In a recent study published in Cell, Zhang et al. broadly identify proteins modified during oxidative stress induced by H₂O₂ or chemotherapy drugs and establish the DNA damage protein CHK1 as a key regulator of mitochondrial ROS.

Oxidants are double-edged swords. At low concentrations, reactive oxygen species (ROS), including the archetype H₂O₂, facilitate key biological processes, including proliferation and defense against infectious agents in an “oxidative eustress” environment. In contrast, high ROS levels drive aberrant signaling and cause damage to DNA, protein, and lipids, resulting in a state referred to as “oxidative distress.”¹ How this oxidative distress affects various cellular components to alter biological functions is incompletely understood.