Inhibition of low‐density lipoprotein oxidation by nitric oxide Potential role in atherogenesis

Hogg, Neil; Kalyanaraman, B.; Joseph, Joy; Struck, Andrew; Parthasarathy, S.

doi:10.1016/0014-5793(93)81706-6

Cited by 381 publications

(186 citation statements)

References 34 publications

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“…The former effect is attributed to the formation of the toxic peroxynitrite after reaction with O 2 Ϫ [11]. The latter effect is not well defined, although inhibition of oxidative killing of Chinese hamster V79 cells [27], attenuation of low-density lipoprotein oxidation [28], and prevention of myocardial ischemiareperfusion injury [10] have been demonstrated. Our goal was to understand the interactive role of NO and ROI in cellular events that culminate in PMN-mediated EC injury.…”

Section: Discussionmentioning

confidence: 99%

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

Kausalya

Nath

1998

Journal of Leukocyte Biology

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Section: Discussionmentioning

confidence: 99%

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

Kausalya

Nath

1998

Journal of Leukocyte Biology

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“…Human monocytes were isolated from buffy coats of healthy donors as previously described (36). After Ficoll gradient centrifugation, monocytes were cultured under adherent conditions in six-well plates in RPMI 1640 supplemented with 10% human serum AB, 1% nonessential amino acids, 1 mM sodium pyruvate, 2 mM L-glutamine, 100 U/ml penicillin, and 100 FIGURE 1.…”

Section: Culture Of Human Primary Monocyte-derived Macrophagesmentioning

confidence: 99%

Dualism of Oxidized Lipoproteins in Provoking and Attenuating the Oxidative Burst in Macrophages: Role of Peroxisome Proliferator-Activated Receptor-γ

Fischer

Knethen

Brüne

2002

The Journal of Immunology

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Activation and deactivation of macrophages are of considerable importance during the development of various disease states, atherosclerosis among others. Macrophage activation is achieved by oxidized lipoproteins (oxLDL) and is determined by oxygen radical (ROS) formation. The oxidative burst was measured by flow cytometry and quantitated by oxidation of the redox-sensitive dye dichlorodihydrofluorescein diacetate. Short-time stimulation dose-dependently elicited ROS formation. Diphenylene iodonium prevented ROS formation, thus pointing to the involvement of a NAD(P)H oxidase in producing reduced oxygen species. In contrast, preincubation of macrophages with oxLDL for 16 h showed an attenuated oxidative burst upon a second contact with oxLDL. Taking into account that oxLDL is an established peroxisome proliferator-activated receptor-γ (PPARγ) agonist and considering the anti-inflammatory properties of PPARγ, we went on and showed that a PPARγ agonist such as ciglitazone attenuated ROS formation. Along that line, major lipid peroxidation products of oxLDL, such as 9- and 13-hydroxyoctadecadienoic acid, shared that performance. Supporting evidence that PPARγ activation accounted for reduced ROS generation came from studies in which proliferator-activated receptor response element decoy oligonucleotides, but not a mutated oligonucleotide, supplied in front of oxLDL delivery regained a complete oxidative burst upon cell activation. We conclude that oxLDL not only elicits an oxidative burst upon first contact, but also promotes desensitization of macrophages via activation of PPARγ. Desensitization of macrophages may have important consequences for the behavior of macrophages/foam cells in atherosclerotic lesions.

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“…In conprotection against AS-mediated cytotoxicity. Treat-trast, NO can protect cells from damage caused by reacment of V79 cells with L-buthionine sulfoximine to re-tive oxygen species (ROS) (4-6), as a result of different duce intracellular glutathione markedly enhanced AS chemical reactions than those involving RNOS (7)(8)(9)(10).…”

mentioning

confidence: 99%

The Cytotoxicity of Nitroxyl: Possible Implications for the Pathophysiological Role of NO

Wink

Feelisch

Fukuto

et al. 1998

Archives of Biochemistry and Biophysics

206

167

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or superoxide, can generate reactive nitrogen oxide spe-AS was found to be cytotoxic to Chinese hamster V79 cies (RNOS) 2 , which can oxidize nitrate, or nitrosate, lung fibroblast cells over a concentration range of 2-4 mM. The presence of equimolar ferricyanide (Fe(III)-other biomolecules (2, 3). RNOS are proposed to medi-(CN 6 ) 30 ), which converts NO 0 to NO, afforded dramatic ate various toxic and cytotoxic mechanisms. In conprotection against AS-mediated cytotoxicity. Treat-trast, NO can protect cells from damage caused by reacment of V79 cells with L-buthionine sulfoximine to re-tive oxygen species (ROS) (4-6), as a result of different duce intracellular glutathione markedly enhanced AS chemical reactions than those involving RNOS (7-10).cytotoxicity, which suggests that GSH is critical for NO participates in chemical reactions associated cellular protection against the toxicity of NO 0 . Fur-with both oxidative and nitrosative stress which can ther experiments showed that low molecular weight have deleterious consequences in vivo. Studies suggest transition metal complexes associated with the forma-that there exists a balance between NO and two of tion of reactive oxygen species are not involved in AS-the major reactive nitrogen oxide species, dinitrogen mediated cytotoxicity since metal chelators had no ef-trioxide (N 2 O 3 ) and peroxynitrite (ONOO 0 ) (11-13) fect. However, under aerobic conditions, AS was more that can determine the toxicological outcome under toxic than under hypoxic conditions, suggesting that oxygen dramatically enhanced AS-mediated cytotoxicity. At a molecular level, AS exposure resulted in DNA 2 Abbreviations used: RNOS, reactive nitrogen oxide species; AS, double strand breaks in whole cells, and this effect was Angelis's salt; DETAPAC, diethylenetriaminepentaacetic acid; DF, desferrioxime; TPH, tempol-H; NADPH, b-nicotinamide adenine dinucleotide phosphate; PBS, phosphate-buffered saline; GSH, intra-1 To whom correspondence and reprint requests should be ad-cellular glutathione; ER, enhancement ratio; ESR, electron spin resonance. dressed. Fax: (301) 480-2238. 66

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Inhibition of low‐density lipoprotein oxidation by nitric oxide Potential role in atherogenesis

Cited by 381 publications

References 34 publications

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

Dualism of Oxidized Lipoproteins in Provoking and Attenuating the Oxidative Burst in Macrophages: Role of Peroxisome Proliferator-Activated Receptor-γ

The Cytotoxicity of Nitroxyl: Possible Implications for the Pathophysiological Role of NO

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