to the control group causing multiple organ failure.

Oxidative Modification of Low-Density Lipoprotein and Atherogenetic Risk in β-Thalassemia

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3936-3942 ◽  
Author(s):  
M.A. Livrea ◽  
L. Tesoriere ◽  
A. Maggio ◽  
D. D’Arpa ◽  
A.M. Pintaudi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Lipid Hydroperoxides ◽  
Low Density ◽  
Healthy Controls ◽  
The Mean ◽  
Β Carotene

Abstract We investigated the oxidative state of low-density lipoprotein (LDL) in patients with β-thalassemia to determine whether there was an association with atherogenesis. Conjugated diene lipid hydroperoxides (CD) and the level of major lipid antioxidants in LDL, as well as modified LDL protein, were evaluated in 35 β-thalassemia intermedia patients, aged 10 to 60, and compared with age-matched healthy controls. Vitamin E and β-carotene levels in LDL from patients were 45% and 24% of that observed in healthy controls, respectively. In contrast, the mean amount of LDL-CD was threefold higher and lysil residues of apo B-100 were decreased by 17%. LDL-CD in thalassemia patients showed a strong inverse correlation with LDL vitamin E (r = −0.784; P &lt; .0001), while a negative trend was observed with LDL-β–carotene (r = −0.443; P = .149). In the plasma of thalassemia patients, malondialdehyde (MDA), a byproduct of lipid peroxidation, was increased by about twofold, while vitamin E showed a 52% decrease versus healthy controls. LDL-CD were inversely correlated with plasma vitamin E (r = −0.659; P &lt; .0001) and correlated positively with plasma MDA (r = 0.621; P &lt; .0001). Plasma ferritin was positively correlated with LDL-CD (r = 0.583; P =.0002). No correlation was found between the age of the patients and plasma MDA or LDL-CD. The LDL from thalassemia patients was cytotoxic to cultured human fibroblasts and cytotoxicity increased with the content of lipid peroxidation products. Clinical evidence of mild to severe vascular complications in nine of the patients was then matched with levels of LDL-CD, which were 36% to 118% higher than the mean levels of the patients. Our results could account for the incidence of atherogenic vascular diseases often reported in β-thalassemia patients. We suggest that the level of plasma MDA in β-thalassemia patients may represent a sensitive index of the oxidative status of LDL in vivo and of its potential atherogenicity.

scholarly journals Age-related characteristics of lipid peroxidation and antioxidant defense system of ostriches (Struthio camelus domesticus)

2020 ◽  
Vol 10 (1) ◽  
pp. 168-174
Author(s):  
V. M. Polishchuk ◽  
S. I. Tsekhmistrenko ◽  
S. A. Polishchuk ◽  
N. V. Ponomarenko ◽  
N. V. Rol ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Glutathione Reductase ◽  
Antioxidant System ◽  
Free Radical Oxidation ◽  
Antioxidant Defense System ◽  
Egg Laying ◽  
Lipid Hydroperoxides ◽  
Diene Conjugates ◽  
Radical Oxidation ◽  
Age Related

We studied the intensity of lipid peroxidation (LPO) and the status of antioxidant system in blood of 6-60 months ostriches. We proved that specific functioning of the antioxidant system and the accumulation of lipid peroxidation intermediates characterized each period of ostrich life cycle. Thus, the period of puberty was accompanied by intensification of lipid peroxidation in ostrich blood serum and this was confirmed by a significant increase in the amount of TBA-reactive substances. This could be the consequence of the insufficient activity of enzymes of the antioxidant system (catalase, glutathione-S-transferase, glutathione reductase). The egg-laying peak was characterized by the increased body metabolism, which caused the activation of free-radical oxidation. The concentration of lipid hydroperoxides and diene conjugates increased and the TBA-reactive substances did not change significantly. Antioxidant protection of the blood during this period was mainly caused by the significant concentration of ceruloplasmin and reduced glutathione due to the increased activity of glutathione reductase. We supposed that the period of puberty and intensive period of egg laying in ostriches should be referred as the periods of stress of metabolic processes with increased intensity of lipid oxidation, associated with the certain changes in ostrich physiological and functional state.

Lipid peroxidation and its significance in the pathology of internal organs

1986 ◽  
Vol 67 (3) ◽  
pp. 200-203
Author(s):  
I. G. Salikhov ◽  
K. N. Agisheva
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Cell Membrane ◽  
Oxidation Reaction ◽  
Lipid Hydroperoxide ◽  
Free Radical Oxidation ◽  
Cell Membrane Permeability ◽  
Internal Organs ◽  
Radical Oxidation ◽  
A Chain

Lipid peroxidation is a chain free-radical oxidation reaction of lipids by molecular oxygen, the product of which is lipid hydroperoxide. The most important effect of lipid peroxidation products on cell membrane permeability. Peroxidation or a mechanism close to it is involved in the regulation of the transport of substances across membranes in normally metabolizing cells.

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