Brightness and shadows of mitochondrial ROS in the brain

Mitochondrial reactive oxygen species (mROS) have been generally considered harmful byproducts wanted to clear when elevated to avoid brain damage. However, the abundance of mROS in astrocytes is very high-about one order of magnitude above that in neurons-, despite they are essential to preserve cell metabolism and animal behavior. Here, we have focused on this apparent ambiguity by discussing (i) the intrinsic mechanisms ac-counting for the higher production of mROS by the mitochondrial respiratory chain in astrocytes than in neurons, (ii) the specific molecular targets of astrocytic beneficial mROS, and (iii) how decreased astrocytic mROS causes excess neuronal mROS leading to cellular and organismal damage. We hope that this mini-review serves to clarifying the apparent controversy on the beneficial versus deleterious faces of ROS in the brain from molecular to higher-order organismal levels.

Automated summary

This mini-review focuses on the contradiction between the high abundance of mitochondrial reactive oxygen species (mROS) in astrocytes and their essential role in cell metabolism and animal behavior. It discusses the mechanisms underlying the higher production of mROS in astrocytes compared to neurons, the specific molecular targets of astrocytic beneficial mROS, and the consequences of decreased astrocytic mROS leading to excess neuronal mROS and cellular damage. It aims to clarify the controversy surrounding the beneficial versus deleterious effects of ROS in the brain.