Pro-oxidative synergic bactericidal effect of NO: kinetics and inhibition by nitroxides

Yadav, Reeta; Samuni, Yuval; Abramson, Alex; Zeltser, Rephael; Casap, Nardy; Kabiraj, Tonmoy K.; Banach, Maureen; Samuni, Uri

doi:10.1016/j.freeradbiomed.2013.10.012

Cited by 14 publications

(10 citation statements)

References 65 publications

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“…However, it failed to affect the expression of TGF-β3 mRNA in activated microglia around regenerating motoneurons and astrocytes 58 . It was also reported that the protein expressions of TGF-β type II receptor and Smad3 were rapidly upregulated in neurons of the ipsilateral cortex and CA1 region of the hippocampus after stab wound injury 59 .…”

Section: Expressions Of Tgf-β Following Nerve Injurymentioning

confidence: 94%

The Regulatory Effects of Transforming Growth Factor-β on Nerve Regeneration

2017

Cell Transplant

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Transforming growth factor-b (TGF-b) belongs to a group of pleiotropic cytokines that are involved in a variety of biological processes, such as inflammation and immune reactions, cellular phenotype transition, extracellular matrix (ECM) deposition, and epithelial-mesenchymal transition. TGF-b is widely distributed throughout the body, including the nervous system. Following injury to the nervous system, TGF-b regulates the behavior of neurons and glial cells and thus mediates the regenerative process. In the current article, we reviewed the production, activation, as well as the signaling pathway of TGF-b. We also described altered expression patterns of TGF-b in the nervous system after nerve injury and the regulatory effects of TGF-b on nerve repair and regeneration in many aspects, including inflammation and immune response, phenotypic modulation of neural cells, neurite outgrowth, scar formation, and modulation of neurotrophic factors. The diverse biological actions of TGF-b suggest that it may become a potential therapeutic target for the treatment of nerve injury and regeneration.

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Section: Expressions Of Tgf-β Following Nerve Injurymentioning

confidence: 94%

The Regulatory Effects of Transforming Growth Factor-β on Nerve Regeneration

2017

Cell Transplant

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“…Opposite effects of NO are particularly evident for cells subjected to oxidative stress where NO enhanced the killing of E. coli (71)(72)(73)(74)(75)(76)(77), but protected B. subtilis and Neisseria meningitidis (74,78) as is the case with mammalian cells (79,80). Aceto-HX alone has no effect on the viability of bacterial cells suspended in Luria-Bertani medium (LB), but potentiates the killing induced by H 2 O 2 or H 2 O 2 and MbFe III of both E. coli ( Figure 4) and B. subtilis ( Figure 5).…”

Section: Effects Of Hxs On Cells Subjected To Oxidative Stressmentioning

confidence: 99%

“…There is a clear distinction between the effects of NO and HNO on H 2 O 2 induced killing of E. coli where only NO, but not HNO, demonstrates a synergistic prooxidative effect (71)(72)(73)(74)(75)(76)(77). In the case of B. subtilis, NO protected the cells (74,78) whereas in most cases HNO enhanced the killing induced by H 2 O 2 (47).…”

Section: Effects Of Hxs On Cells Subjected To Oxidative Stressmentioning

confidence: 99%

Oxidation Mechanism of Hydroxamic Acids Forming HNO and NO

Goldstein¹,

Samuni²

2015

NOx Related Chemistry

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“…For example, Pacelli and colleagues observed that simultaneous exposure to 1 mM H 2 O 2 and 1 mM diethylamine (DEA) NONOate, a NO· donor, led to increased killing of different strains of Escherichia coli (18). Similarly, Yadav and coworkers found that millimolar concentrations of H 2 O 2 and NO· donors enhanced killing of E. coli as well as Actinobacillus actinomycetemcomitans, Actinomyces viscosus, Streptococcus mutans, and Streptococcus sobrinus (17). On the other hand, Gusarov and Nudler found that 30 M boluses of NO· delivered right before 10 mM boluses of H 2 O 2 protected Bacillus subtilis from cell death through reactivation of a catalase and inhibition of thioredoxin and thioredoxin reductase, which limited Fenton chemistry (19).…”

