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Physiologic Implications of Reactive Oxygen Species Production by Mitochondrial Complex I Reverse Electron Transport

1
Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
2
Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
*
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(8), 285; https://doi.org/10.3390/antiox8080285
Received: 27 June 2019 / Revised: 1 August 2019 / Accepted: 2 August 2019 / Published: 6 August 2019
(This article belongs to the Special Issue Mitochondria-Targeted Antioxidants)
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Abstract

Mitochondrial reactive oxygen species (ROS) can be either detrimental or beneficial depending on the amount, duration, and location of their production. Mitochondrial complex I is a component of the electron transport chain and transfers electrons from NADH to ubiquinone. Complex I is also a source of ROS production. Under certain thermodynamic conditions, electron transfer can reverse direction and reduce oxygen at complex I to generate ROS. Conditions that favor this reverse electron transport (RET) include highly reduced ubiquinone pools, high mitochondrial membrane potential, and accumulated metabolic substrates. Historically, complex I RET was associated with pathological conditions, causing oxidative stress. However, recent evidence suggests that ROS generation by complex I RET contributes to signaling events in cells and organisms. Collectively, these studies demonstrate that the impact of complex I RET, either beneficial or detrimental, can be determined by the timing and quantity of ROS production. In this article we review the role of site-specific ROS production at complex I in the contexts of pathology and physiologic signaling. View Full-Text
Keywords: reactive oxygen species; mitochondrial complex I; reverse electron transport; superoxide; hydrogen peroxide; ischemia reperfusion injury; oxidative damage reactive oxygen species; mitochondrial complex I; reverse electron transport; superoxide; hydrogen peroxide; ischemia reperfusion injury; oxidative damage
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Onukwufor, J.O.; Berry, B.J.; Wojtovich, A.P. Physiologic Implications of Reactive Oxygen Species Production by Mitochondrial Complex I Reverse Electron Transport. Antioxidants 2019, 8, 285.

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