The roles of hydrogen peroxide and superoxide as messengers in the activation of transcription factor NF-κB

Schmidt, Kerstin; Amstad, Paul; Cerutti, Peter; Baeuerle, Patrick A.

doi:10.1016/1074-5521(95)90076-4

Cited by 433 publications

(255 citation statements)

References 41 publications

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“…Together with the present findings of induction of cPLA 2 expression by ferrous ammonium citrate, they indicate that cPLA 2 could be induced by free radicals. One possibility is that ferrous ammonium citrate-mediated oxidative stress can induced the expression of nuclear factor-kappa B (NF-κB) [34], which is one of the oxidative stress-responsive transcription factors that has been reported to have binding sites on the cPLA 2 promoter, and this binding may induce the expression of cPLA 2 [35][36][37]. The transcription factor, fos is also increased in times of oxidative stress, and increased fos could have bound to the activator protein-1 (AP-1) binding site of cPLA 2 promoter, and induced the expression of cPLA 2 [36].…”

Section: Discussionmentioning

confidence: 99%

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

et al. 2005

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-The present study was carried out to elucidate the effect of a single episode of oxidative stress on pyramidal neurons of the rat hippocampus. A significant increase in the number of neurons that were immunolabeled for the toxic lipid peroxidation product, 4-hydroxynonenal (HNE) was observed in field CA3 of the hippocampus, at 1 day, 7 days and 14 days after intracerebroventricular injection of 1 µL of 5mM ferrous ammonium citrate, compared to ammonium citrate injected controls at these time points. The number of HNE positive cells was fewer at 14 days, compared to 1 day, after ferrous ammonium citrate injection. The changes in HNE imunoreactivity were paralleled by changes in cytoplasmic phospholipase A 2 (cPLA 2 ) labeling in the pyramidal neurons in adjacent sections, suggesting that some of the HNE could have arisen as a result of peroxidation of arachidonic acid that was released by cPLA 2 . Interestingly, despite the HNE and cPLA 2 labeling, no loss of neurons was observed in adjacent Nissl and Fluoro-Jade stained sections. Electron microscopy also showed that the HNE or cPLA 2 labeled cells had features of injured neurons, rather than necrotic neurons. The reduction of HNE immunoreactivity in neurons at 14 days after oxidative injury, and the absence of cell loss at any of the time intervals, shows that hippocampal pyramidal neurons have remarkable ability to recover from a single episode of oxidative stress, if repeated injury such as seizures / excitotoxicity could be avoided.iron / neurodegeneration / 4-hydroxynonenal / cytosolic phospholipase A 2 / lipid peroxidation / antioxidant defenses Abbreviations: AP-1: activator protein-1; CA: cornu ammonis; cPLA 2 : cytosolic phospholipase A 2;

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Section: Discussionmentioning

confidence: 99%

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

et al. 2005

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“…4 Such reactive oxygen species may act as intracellular second messengers via activation of the inactive cytoplasmic form of NF-B by the release of the inhibitory subunit I B␣. 50 N-acetyl-L-cysteine and pyrrolidine dithiocarbamate have been shown to inhibit NF-B activation in vitro and in vivo and subsequently the induction of pro-inflammatory cytokines and intracellular adhesion molecule-1. 51,52 Therefore, the inhibition of carrageenin-induced edema formation by ODN decoy may also depend on the reduced expression of cell adhesion molecules or cytokines through a NF-B-dependent mechanism.…”

Section: Discussionmentioning

confidence: 99%

Local administration of transcription factor decoy oligonucleotides to nuclear factor-κB prevents carrageenin-induced inflammation in rat hind paw

et al. 2000

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The transcription factor nuclear factor-B (NF-B) plays a key role in the expression of several genes involved in the inflammatory process. In the present study we investigated in an acute model of inflammation, the carrageenin-induced hind paw edema, the anti-inflammatory effect of double stranded oligodeoxynucleotides (ODN) with consensus nuclear factor-B (NF-B) sequence as transcription factor decoys (TFD) to inhibit NF-B binding to native DNA sites. Local administration of wild-type, but not mutant-ODN decoy, dose-dependently inhibited edema formation induced by carrageenin in rat paw. Molecular analysis performed on soft tissue obtained from inflamed paw demonstrated: (1) an

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“…27,28 In this condition, altered redox state has been adscribed to increased production of proinflammatory cytokines such as TNF␣. 27 The relationship between ROS and TNF␣ is bidirectional in that TNF␣ induces oxidative stress but also ROS activate latent nuclear factor B 29 and increase TNF␣ 30 In addition to increasing the production of ROS, TNF␣ also induces the synthesis of Mn-SOD, 31,32 and this latter effect can protect the cell against the cytotoxic effects of TNF␣. 31,32 As shown in the present report (which confirms our previous studies 7 ), this cytokine is overexpressed in PBMC and in the liver in chronic hepatitis C. It thus seems possible that TNF␣ might participate in causing oxidative stress and Mn-SOD overexpression in PBMC in this condition.…”

Section: Discussionmentioning

confidence: 99%

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

Larrea

Beloqui

Muñoz-Navas

et al. 1998

Free Radical Biology and Medicine

109

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Abstract-It has been reported that hepatitis C virus (HCV) may cause oxidative stress in infected cells. Patients with chronic hepatitis C exhibit an increased production of tumor necrosis factor-␣ (TNF␣), a cytokine that can produce oxidative stress by stimulating the generation of reactive oxygen species (ROS). Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme. To investigate cell defense against oxidative stress in HCV infection, we analyzed Mn-SOD mRNA in liver and in peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis C. Mn-SOD expression in PBMC was significantly increased in patients with HCV infection. Patients with sustained virological and biochemical response after therapy showed significantly lower Mn-SOD than patients with positive viremia. By contrast, Mn-SOD expression was not enhanced in the liver of patients with chronic hepatitis C. The values of Mn-SOD mRNA did not correlate with TNF␣ mRNA expression, viral load, or liver disease activity. Our results indicate that in HCV infection an induction of Mn-SOD was present in PBMC but absent in the liver, suggesting that this organ could be less protected against oxidative damage. Oxidative stress could participate in the pathogenesis of HCV infection.

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The roles of hydrogen peroxide and superoxide as messengers in the activation of transcription factor NF-κB

Cited by 433 publications

References 41 publications

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

Local administration of transcription factor decoy oligonucleotides to nuclear factor-κB prevents carrageenin-induced inflammation in rat hind paw

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

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