Cited by 715Mitochondrial Function and PathologyRedox biology and oxidative stressCell death mechanisms and regulation

Superoxide flashes in single mitochondria

Open access
Wang, Wang, Fang, Huaqiang, Groom, Linda, Cheng, Aiwu, Zhang, Wanrui, Liu, Jie, Wang, Xianhua, Li, Kaitao +12 more·2008·Cell

Abstract

In quiescent cells, mitochondria are the primary source of reactive oxygen species (ROS), which are generated by leakiness of the electron transport chain (ETC). High levels of ROS can trigger cell death, whereas lower levels drive diverse and important cellular functions. We show here by employing a newly developed mitochondrial matrix-targeted superoxide indicator, that individual mitochondria undergo spontaneous bursts of superoxide generation, termed "superoxide flashes." Superoxide flashes occur randomly in space and time, exhibit all-or-none properties, and provide a vital source of superoxide production across many different cell types. Individual flashes are triggered by transient openings of the mitochondrial permeability transition pore stimulating superoxide production by the ETC. Furthermore, we observe a flurry of superoxide flash activity during reoxygenation of cardiomyocytes after hypoxia, which is inhibited by the cardioprotective compound adenosine. We propose that superoxide flashes could serve as a valuable biomarker for a wide variety of oxidative stress-related diseases.

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Crossref · 10.1016/j.cell.2008.06.017

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  • Alterations in mPTP function contribute to the aging-related loss of muscle mass and function.

    “Alterations in mPTP function are undoubtedly contributing to the aging-related loss of muscle mass and function, since mPTP opening can trigger several atrophy-regulating pathways.”

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  1. Wallace DC A mitochondrial paradigm for degenerative diseases and ageing Novartis Found Symp 2001b 235 247 263 discussion 263-246 11280029

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Authors
Wang, W., Fang, H., Groom, L., Cheng, A., Zhang, W., Liu, J., Wang, X., Li, K., Han, P., Zheng, M., Yin, J., Wang, W., Mattson, M. P., Kao, J. P. Y., Lakatta, E. G., Sheu, S.-S., Ouyang, K., Chen, J., Dirksen, R. T., & Cheng, H.
Affiliations
  • National Institutes of Health (US)
  • Peking University (CN)
  • University of Rochester Medicine (US)
  • University of Maryland, Baltimore (US)
  • University of California San Diego (US)
Corresponding author
  • Wang, Wang
  • Cheng, Heping
Venue
Cell
Publisher
Elsevier BV
Published
2008-07
Volume
134
Issue
2
Pages
279-290
ISSN
0092-8674 (ISSN-L)
OpenAlex
W1993039541
Cited by
715
References
58
Citations by year
2026: 11 · 2025: 20 · 2024: 24 · 2023: 12 · 2022: 23 · 2021: 34 · 2020: 36 · 2019: 44 · 2018: 43 · 2017: 45 · 2016: 52 · 2015: 57 · 2014: 60 · 2013: 50 · 2012: 60
FWCI
19.77
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL 33333, R01-HL-093671, R01HL033333)
  • National Institute of General Medical Sciences (R01GM056481)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R29AR044657, AR-44657, R01AR044657)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
mitochondrial superoxide, reactive oxygen species, mitochondrial permeability transition pore, mitochondrial matrix, hypoxia/reoxygenation, cardiomyocytes, adenosine, oxidative stress biomarkers, cell death
MeSH terms
Adenoviridae, Animals, Cells, Cultured, Humans, Luminescent Proteins, Mitochondria, Neurons, Superoxides, Cell Hypoxia, Reactive Oxygen Species, Oxidative Stress, Muscle Cells, Myocytes, Cardiac, Cell Line, Tumor

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