Peroxynitrite: an endogenous oxidizing and nitrating agent

Ducrocq, Claire; Blanchard, B.; Pignatelli, Brigitte; Ohshima, Hiroshi

doi:10.1007/s000180050357

Cited by 254 publications

(174 citation statements)

References 96 publications

(127 reference statements)

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“…Important sources of endogenous oxygen radicals are phagocytic cells such as neutrophils and macrophages [32]. It has been proposed that reactive oxygen species (ROS) including nitrogen oxide generated in inflamed tissues can cause injury to target cells and also damage DNA, which contributes to carcinogenic processes [33][34][35]. Based on the above overall model, two mechanisms for nickel-induced oxidative DNA damage have been proposed as follows: all the nickel compounds tested induced indirect damage through inflammation, and Ni 3 S 2 also showed direct oxidative DNA damage through H 2 O 2 formation.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity and apoptotic effects of nickel oxide nanoparticles in cultured HeLa cells.

Ada

Türk²,

Oğuztüzün³

et al. 2011

Folia Histochem Cytobiol.

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Abstract:The aim of this study was to observe the cytotoxicity and apoptotic effects of nickel oxide nanoparticles on human cervix epithelioid carcinoma cell line (HeLa). Nickel oxide precursors were synthesized by an nickel sulphate-excess urea reaction in boiling aqueous solution. The synthesized NiO nanoparticles (<200 nm) were investigated by X-ray diffraction analysis and transmission electron microscopy techniques. For cytotoxicity experiments, HeLa cells were incubated in 50-500 μg/mL NiO for 2, 6, 12 and 16 hours. The viable cells were counted with a haemacytometer using light microscopy. The cytotoxicity was observed low in 50-200 μg/mL concentration for 16 h, but high in 400-500 μg/mL concentration for 2-6 h. HeLa cells' cytoplasm membrane was lysed and detached from the well surface in 400 μg/mL concentration NiO nanoparticles. Double staining and M30 immunostaining were performed to quantify the number of apoptotic cells in culture on the basis of apoptotic cell nuclei scores. The apoptotic effect was observed 20% for 16 h incubation.

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity and apoptotic effects of nickel oxide nanoparticles in cultured HeLa cells.

Ada

Türk²,

Oğuztüzün³

et al. 2011

Folia Histochem Cytobiol.

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“…It inactivates mitochondrial aconitase by interacting with its iron-sulfur cluster [9]. The most common peroxynitrite-induced change in peptide chains is thiol oxidation of cysteines resulting in disulfide bonds or thiyl radicals that can react with oxygen to generate more reactive oxygen species or with NO to form nitrosothiols [15]. Cysteine modifications by peroxynitrite cause inactivation of several enzymes involved in generation of ATP including glyceraldehyde-3-phosphate dehydrogenase, NADH dehydrogenase, succinate dehydrogenase, cytochrome c reductase, and ATP synthase [10,12,17].…”

Section: Discussionmentioning

confidence: 99%

“…Peroxynitrite is a strong oxidant that can damage macromolecules by reacting with them directly [9][10][11][12][13][14][15][16][17][18] or it can generate other strong oxidants such as hydroxyl or carbonate radicals [19]. Peroxynitrite is generated from nitric oxide (NO) and superoxide radicals [20].…”

Section: Introductionmentioning

confidence: 99%

Blockade of neuronal nitric oxide synthase reduces cone cell death in a model of retinitis pigmentosa

Komeima

Usui

Shen

et al. 2008

Free Radical Biology and Medicine

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Retinitis pigmentosa (RP) is a group of diseases in which many different mutations cause rod photoreceptor cells to die and then gradually cone photoreceptors die due to progressive oxidative damage. In this study, we have shown that peroxynitrite-induced nitrosative damage also occurs. In the rd1 mouse model of RP, there was increased staining for S-nitrosocysteine and nitrotyrosine protein adducts that are generated by peroxynitrite. Peroxynitrite is generated from nitric oxide (NO) and superoxide radicals. After degeneration of rods, injection of hydroethidine resulted in strong fluorescence in the retina of rd1 mice indicating high levels of superoxide radicals, and this was reduced, as was nitrotyrosine staining, by apocynin suggesting that over action of NADP(H) oxidase is at least partially responsible. Treatment of rd1 mice with a mixture of nitric oxide synthase (NOS) inhibitors markedly reduced S-nitrosocysteine and nitrotyrosine staining and significantly increased cone survival, indicating that NO-derived peroxynitrite contributes to cone cell death. Treatment with 7-nitroindazole, a relatively specific inhibitor of neuronal NOS, also significantly reduced cone cell death, but aminoguanidine, a relatively specific inhibitor of inducible NOS, did not. These data suggest that NO generated by neuronal NOS exacerbates oxidative damage to cones in RP and that combined therapy to reduce NO and oxidative stress should be considered.

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“…The product of O 2 . ϩ NO, ONOO Ϫ , mostly rearranges to form biologically inert nitrite or reacts with GSH to form the NO donor GSNO (19,23,24). However, when the [NO] approaches that of SOD, the resulting high levels of ONOO Ϫ produce a number of cell-damaging effects (19,24).…”

mentioning

confidence: 99%

Activation of Constitutive Nitric-oxide Synthase Activity Is an Early Signaling Event Induced by Ionizing Radiation

Leach

Black

Schmidt‐Ullrich

et al. 2002

Journal of Biological Chemistry

130

114

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Ionizing radiation at clinical dose levels activates both pro-and anti-proliferative signal transduction pathways, the balance of which determines cell fate. The initiating and amplifying mechanisms involved in the activation are poorly understood. We demonstrate that one mechanism involves stimulation of constitutive nitric-oxide synthase (NOS) activity. NOS activity of Chinese hamster ovary cells was measured by the arginine 3 citrulline conversion assay. Irradiation stimulated a transient activation of NOS with maximal activity at 5 min of post-irradiation. Western blot analysis and genetic manipulation by overexpression of wild type or dominant negative NOS mutant identify the radiationinduced isoform as NOS-1. Further evidence that NOS-1 is activated by radiation was the demonstration of radiation-induced cGMP formation in cells transiently transfected with the NO-dependent soluble guanylate cyclase. Protein Tyr nitration, a footprint of peroxynitrite formation, followed radiation exposure and was inhibited by expression of a dominant negative NOS-1 mutant. Radiation-induced ERK1/2 kinase activity, a cytoprotective response to radiation, was also blocked by inhibiting NOS activity. These experiments establish NOdependent signal transduction pathways as being radioresponsive. Given the lipophilic and relatively stable properties of NO, these results also suggest a possible mechanism by which ionization events in one cell may activate signaling processes in adjacent cells.

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Peroxynitrite: an endogenous oxidizing and nitrating agent

Cited by 254 publications

References 96 publications

Cytotoxicity and apoptotic effects of nickel oxide nanoparticles in cultured HeLa cells.

Cytotoxicity and apoptotic effects of nickel oxide nanoparticles in cultured HeLa cells.

Blockade of neuronal nitric oxide synthase reduces cone cell death in a model of retinitis pigmentosa

Activation of Constitutive Nitric-oxide Synthase Activity Is an Early Signaling Event Induced by Ionizing Radiation

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