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Mitochondrial ROS Generation and Its Regulation: Mechanisms Involved in H 2 O 2 Signaling
Abstract
Mitochondria are the main source of reactive oxygen species in the cell. These reactive oxygen species have long been known as being involved in oxidative stress. This is a review of the mechanisms involved in reactive oxygen species generation by the respiratory chain and some of the dehydrogenases and the control by thermodynamic and kinetic constraints. Mitochondrial ROS produced at the level of the bc1 complex as well at the level of complex I are discussed. It was recognized more than a decade ago that they can also function as signaling molecules. This signaling role will be developed both in terms of mechanism and in terms of mitochondrial ROS signaling. The notion that hydrogen peroxide acts not only as a damaging oxidant but also as a signaling molecule was proposed more than a decade ago. Hydrogen peroxide signaling can be either direct (oxidation of its target) or indirect (involving peroxiredoxins, for example). The consequences of ROS signaling on crucial biologic processes such as cell proliferation and differentiation are discussed. Antioxid. Redox Signal. 14, 459—468.
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“It is well established that mitochondria produce ROS as a consequence of electron leak during respiration (223, 349).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [349]
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“Although some increases in ROS can stimulate these essential pathways, there is a threshold range of concentrations beyond which ROS become harmful (83, 206, 349).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [349]
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“Many of the ROS-mediated cellular signals paradoxically protect the cell against oxidative stress, but above a given threshold ROS become harmful and induce oxidative stress [268].”
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“The overload of ROS leads to the loss of MMP, which is considered a characteristic of the initiation phase of the intrinsic apoptosis pathway [36,37].”
BackgroundRedox and Reactive Oxygen Species Regulation of Mitochondrial Cytochrome c Oxidase Biogenesis
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“The selected damaging agent in this study was H2O2 because it exhibits either direct (oxidation of its target) or indirect (involving peroxiredoxins) signaling [18] and induction of oxidative stress [20–22].”
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“Consistent with mitochondria being the major source of ROS in eukaryotic cells (21, 46, 52), our findings demonstrate that CTX injection results in rapid ROS production by mitochondria.”
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“Singly reduced semiquinone is believed to be capable of donating its free electron to oxygen at complex III, leading to formation of superoxide anion which is the precursor of other damaging oxygen species (Nakamura & Hayashi, 1994; Rigoulet et al., 2010; Turrens, 2003).”
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“At the cellular level, ROS are generated as metabolic byproducts of normal biological processes, with oxidative phosphorylation in mitochondria as the primary source in eukaryotic cells [20].”
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“2011), and studies have shown that excessive ROS can cause mitochondrial permeability transport pore opening and mitochondrial dysfunction, which leads to caspase-3 activity (Li et al. 1997; Schon and Manfredi 2003; Rigoulet et al. 2011).”
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“It is difficult to predict whether this decrease would have a negative role in tumorigenesis, but ROS has been described as a signaling molecule promoting growth (Rigoulet et al., 2011).”
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“ROS accumulation can oxidative major macromolecules such as lipids, proteins, and DNA leading to cellular damage [5].”
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“The antioxidant properties of these molecules could also be associated with their capacity to modulate the mitochondrial function, keeping in mind that mitochondria constitute a main source of ROS [65].”
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Metadata
- Authors
- Rigoulet, M., Yoboue, E. D., & Devin, A.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2011-02
- Volume
- 14
- Issue
- 3
- Pages
- 459-468
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W1985730402
- Semantic Scholar
- 72f038ebb891d7e56acea1d3220662223a95864f
- Cited by
- 394
- References
- 112
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 13 · 2023: 24 · 2022: 25 · 2021: 41 · 2020: 23 · 2019: 24 · 2018: 26 · 2017: 25 · 2016: 19 · 2015: 31 · 2014: 25 · 2013: 37 · 2012: 44
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Agence Nationale de la Recherche
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- mitochondrial reactive oxygen species, hydrogen peroxide signaling, oxidative stress, electron transport chain, bc1 complex, complex I, dehydrogenase, peroxiredoxin, cell proliferation, cell differentiation
- MeSH terms
- Animals, Electron Transport, Hydrogen Peroxide, Mitochondria, Models, Molecular, Oxygen, Protein Conformation, Signal Transduction, Oxidants, Reactive Oxygen Species, Oxidative Stress, Cell Proliferation
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