Chemistry and biology of reactive oxygen species in signaling or stress responses
Open accessAbstract
Reactive oxygen species (ROS) are a family of molecules that are continuously generated, transformed and consumed in all living organisms as a consequence of aerobic life. The traditional view of these reactive oxygen metabolites is one of oxidative stress and damage that leads to decline of tissue and organ systems in aging and disease. However, emerging data show that ROS produced in certain situations can also contribute to physiology and increased fitness. This Perspective provides a focused discussion on what factors lead ROS molecules to become signal and/or stress agents, highlighting how increasing knowledge of the underlying chemistry of ROS can lead to advances in understanding their disparate contributions to biology. An important facet of this emerging area at the chemistry-biology interface is the development of new tools to study these small molecules and their reactivity in complex biological systems.
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Mitochondrial reactive oxygen species can oxidize mitochondrial nucleic acids, cause aberrant protein expression, induce post-translational oxidation, lipid peroxidation and oxidative damage to nuclear DNA and/or mitochondrial DNA.
“Mitochondrial ROS can oxidize mitochondrial nucleic acids, causing the expression of aberrant proteins, and/or directly induce post-translational oxidation of local proteins, lipid peroxidation and oxidative damage to nuclear DNA and/or mtDNA60,66,67”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [66]
The “Mitochondria and electron transfer” section says mitochondria generate ROS, and “Chemical targets and reactions mediated by ROS” says ROS can modify proteins, lipids, DNA and RNA. The copy does not specifically link mitochondrial ROS to aberrant protein expression, lipid peroxidation, or damage to nuclear versus mitochondrial DNA. No page numbers are provided in the indexed passages. (LLM, conf=0.85)
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References 101 · Cited by 1,821
- Authors
- Dickinson, B. C., & Chang, C. J.
- Affiliations
- University of California, Berkeley (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Chang, Christopher J
- Venue
- Nature Chemical Biology
- Published
- 2011-07-18
- Volume
- 7
- Issue
- 8
- Pages
- 504-511
- ISSN
- 1552-4450 (ISSN-L)
- 1552-4469
- PMC
- PMC3390228
- OpenAlex
- W1989987141
- Cited by
- 1,821
- References
- 101
- Citations by year
- 2026: 77 · 2025: 120 · 2024: 133 · 2023: 169 · 2022: 174 · 2021: 165 · 2020: 162 · 2019: 154 · 2018: 119 · 2017: 124 · 2016: 104 · 2015: 91 · 2014: 89 · 2013: 77 · 2012: 57
- FWCI
- 29.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Chemical Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM066698, GM-79465, R01GM079465)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- reactive oxygen species, oxidative stress, redox signaling, stress response, aging
- MeSH terms
- Amino Acids, Cell Movement, Circadian Rhythm, Electron Transport, Endoplasmic Reticulum, Gene Expression Regulation, Mitochondria, Oxidation-Reduction, Proteins, Stress, Physiological, Molecular Structure, Signal Transduction, Reactive Oxygen Species, Protein Folding
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