Steven J. Sollott

TL;DR: The mechanism of mitochondrial RIRR highlights the central role of mitochondria-formed ROS, and all of the known ROS-producing sites and their relevance to the mitochondrial ROS production in vivo are discussed.

TL;DR: A new model enabling incremental ROS accumulation in individual mitochondria in isolated cardiac myocytes via photoactivation of tetramethylrhodamine derivatives, which also served to report the mitochondrial transmembrane potential is devised, which is termed mitochondrial “ROS-induced ROS release” (RIRR).

TL;DR: Additional potential mechanisms for which ΔΨm is essential for maintenance of cellular health and viability are proposed and recommendations how to accurately measure ΔΩm in a cell are provided and potential sources of artifacts are discussed.

TL;DR: R could be a general cell biology phenomenon relevant to the processes of programmed mitochondrial destruction and cell death, and may contribute to other mechanisms of post-ischemic pathologies, including arrhythmias.

TL;DR: It is shown that reoxygenation after prolonged hypoxia reduces the reactive oxygen species (ROS) threshold for the mitochondrial permeability transition (MPT) in cardiomyocytes and that cell survival is steeply negatively correlated with the fraction of depolarized mitochondria.