Human vascular smooth muscle cells and endothelial cells lack catalase activity and are susceptible to hydrogen peroxide

Sato, Masao; Yoshioka, Kazunori; Nobunaga, Masashi; Yoshida, Kōji

doi:10.1007/bf00916279

Cited by 84 publications

(40 citation statements)

References 33 publications

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“…Our findings agree with previous data that catalase was unchanged in the aortas of Gpx1-deficient mice (33). Although catalase overexpression has been shown to limit lesion formation in apolipoprotein E-deficient mice (39), its role as a major player in the protection against atherosclerosis is questionable because catalase enzymatic activity is known to be particularly low in the vasculature (44). The expression profiles of other enzymes implicated in cellular antioxidant defense were also investigated in this study.…”

Section: Lack Of Gpx1 Does Not Increase Murine Atherosclerosissupporting

confidence: 82%

Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet

Witting

Stefanovic

Pete

et al. 2006

Journal of Lipid Research

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Oxidative stress is thought to contribute to the initiation and progression of atherosclerosis. As glutathione peroxidase-1 (Gpx1) is an antioxidant enzyme that detoxifies lipid hydroperoxides, we tested the impact of Gpx1 deficiency on atherosclerotic processes and antioxidant enzyme expression in mice fed a high-fat diet (HFD). After 12 weeks of HFD, atherosclerotic lesions at the aortic sinus were of similar size in control and Gpx1-deficient mice. However, after 20 weeks of HFD, lesion size increased further in control but not in Gpx1-deficient mice, even though plasma and aortic wall markers of oxidative damage did not differ between groups. In control mice, the expression of Gpx1 increased and that of Gpx3 decreased at the aortic sinus after 20 weeks of HFD, with no change in the expression of Gpx2, Gpx4, catalase, peroxiredoxin-6, glutaredoxin-1 and -2, or thioredoxin-1 and -2. By comparison, in Gpx1-deficient mice, the expression of antioxidant genes was unaltered except for a decrease in glutaredoxin-1 and an increase in glutaredoxin-2. These changes were associated with increased expression of the proinflammatory marker monocyte chemoattractant protein-1 in control mice but not in Gpx1-deficient mice. In summary, a specific deficiency in Gpx1 was not accompanied by an increase in markers of oxidative damage or increased atherosclerosis in a murine model of HFD-induced atherogenesis.-de Haan,

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Section: Lack Of Gpx1 Does Not Increase Murine Atherosclerosissupporting

confidence: 82%

Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet

Witting

Stefanovic

Pete

et al. 2006

Journal of Lipid Research

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“…Among the oxygen radicals. HP may be responsible for the killing of cultured endothelial eells [20], fibroblasts [21] and vascular smooth muscle cells [22]. HP can activate latent collagenase, and inhibit collagen gelation and proteoglycan synthesis by cartilage [23 25], It has been shown that latent collagenase is activated by HP-related products [26].…”

Section: [Ntroductionmentioning

confidence: 99%

Activation of complement in normal serum by hydrogen peroxide and hydrogen peroxide-related oxygen radicals produced by activated neutrophils

