Activation by nitric oxide of an oxidative-stress response that defends Escherichia coli against activated macrophages.

Nunoshiba, Tatsuo; deRojas-Walker, Teresa; Wishnok, John S.; Tannenbaum, Steven R.; Demple, Bruce

doi:10.1073/pnas.90.21.9993

Cited by 289 publications

(247 citation statements)

References 36 publications

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“…(iii) Nitric oxide (or perhaps a more reactive derivative thereof) could induce the regulon under anaerobic conditions (29). Therefore, the following theory was proposed (11,30 generators accomplish this by depleting the cell of NAD(P)H through redox cycling.…”

Section: Discussionmentioning

confidence: 99%

Regulation of the soxRS Oxidative Stress Regulon

Gaudu

Moon

Weiss

1997

Journal of Biological Chemistry

133

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Section: Discussionmentioning

confidence: 99%

Regulation of the soxRS Oxidative Stress Regulon

Gaudu

Moon

Weiss

1997

Journal of Biological Chemistry

133

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“…13,[43][44][45][46] Thus, oxidative damage is expected to occur predominantly inside the cell, since superoxide does not readily cross cell membranes. 47 A significant antibacterial process related to oxidative stress is peroxynitrite-dependent lipid peroxidation, which stems from OH and NO 2 radicals derived from peroxynitrous acid (HOONO; Fig. 8).…”

Section: Confocal Microscopy Studiesmentioning

confidence: 99%

Bactericidal Efficacy of Nitric Oxide-Releasing Silica Nanoparticles

Hetrick

Shin²,

Stasko³

et al. 2008

ACS Nano

322

380

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The utility of nitric oxide (NO)-releasing silica nanoparticles as a novel antibacterial is demonstrated against Pseudomonas aeruginosa. Nitric oxide-releasing nanoparticles were prepared via co-condensation of tetraalkoxysilane with aminoalkoxysilane modified with diazeniumdiolate NO donors, allowing for the storage of large NO payloads. Comparison of the bactericidal efficacy of the NO-releasing nanoparticles to 1-[2-(carboxylato)pyrrolidin-1-yl]diazen-1-ium-1,2-diolate (PROLI/NO), a small molecule NO donor, demonstrated enhanced bactericidal efficacy of nanoparticle-derived NO and reduced cytotoxicity to healthy cells (mammalian fibroblasts). Confocal microscopy revealed that fluorescently-labeled NO-releasing nanoparticles associated with the bacteria, providing rationale for the enhanced bactericidal efficacy of the nanoparticles. Intracellular NO concentrations were measurable when the NO was delivered from nanoparticles as opposed to PROLI/NO. Collectively, these results demonstrate the advantage of delivering NO via nanoparticles for antimicrobial applications.Keywords nitric oxide; silica nanoparticle; antibacterial; bactericidal; cytotoxicity; reactive nitrogen species; reactive oxygen species Antibiotic resistance has resulted in bacterial infections becoming the most common cause of infectious disease-related death. 1,2 In the United States alone, nearly 2 million people per year acquire infections during a hospital stay, of which approximately 90,000 die. 2 The primary culprits behind such deadly infections are antibiotic-resistant pathogens, which are responsible for approximately 70% of all lethal nosocomial infections. The growing danger of life-threatening infections and the rising economic burden of resistant bacteria have created a demand for new antibacterial therapeutics.The use of nanoparticles as delivery vehicles for bactericidal agents represents a new paradigm in the design of antibacterial therapeutics. To date, most antibacterial nanoparticles have been engineered using traditional antibiotics that are either incorporated within the particle scaffold or attached to the exterior of the particle. In many cases, such particles have exhibited greater efficacy than their constituent antibiotics alone. For example, Gu et al. reported that vancomycin-capped gold nanoparticles exhibited a 64-fold improvement in efficacy over vancomycin alone. 3 Similarly, silver nanoparticles have schoenfisch@unc.edu. Supporting Information Available: Synthesis of FITC-modified silica nanoparticles, AFM analysis of nanoparticle dimensions, scavenging of NO by TSB, and confocal fluorescence microscopy images of PROLI/NO-treated P. aeruginosa cells. This material is available free of charge via the Internet at http://pubs.acs.org. NIH Public AccessAuthor Manuscript ACS Nano. Author manuscript; available in PMC 2013 February 13. shown greater antibacterial activity than silver ion (Ag + ) in solution due to the direct toxicity of the particles and tunable release of Ag + based on nanocomposite size. [4][...

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“…Although H 2 O 2 can oxidize SoxR Fe, it does so without stimulating biological activity. NO does not oxidize SoxR but NO modulates biological activity in vivo (Nunoshiba et al, 1995). As pointed out by Marshall et al (2000), no eucaryotic homologs of SoxR have been described nor have eucaryotic transcription factors with redox-sensitive transition metals been identified.…”

Section: Transcription Factors As Ros/rns Sensorsmentioning

confidence: 99%

Biological chemistry of reactive oxygen and nitrogen and radiation-induced signal transduction mechanisms

2003

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In the past few years, nuclear DNA damage-sensing mechanisms activated by ionizing radiation have been identified, including ATM/ATR and the DNA-dependent protein kinase. Less is known about sensing mechanisms for cytoplasmic ionization events and how these events influence nuclear processes. Several studies have demonstrated the importance of cytoplasmic signaling pathways in cytoprotection and mutagenesis. For cytoplasmic signaling, radiation-stimulated reactive oxygen species (ROS) and reactive nitrogen species (RNS) are essential activators of these pathways. This review summarizes recent studies on the chemistry of radiation-induced ROS/ RNS generation and emphasizes interactions between ROS and RNS and the relative roles of cellular ROS/ RNS generators as amplifiers of the initial ionization events. Cellular mechanisms for regulating ROS/RNS levels are discussed. The mechanisms by which cells sense ROS/RNS are examined in terms of how ROS/RNS modify protein structure and function, for example, interactions with metal-thiol clusters, protein tyrosine nitration, protein cysteine oxidation, S-thiolation and Snitrosylation. We propose that radiation-induced ROS are the initiators and that nitric oxide (NO ) or derivatives are the effectors activating these signal transduction pathways. In responding to cellular ionization events, the cell converts an oxidative signal to a nitrosative one because ROS are too reactive and unspecific in their reactions for regulatory purposes and the cell is equipped to precisely modulate NO levels.

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Activation by nitric oxide of an oxidative-stress response that defends Escherichia coli against activated macrophages.

Cited by 289 publications

References 36 publications

Regulation of the soxRS Oxidative Stress Regulon

Regulation of the soxRS Oxidative Stress Regulon

Bactericidal Efficacy of Nitric Oxide-Releasing Silica Nanoparticles

Biological chemistry of reactive oxygen and nitrogen and radiation-induced signal transduction mechanisms

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