Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Aug 5:2019:6175804.
doi: 10.1155/2019/6175804. eCollection 2019.

ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells

Affiliations
Review

ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells

Anastasiya V Snezhkina et al. Oxid Med Cell Longev. .

Abstract

Reactive oxygen species (ROS) are by-products of normal cell activity. They are produced in many cellular compartments and play a major role in signaling pathways. Overproduction of ROS is associated with the development of various human diseases (including cancer, cardiovascular, neurodegenerative, and metabolic disorders), inflammation, and aging. Tumors continuously generate ROS at increased levels that have a dual role in their development. Oxidative stress can promote tumor initiation, progression, and resistance to therapy through DNA damage, leading to the accumulation of mutations and genome instability, as well as reprogramming cell metabolism and signaling. On the contrary, elevated ROS levels can induce tumor cell death. This review covers the current data on the mechanisms of ROS generation and existing antioxidant systems balancing the redox state in mammalian cells that can also be related to tumors.

PubMed Disclaimer

Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper.

Figures

Figure 1
Figure 1
Main sources of ROS production in normal and tumor cells.

References

    1. Zhang J., Wang X., Vikash V., et al. ROS and ROS-mediated cellular signaling. Oxidative Medicine and Cellular Longevity. 2016;2016:18. doi: 10.1155/2016/4350965.4350965 - DOI - PMC - PubMed
    1. Alfadda A. A., Sallam R. M. Reactive oxygen species in health and disease. Journal of Biomedicine and Biotechnology. 2012;2012:14. doi: 10.1155/2012/936486.936486 - DOI - PMC - PubMed
    1. Kudryavtseva A. V., Krasnov G. S., Dmitriev A. A., et al. Mitochondrial dysfunction and oxidative stress in aging and cancer. Oncotarget. 2016;7(29):44879–44905. doi: 10.18632/oncotarget.9821. - DOI - PMC - PubMed
    1. Storz P. Reactive oxygen species in tumor progression. Frontiers in Bioscience. 2005;10(1-3):1881–1896. doi: 10.2741/1667. - DOI - PubMed
    1. Dansen T. B., Wirtz K. W. The peroxisome in oxidative stress. IUBMB Life. 2001;51(4):223–230. - PubMed

MeSH terms