Sato

Nonaka

Nishimukai

et al. 1992

Clinical and Experimental Immunology

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SUMMARYNeutrophils activated by soluble parliculate stimuli generate superoxide anion and subsequently form hydrogen peroxide and other oxygen radicals. The effect o\' hydrogen peroxide on the complement system in normal serum was investigated. Treatment of normal serum with hydrogen peroxide resulted in a diminution ofthe haemolytic activity ofthe total and alternative complement pathways and the haemolytic titres of C3 and C^ but not of C2. in normal scrum. These decreases in complcEiient aclivity depended on the conccntraiion of hydrogen peroxide added to the serum. Immunoelectrophoretic analysis of hydrogen peroxide-treated serum showed ihat C3 and C5 proteins were activated. Complemeni degradation products C3a and C5a were produced in normal serum treated with hydrogen peroxide, and 20 mM EDTA abolished C3a and C5a production in hydrogen peroxide-treated scrum but 20 mM Mg-EGTA did not, Cataiase completely abolished and dimethylsulphoxidc and t>-mannitol. hydroxyl radical scavengers, partially inhibited the hydrogen peroxide-mediated complement activation. Hypochlorite. ineubated with normal serum, significantly inhibited scrum haemolytic activity, and sodium thiosulphale. a reducing agent, abolished the effect of hypochlorite. Nonnal scrum incubaled with activated neutrophils showed neutrophil chemotactic activity and decreased serum haemolytic activity, and the addition of catalase or mcthionine (5 niM) completely abolished the elTects of activated neutrophils. These results suggest that hydrogen peroxide activates complement via an alternative pathway of complement activalion and that hydroxyl radicals and other hydrogen peroxide-related species such as hypochlorite are most likely involved in hydrogen peroxidc-mcdialcd complement activation. Complement aclivation by oxygen radicals produced by activated nentrophils may be one of the mechanisms by which complement is activated in human immune complex diseases. Keywords hydrogen peroxide hypochlorite complement aetivation neutrophils[NTRODUCTION The aclivation of the complement system by immune eomplexes via the classical pathway may be involved in initiating and sustaining the inllammatory process and subsequent tissue injury in immune complex diseases such as systemic lupus erylhematosus (SLF.) and rheumatoid arlhritis (RA), The aclivation of complement at sites of immune complex deposition in tissue plays an important role in the pathogenesis of vascular injury in such diseases. Complement fragments generated from the native complement components following aetivation of complement, arc biologically active, act as inflammatory mediators and produce tissue damage by stimulating the

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“…Studies that used the manipulation of genes for antioxidant enzymes 11,12 to test the effects of oxidants on cells also corroborate the assumption that intracellular oxidative stress might play an important role in the transduction of oxidative stress from external sources to intracellular sites. Previously, Shingu et al 13 showed that endothelial cells and smooth muscle cells have very low levels of catalase activity and therefore are more susceptible to damage by H 2 O 2 . Several studies had attempted to overexpress catalase enzyme in various cell types and looked for the effect of this enzyme in preventing oxidation-related damage.…”

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confidence: 99%

Overexpression of Human Catalase Gene Decreases Oxidized Lipid-Induced Cytotoxicity in Vascular Smooth Muscle Cells

Santanam

Augé

Zhou

et al. 1999

ATVB

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Abstract-Reactive oxygen metabolites such as hydrogen peroxide (H 2 O 2 ) and oxidized fatty acids are proinflammatory and are involved in the pathophysiology of various diseases including atherosclerosis. The effects of these oxidants could be inhibited by the external addition of an antioxidant, suggesting the promotion or propagation of further oxidation. In this study, we describe the stable overexpression of human catalase in smooth muscle cells and the resistance of these cells to cytotoxicity induced not only by the addition of H 2 O 2 but also by the addition of 13-hydroperoxyoctadecadienoic acid (13-HPODE). The results pose an intriguing possibility of the generation of H 2 O 2 from a peroxidized fatty acid. Accordingly, incubation of cells with both 13-HPODE and 13-hydroxyoctadecadienoic acid resulted in the generation of intracellular H 2 O 2 . To explain the observed results by which catalase could overcome the effects of 13-HPODE, we propose that oxidized fatty acids are degraded in the cellular peroxisomes, resulting in the generation of H 2 O 2 . In other words, the cellular effects of peroxidized fatty acids could be attributed to the generation of H 2 O 2 .

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Human vascular smooth muscle cells and endothelial cells lack catalase activity and are susceptible to hydrogen peroxide

Cited by 84 publications

References 33 publications

Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet

Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet

Activation of complement in normal serum by hydrogen peroxide and hydrogen peroxide-related oxygen radicals produced by activated neutrophils

Overexpression of Human Catalase Gene Decreases Oxidized Lipid-Induced Cytotoxicity in Vascular Smooth Muscle Cells

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