mentioning

confidence: 99%

“…The physiological interactions of concurrent NO· and H 2 O 2 stresses, which can be encountered within phagosomes (3,(14)(15)(16), are not well understood. In vitro studies have suggested that NO· can both reduce and enhance killing by high concentrations of H 2 O 2 depending on the organism and treatment conditions (17)(18)(19)(20). For example, Pacelli and colleagues observed that simultaneous exposure to 1 mM H 2 O 2 and 1 mM diethylamine (DEA) NONOate, a NO· donor, led to increased killing of different strains of Escherichia coli (18).…”

mentioning

confidence: 99%

Transcriptional Regulation Contributes to Prioritized Detoxification of Hydrogen Peroxide over Nitric Oxide

2019

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Hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO·) are toxic metabolites that immune cells use to attack pathogens. These antimicrobials can be present at the same time in phagosomes, and it remains unclear how bacteria deal with these insults when simultaneously present. Here, using Escherichia coli, we observed that simultaneous exposure to H 2 O 2 and NO· leads to prioritized detoxification, where enzymatic removal of NO· is impeded until H 2 O 2 has been eliminated. This phenomenon is reminiscent of carbon catabolite repression (CCR), where preferred carbon sources are catabolized prior to less desirable substrates; however, H 2 O 2 and NO· are toxic, growth-inhibitory compounds rather than growth-promoting nutrients. To understand how NO· detoxification is delayed by H 2 O 2 whereas H 2 O 2 detoxification proceeds unimpeded, we confirmed that the effect depended on Hmp, which is the main NO· detoxification enzyme, and used an approach that integrated computational modeling and experimentation to delineate and test potential mechanisms. Plausible interactions included H 2 O 2 -dependent inhibition of hmp transcription and translation, direct inhibition of Hmp catalysis, and competition for reducing equivalents between Hmp and H 2 O 2 -degrading enzymes. Experiments illustrated that Hmp catalysis and NAD(P)H supply were not impaired by H 2 O 2 , whereas hmp transcription and translation were diminished. A dependence of this phenomenon on transcriptional regulation parallels CCR, and we found it to involve the transcriptional repressor NsrR. Collectively, these data suggest that bacterial regulation of growth inhibitor detoxification has similarities to the regulation of growth substrate consumption, which could have ramifications for infectious disease, bioremediation, and biocatalysis from inhibitor-containing feedstocks. IMPORTANCE Bacteria can be exposed to H 2 O 2 and NO· concurrently within phagosomes. In such multistress situations, bacteria could have evolved to simultaneously degrade both toxic metabolites or preferentially detoxify one over the other. Here, we found that simultaneous exposure to H 2 O 2 and NO· leads to prioritized detoxification, where detoxification of NO· is hampered until H 2 O 2 has been eliminated. This phenomenon resembles CCR, where bacteria consume one substrate over others in carbon source mixtures. Further experimentation revealed a central role for transcriptional regulation in the prioritization of H 2 O 2 over NO·, which is also important to CCR. This study suggests that regulatory scenarios observed in bacterial consumption of growth-promoting compound mixtures can be conserved in bacterial detoxification of toxic metabolite mixtures.

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Pro-oxidative synergic bactericidal effect of NO: kinetics and inhibition by nitroxides

Cited by 14 publications

References 65 publications

The Regulatory Effects of Transforming Growth Factor-β on Nerve Regeneration

The Regulatory Effects of Transforming Growth Factor-β on Nerve Regeneration

Oxidation Mechanism of Hydroxamic Acids Forming HNO and NO

Transcriptional Regulation Contributes to Prioritized Detoxification of Hydrogen Peroxide over Nitric Oxide

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