Defining roles of specific reactive oxygen species (ROS) in cell biology and physiology

Research output: Contribution to journalReviewResearchpeer-review

  • Helmut Sies
  • Vsevolod V. Belousov
  • Navdeep S. Chandel
  • Davies, Michael J.
  • Dean P. Jones
  • Giovanni E. Mann
  • Michael P. Murphy
  • Masayuki Yamamoto
  • Christine Winterbourn

‘Reactive oxygen species’ (ROS) is a generic term that defines a wide variety of oxidant molecules with vastly different properties and biological functions that range from signalling to causing cell damage. Consequently, the description of oxidants needs to be chemically precise to translate research on their biological effects into therapeutic benefit in redox medicine. This Expert Recommendation article pinpoints key issues associated with identifying the physiological roles of oxidants, focusing on H2O2 and O2.–. The generic term ROS should not be used to describe specific molecular agents. We also advocate for greater precision in measurement of H2O2, O2.– and other oxidants, along with more specific identification of their signalling targets. Future work should also consider inter-organellar communication and the interactions of redox-sensitive signalling targets within organs and whole organisms, including the contribution of environmental exposures. To achieve these goals, development of tools that enable site-specific and real-time detection and quantification of individual oxidants in cells and model organisms are needed. We also stress that physiological O2 levels should be maintained in cell culture to better mimic in vivo redox reactions associated with specific cell types. Use of precise definitions and analytical tools will help harmonize research among the many scientific disciplines working on the common goal of understanding redox biology.

Original languageEnglish
JournalNature Reviews Molecular Cell Biology
Pages (from-to)1-17
ISSN1471-0072
DOIs
Publication statusAccepted/In press - 2022

Bibliographical note

Funding Information:
Generous support is acknowledged: G.E.M., British Heart Foundation (FS19/25/34277, FS16/67/32548), Heart Research UK (RG2672) and King’s Together Strategic Award; M.J.D., Novo Nordisk Foundation (Laureate grants NNF13OC0004294 and NNF20SA0064214); D.P.J., P30-ES019776, R21-ES031824, R01-ES023485, U2C-ES030163 and RC2-DK118619; M.P.M., Medical Research Council UK (MC_U105663142) and a Wellcome Trust Investigator Award (110159/A/15Z); V.V.B., Ministry of Science and Higher Education, Russian Federation (grant 075-15-2019-1789); and H.S., Deutsche Forschungsgemeinschaft, National Foundation for Cancer Research.

Publisher Copyright:
© 2022, Springer Nature Limited.

ID: 303170301