Mitochondrial ROS metabolism: 10 Years later

Abstract

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 p66shc 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.

Metabolism of Preimplantation Embryo Development

“…It should be noted that OXPHOS-associated ROS is not the only endogenous ROS produced. However, given the central importance of OXPHOS to the metabolic needs of an aerobic organism, it is likely that ROS produced by the mitochondria plays a major role during active metabolic processes that require efficient ATP production (Andreyev, Kushnareva, Murphy, & Starkov, 2015;Balaban, Nemoto, & Finkel, 2005).…”

Mitochondria and aging: A role for the mitochondrial transition pore?

“…The electron leakage in the electron transport chain during respiration is generally considered as the main source of mitochondrial ROS but other mitochondrial enzymatic systems, such as monoamine oxidase and cytochrome b5 reductase in the outer membranes, cytochromes P450 enzymes in the inner membranes, or several matrix enzymes such as aconitase, can also produce ROS (Andreyev, Kushnareva, Murphy, & Starkov, 2015; Andreyev, Kushnareva, & Starkov, 2005). Although mitochondria are not always considered as the main producer of ROS in the cell (NADPH or xantine oxidases being able to produce high levels of ROS), the respiratory chain produces ROS continuously.…”

The transcription factor NR4A3 controls CD103+ dendritic cell migration

“…Oxidative phosphorylation inevitably accompanies ROS production (45), and GM-CSF highly increases ROS production in BMDCs (46). We asked whether the lower basal respiratory capacity of Nr4a3 -/-BMDCs is due to a smaller quantity of mitochondria or to a mitochondrial functional defect.…”