Reaction of Phosphatidylcholine Hydroperoxide in Human Plasma: The Role of Peroxidase and Lecithin:Cholesterol Acyltransferase

Nagata, Yutaka; Yamamoto, Yorihiro; Niki, Etsuo

doi:10.1006/abbi.1996.0187

Cited by 34 publications

(30 citation statements)

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“…As the antioxidative side plasma lecithin:cholesterol acyltransferase (LCAT) and apolipoprotein A-I (apoA-I) were studied. These substances are known to eliminate LOOH [11,12,13,14,15, 21, 22]. From a comprehensive evaluation of these parameters we found that CE-OOH was specifically decreased in relation to apoA-I even under the pro-oxidative conditions of HD which leaded us to conclude HD is antioxidative.…”

Section: Introductionmentioning

confidence: 82%

Elimination of Lipid Peroxide during Hemodialysis

Obara

Hirayama²,

Gotoh³

et al. 2007

Nephron Clin Pract

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Background/Aims: This study is aimed to show the antioxidative effect of hemodialysis (HD) by demonstrating the elimination of toxic lipid peroxides. Methods: Blood samples were obtained from patients on regular maintenance HD before and 15, 30, 60, 120 and 240 min after the start of each HD session. Plasma cholesteryl ester hydroperoxide (CE-OOH), phosphatidylcholine hydroperoxide (PC-OOH), and eliminators of lipid peroxides (LOOH) such as apolipoprotein A-I (apoA-I) and lecithin:cholesterol acyltransferase (LCAT) were investigated. The hydroxyl radical scavenging activity was measured for the evaluation of the pro-oxidative side. Results: CE-OOH and PC-OOH were elevated in patients with chronic kidney disease both on and not on HD, while these values were much higher in HD patients. CE-OOH quickly dropped during the first 30 min of HD, then gradually decreased until 240 min. CE-OOH concentrations were related to those of apoA-I. In contrast, PC-OOH showed an increase 30 min after the start of HD, a change which resembled that of LCAT and was the reverse of the hydroxyl radical scavenging activity. Conclusion: These results demonstrate the antioxidative action through CE-OOH elimination involving apoA-I. The pro- and antioxidative effects of HD on LOOH are not uniform but PC-OOH is mainly influenced prooxidatively.

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Section: Introductionmentioning

confidence: 82%

Elimination of Lipid Peroxide during Hemodialysis

Obara

Hirayama²,

Gotoh³

et al. 2007

Nephron Clin Pract

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“…Phosphatidylcholine is one of the major components of human lipoproteins, and PCOOH is expected to be an important product of the oxidation of low-density lipoproteins [15]. HD using bioincompatible membranes induces neutrophil activation as evidenced by overexpression of adhesion molecules, elevation of cytosolic calcium, release of polymorphonuclear leukocyte granular enzymes, and generation of reactive oxygen species [6]which cause lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Hemodialysis Does Not Influence the Peroxidative State Already Present in Uremia

Hirayama

Nagase

Gotoh

et al. 2000

Nephron

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Hemodialysis (HD) patients are exposed to high oxidative stress, however, the nature of this stress is still unclear. In this study, we employed a specific lipid peroxidative product, phosphatidylcholine hydroperoxide (PCOOH), and evaluated the peroxidative effect of end stage renal disease by measuring thiobarbituric acid reactive substances (TBARS) and PCOOH in both plasma and erythrocyte membrane. We also surveyed plasma TBARS and PCOOH before and after HD sessions thereby assessing oxidative stress by a single HD procedure. The plasma TBARS level of healthy controls was 2.9 ± 0.4 nmol/ml. Those of HD patients before and after HD session were 5.1 ± 1.4 and 3.1 ± 0.5 nmol/ml, respectively, and the pre-HD plasma TBARS levels were significantly higher than those of controls and after HD. The Plasma PCOOH concentration of patients before HD was 119.7 ± 58.4 pmol/ml and was significantly higher than that of controls which was 88.6 ± 14.3 pmol/ml. After HD, the plasma PCOOH level decreased to 103.2 ± 36.0 pmol/ml, which was still significantly higher than that of controls. In erythrocytes, the PCOOH level of patients was 259.3 ± 105.4 nmol/g RBC and was significantly higher than that of controls with 88.6 ± 32.0 nmol/g RBC. Analyzed with respect to the cause of renal disease, the polycystic kidney disease patients showed significantly lower plasma PCOOH levels than the others. These results suggest that there is an increase of lipid peroxidation in both plasma and erythrocytes of HD patients, though this oxidative stress was not brought about by HD.

