Nitrosative Stress: Activation of the Transcription Factor OxyR
Open accessAbstract
Hydrogen peroxide (H2O2) imposes an oxidative stress to Escherichia coli that is manifested by oxidation of glutathione and related redox-sensitive targets. OxyR is a thiol-containing transcriptional activator whose oxidation controls the expression of genes involved in H2O2 detoxification. Here we report that certain S-nitrosothiols (RSNOs) impose what we term a "nitrosative stress" to E. coli, evidenced by lowering of intracellular thiol and the transcriptional activation of OxyR by S-nitrosylation. This cellular and genetic response determines the metabolic fate of RSNOs and thereby contributes to bacterial rescue from stasis. Our studies reveal that signaling by S-nitrosylation can extend to the level of transcription and describe a metabolic pathway that constitutes an adaptation to nitrosative stress.
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Higher NO concentrations (>1 μM) can lead to oxidative stress and nitrative and nitrosative stress via peroxynitrite and nitrosating species, and in combination with oxygen can trigger posttranslational modification of proteins, lipids, and DNA.
“Higher concentrations of NO (>1 μM) can lead not only to oxidative stress but also nitrative and nitrosative stress via the generation of peroxynitrite and nitrosating species”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [412]
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- Authors
- Hausladen, A., Privalle, C. T., Keng, T., DeAngelo, J., & Stamler, J. S.
- Affiliations
- Duke University (US)
- Corresponding author
- Stamler, Jonathan S
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1996-09
- Volume
- 86
- Issue
- 5
- Pages
- 719-729
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2007013508
- Cited by
- 359
- References
- 66
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 6 · 2019: 7 · 2018: 13 · 2017: 3 · 2016: 9 · 2015: 5 · 2014: 9 · 2013: 10 · 2012: 9
- FWCI
- 7.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1k08hl002582-01, 5r01hl052529-05)
- National Heart, Lung, and Blood Institute (HL02582, HL 52529)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- nitrosative stress, OxyR, S-nitrosylation, S-nitrosothiols, hydrogen peroxide, oxidative stress, Escherichia coli, thiol oxidation, transcriptional activation, hydrogen peroxide detoxification, glutathione, bacterial adaptation
- MeSH terms
- Aerobiosis, Anaerobiosis, Catalase, Cysteine, DNA-Binding Proteins, Enzyme Induction, Escherichia coli, Glutathione, Hydrogen Peroxide, Mercaptoethanol, Nitric Oxide, Nitroso Compounds, Oxidation-Reduction, Repressor Proteins, Transcription Factors, Transcriptional Activation, Gene Expression Regulation, Bacterial, Oxidants, Oxidative Stress, S-Nitrosothiols, Escherichia coli Proteins
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