Detection of Peroxynitrite-Induced Protein and DNA Modifications

Lorch, Scott A.; Lightfoot, Richard; Ohshima, Hiroshi; Virág, László; Chen, Qiping; Hertkorn, Caryn; Weiss, Marie; Souza, José Maria de; Ischiropoulos, Harry; Yermilov, Vladimir; Pignatelli, Brigitte; Masuda, Mituharu; Szabó, Csaba

doi:10.1385/1-59259-274-0:247

Cited by 8 publications

(8 citation statements)

References 2 publications

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“…They are formed initially in situ in the phospholipid domain of cell membranes subject to ROS attack and are then cleaved by phospholipases, released extracellularly, circulated, and excreted in urine. 25,30,31 A range of mass spectroscopic assays have emerged on the basis of authentic standards for individual F 2 iPs. [32][33][34][35][36][37][38] Current immunoassays directed against iPF 2␣ -III (also known as 8-iso PGF 2␣ ) are more commonly used.…”

Section: Monitoring Ros Formation In Vivomentioning

confidence: 99%

Oxidative Stress and Cardiovascular Injury

2003

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Section: Monitoring Ros Formation In Vivomentioning

confidence: 99%

Oxidative Stress and Cardiovascular Injury

2003

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“…Peroxynitrite readily reacts with proteins to form 3-nitrotyrosine, tyrosine dimers or oxidation of thiol groups [9][10][11][12] which can either lead to inactivation or enhanced degradation [13][14][15][16] of the proteins. Further, peroxynitrite can also cause adduct formation, oxidation and strand breaks in DNA [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Differential patterns of peroxynitrite mediated apoptosis in proximal tubular epithelial cells following ATP depletion recovery

et al. 2008

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Ischemia-reperfusion injury (IRI) is characterized by ATP depletion in the ischemic phase, followed by a rapid increase in reactive oxygen species, including peroxynitrite in the reperfusion phase. In this study, we examined the role of peroxynitrite on cytotoxicity and apoptosis in an in vitro model of ATP depletion-recovery. Porcine proximal tubular epithelial (LLC-PK(1)) cells were ATP depleted for either 2 h (2/2) or 4 h (4/2) followed by recovery in serum free medium for 2 h. A subset of cells was treated with 100 microM of the peroxynitrite scavenger, iron (III) tetrakis (N-methyl-4'pyridyl) porphyrin pentachloride (FeTMPyP) 30 min prior to and during treatment/recovery. Treatment with FeTMPyP reduced cytotoxicity and superoxide levels at both the 2/2 and 4/2 time points, however FeTMPyP decreased nitric oxide only at the 2/2 time point. FeTMPyP also partially blocked caspase-3 and caspase-8 activation at both 2/2 and 4/2 time points. At the 4/2 time point, FeTMPyP also partially inhibited the ATP depletion mediated increase in tumor necrosis factor alpha (TNF-alpha) and decreased Bax and FasL gene expression. These data show that peroxynitrite induces apoptosis by activation of multiple pathways depending on length and severity of insult following ATP depletion-recovery.

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“…Estos métodos continúan perfeccionándose y probablemente surjan nuevos marcadores que nos permitirán medir la acción de los RLO de una manera más exacta y precisa [21][22][23][24] .…”

Section: Monitorización De La Formación De Radicales Libres De Oxígenounclassified

Estrés oxidativo y síndrome de apneas-hipopneas del sueño

Barceló

Barbé

2005

Archivos de Bronconeumología

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Detection of Peroxynitrite-Induced Protein and DNA Modifications

Cited by 8 publications

References 2 publications

Oxidative Stress and Cardiovascular Injury

Oxidative Stress and Cardiovascular Injury

Differential patterns of peroxynitrite mediated apoptosis in proximal tubular epithelial cells following ATP depletion recovery

Estrés oxidativo y síndrome de apneas-hipopneas del sueño

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