REVIEW: Mitochondrial ROS Metabolism: 10 Years Later

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A. Y. Andreyev^1*, Y. E. Kushnareva², A. N. Murphy¹, and A. A. Starkov^3*

¹Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, MC 0601, La Jolla, CA 92093-0601, USA; E-mail: alex_andreyev@mitoexperts.com

²La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA

³Brain and Mind Research Institute, Weill Medical College of Cornell University, 407 East 61st Street, 5th floor, New York, NY 10065, USA; E-mail: ans2024@med.cornell.edu

^* To whom correspondence should be addressed.

Received February 1, 2015; Revision received February 8, 2015

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The role of mitochondria in oxidative stress is well recognized, but many questions are still to be answered. This article is intended to update our comprehensive review in 2005 by highlighting the progress in understanding of mitochondrial reactive oxygen species (ROS) metabolism over the past 10 years. We review the recently identified or re-appraised sources of ROS generation in mitochondria, such as p66^shc protein, succinate dehydrogenase, and recently discovered properties of the mitochondrial antioxidant system. We also reflect upon some controversies, disputes, and misconceptions that confound the field.

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KEY WORDS: mitochondria, reactive oxygen species, p66shc, succinate dehydrogenase, dihydroorotate dehydrogenase, ROS scavenging, oxidative stress

DOI: 10.1134/S0006297915050028

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