Possible involvement of myeloperoxidase in lipid peroxidation

Stelmaszyńska, Teresa; Kukovetz, E.; Egger, G.; Schaur, R. J.

doi:10.1016/0020-711x(92)90237-u

Cited by 85 publications

(37 citation statements)

References 25 publications

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“…The detection of the enzyme in diseased human vascular tissue is strong support for the hypothesis that myeloperoxidase, with its ability to promote lipoprotein oxidation by pathways involving HOCl and tyrosyl radical (47)(48)(49)(50), might be a pivotal agent in the development of atherosclerotic lesions.…”

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confidence: 79%

“…Because C1-is abundant in plasma, one important product of the myeloperoxidase-H202 system is probably HOCl (42)(43)(44)(45), which oxidizes unsaturated lipids (37,38) and reactive protein groups such as thiols, amines, and hemes (39)(40)(41). Recent studies reveal that HOC1 modifies LDL (47)(48)(49), increasing its negative charge and forming products that stimulate cholesterol deposition in macrophages (49). Lipoproteins with similar properties have been isolated from atherosclerotic lesions ( 16,17).…”

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confidence: 99%

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Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions.

et al. 1994

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confidence: 79%

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confidence: 99%

Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions.

et al. 1994

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“…Lipid peroxidation occurs via ROS generated not only by the xanthine-XO system but also by activated NADPH oxidoreductase in neutrophils (39,40). It is also known that MPO mediates lipid peroxidation in the presence of hydrogen peroxide with halide ions (41). In the present study, teprenone pre-administered to compound 48 / 80-treated rats attenuated the increased content of gastric mucosal TBARS, an index of lipid peroxidation, found at 3 h after the treatment in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Teprenone Against Acute Gastric Mucosal Lesions Induced by Compound 48/80, a Mast Cell Degranulator, in Rats

et al. 2003

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Abstract. The protective effect of teprenone, an anti-ulcer drug, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48 / 80 (0.75 mg / kg). Teprenone (50, 100, or 200 mg / kg) was orally administered 0.5 h before compound 48/ 80 treatment. Administered teprenone prevented gastric mucosal lesion development found at 3 h after compound 48 / 80 treatment dose-dependently, although no dose of teprenone affected the decreased gastric mucosal blood flow and increased serum serotonin and histamine concentrations found at 3 h after the tresatment. Increases in the activities of myeloperoxdiase (an index of neutrophil infiltration) and xanthine oxidase and the content of thiobarbituric acid reactive substances (an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus occurred in gastric mucosal tissues at 3 h after compound 48 / 80 treatment. Administered teprenone dose-dependently attenuated all these changes found at 3 h after compound 48 / 80 treatment. These results indicate that orally administered teprenone protects against compound 48 / 80-induced acute gastric mucosal lesions in rats possibly through its stimulatory action on gastric mucus synthesis and secretion and its inhibitory action on neutrophil infiltration and enhanced lipid peroxidation in the gastric mucosal tissue.

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“…42) It is also known that MPO mediates lipid peroxidation in the presence of H 2 O 2 with halide ions. 43) Therefore, a part of the aforementioned reduction of gastric mucosal TBARS content in C48/80-treated rats by vitamin E administration may be due to the inhibitory effect of the administered vitamin on neutrophil infiltration into gastric mucosal tissues. We have reported that an increase in the gastric mucosal activity of XO, an enzyme to generate O 2 Ϫ and H 2 O 2 , in the presence of hyoxanthine or xanthine, is mainly associated with acute gastric mucosal lesion progression in rats treated with C48/80, and have suggested that this increase in gastric mucosal XO activity is closely related to neutrophil infiltration into the gastric mucosal tissue.…”

Section: Discussionmentioning

confidence: 99%

Effect of Oral Vitamin E Administration on Acute Gastric Mucosal Lesion Progression in Rats Treated with Compound 48/80, a Mast Cell Degranulator

Ohta

Kobayashi

Imai

et al. 2006

Biological & Pharmaceutical Bulletin

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Compound 48/80 (C48/80) is known to cause degranulation of connective tissue mast cells, but not mucosal mast cells, with release of serotonin and histamine from the cells. 1,2) We have shown in rats with a single C48/80 treatment that the development of gastric mucosal lesions occurs with decreases in Se-glutathione peroxidase (Se-GSHpx) activity and vitamin E and hexosamine levels and increases in neutrophil infiltration, xanthine oxidase (XO) activity, and lipid peroxide level in the gastric mucosal tissue and that gastric mucosal blood flow changes like ischemia-reperfusion during gastric mucosal lesion development.3) We have also shown in rats treated once with C48/80 that neutrophils infiltrating into the gastric mucosal tissue participate in gastric mucosal lesion formation and progression, while the xanthine-XO system in the gastric mucosal tissue takes part mainly in the lesion progression. 4) Furthermore, it has been shown in rats treated once with C48/80 that acutely released endogenous serotonin contributes to gastric mucosal lesion formation, while released endogenous histamine mainly contributes to the lesion progression, although gastric acid plays no important role in the pathogenesis of the C48/80-induced gastric mucosal lesion.3,5) Ascorbic acid (vitamin C) is a water-soluble antioxidant and it scavenges reactive oxygen species (ROS), such as superoxide radical (O 2 Ϫ ), hydroxyl radical (OH . ), hydrogen peroxide (H 2 O 2 ), singlet oxygen, and hypochlorus acid, by itself and also supports the chainbreaking antioxidant action of vitamin E by reducing vitamin E radical to vitamin E at the liquid/aqueous interface. [6][7][8][9][10][11] In addition, ascorbic acid prevents neutrophil adherence to endothelium by scavenging ROS derived from activated neutrophils.12) Our recent reports have shown that ascorbic acid content decreases with a concomitant decrease in vitamin E content during lesion progression in the gastric mucosa of rats treated once with C48/80 and that gastric mucosal ascorbic acid plays a critical role in the progression of C48/80-induced gastric mucosal lesions, which is closely associated with its antioxidant and anti-inflammatory actions in the gastric mucosa. 13,14) Vitamin E is a lipid-soluble antioxidant and it functions as a chain-breaking antioxidant for lipid peroxidation in cell membranes and also as a scavenger of ROS such O 2 Ϫ , OH . , and singlet oxygen. 15) Vitamin E exerts an anti-inflammatory action by inhibiting the production O 2 Ϫ in activated neutrophils, adhesion of neutrophils to endothelial cells, and transendothelial migration of neutrophils. [16][17][18][19][20] Yoshikawa et al. 21) reported that both a decrease in gastric mucosal vitamin E level and an increase in gastric mucosal lipid peroxidation occurred during the development of ischemia-reperfusion-induced gastric mucosal injury in rats and that the severity of ischemia-reperfusion-induced gastric mucosal injury was enhanced in vitamin E-deficient rats. Naito et al. 22) have shown in nitric oxide-depl...

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Possible involvement of myeloperoxidase in lipid peroxidation

Cited by 85 publications

References 25 publications

Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions.

Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions.

Protective Effect of Teprenone Against Acute Gastric Mucosal Lesions Induced by Compound 48/80, a Mast Cell Degranulator, in Rats

Effect of Oral Vitamin E Administration on Acute Gastric Mucosal Lesion Progression in Rats Treated with Compound 48/80, a Mast Cell Degranulator

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