How mitochondria produce reactive oxygen species

How mitochondria produce reactive oxygen species

2009 | Michael P. MURPHY
The production of reactive oxygen species (ROS) by mammalian mitochondria is crucial due to its role in oxidative damage and retrograde redox signaling. Superoxide (O2•-) is the primary mitochondrial ROS, and its production is influenced by the concentration of potential electron donors, local oxygen concentration, and second-order rate constants. Two modes of mitochondrial operation result in significant O2•- production: (i) when mitochondria are not generating ATP, leading to a high proton motive force (Δp) and reduced coenzyme Q (CoQ) pool; and (ii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix. For actively generating ATP mitochondria, O2•- production is minimal. The generation of O2•- depends on Δp, NADH/NAD+ and CoQH2/CoQ ratios, and local oxygen concentration, which are highly variable and difficult to measure in vivo. Therefore, extrapolating O2•- production rates from isolated mitochondria to in vivo conditions is challenging and can be misleading. Despite these limitations, understanding the factors that favor mitochondrial ROS production is essential for studying pathological oxidative damage and redox signaling.The production of reactive oxygen species (ROS) by mammalian mitochondria is crucial due to its role in oxidative damage and retrograde redox signaling. Superoxide (O2•-) is the primary mitochondrial ROS, and its production is influenced by the concentration of potential electron donors, local oxygen concentration, and second-order rate constants. Two modes of mitochondrial operation result in significant O2•- production: (i) when mitochondria are not generating ATP, leading to a high proton motive force (Δp) and reduced coenzyme Q (CoQ) pool; and (ii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix. For actively generating ATP mitochondria, O2•- production is minimal. The generation of O2•- depends on Δp, NADH/NAD+ and CoQH2/CoQ ratios, and local oxygen concentration, which are highly variable and difficult to measure in vivo. Therefore, extrapolating O2•- production rates from isolated mitochondria to in vivo conditions is challenging and can be misleading. Despite these limitations, understanding the factors that favor mitochondrial ROS production is essential for studying pathological oxidative damage and redox signaling.
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Understanding How mitochondria produce reactive oxygen species