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“…Although identified and purified by its ability to hydrolyze PAF, this LDL-and high density lipoprotein-associated enzyme (62) functions as an oxidized phospholipid phospholipase (63). Other activities have also been suggested to contribute to the accumulation of LPC in oxidized lipoprotein particles (64,65) in conjunction with the PAF acetylhydrolase.…”

Section: Lysophosphatidylcholinementioning

confidence: 99%

Biologically Active Oxidized Phospholipids

McIntyre¹,

Zimmerman²,

Prescott³

1999

Journal of Biological Chemistry

145

105

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Oxidants and free radicals are deleterious in many ways, and organisms employ numerous approaches to block their production or limit their damage. Hydrogen atoms adjacent to olefinic bonds are susceptible to oxidative attack and those between unconjugated olefinic bonds especially so. Lipids are a rich source of these bonds and so are a primary target for oxidative reactions. Lipid oxidation is problematic as the many oxidative chemical reactions are not controlled and constrained by enzymes and may show exponential reaction rates, and some of the products of the attack are highly reactive species that modify proteins and DNA. This review summarizes current information about another outcome of the uncontrolled attack on cellular and circulating phospholipids, the generation of potent biologically active compounds that activate components of the immune and inflammatory systems.The biologically active species discussed here include oxidized phosphatidylcholines with biologic activity similar to platelet-activating factor (PAF), 1 oxidized phosphatidylcholines that stimulate responses through ways other than the PAF receptor, and the lysophosphatidylcholines that result from the enzymatic metabolism of these modified phospholipids. Oxidation products that mimic the properties of a wide variety of arachidonate metabolites are discussed in a separate review in this series (FitzGerald et al. (85)), as is a study of the effects of cholesterol oxidation (Chisolm et al. (86)). We will briefly mention the role of PAF acetylhydrolase in the catabolism of oxidized phospholipids. With the structures of some biologically active oxidation products deciphered, there is physical evidence to show that oxidatively modified phospholipids accumulate in vivo. This suggests that potent biologic mediators can arise from uncontrolled chemical reactions when the antioxidant defenses of the organism are overwhelmed. One area where such newly formed species subvert physiologic events is atherogenesis, but exposure to cigarette smoke, reperfusion injury, and stroke are also likely candidates for inappropriate events initiated or propagated by biologically active oxidized phospholipids. Lipid OxidationOxidative reactions of free fatty acids have been defined (e.g. Refs. 1-3), and oxidation of fatty acyl residues esterified in phospholipids appears to proceed in a similar fashion. The initial oxidative attack on polyunsaturated fatty acids generates alkyl radicals and then with the addition of oxygen, alkoxy radicals and peroxides. Arachidonate when oxidized enzymatically generates hydroperoxyeicosatetraenoates, hydroxyeicosatetraenoates, prostaglandins, and leukotrienes. A larger series of stereo and positional isomers known as isoprostanes, isothromboxanes, and isoleukotrienes (4, 5) is produced when arachidonate is nonenzymatically oxidized by a series of competing chemical reactions.

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Reaction of Phosphatidylcholine Hydroperoxide in Human Plasma: The Role of Peroxidase and Lecithin:Cholesterol Acyltransferase

Cited by 34 publications

References 0 publications

Elimination of Lipid Peroxide during Hemodialysis

Elimination of Lipid Peroxide during Hemodialysis

Hemodialysis Does Not Influence the Peroxidative State Already Present in Uremia

Biologically Active Oxidized Phospholipids

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