Reactive Oxygen Species (Ros-Induced) Ros Release

By D. Zorov, C. Filburn, L. Klotz, Jay L. Zweier, Steven J. Sollott. Journal of Experimental Medicine, 2000

1,306 citations recorded by the source corpus.

We sought to understand the relationship between reactive oxygen species (ROS) and the mitochondrial permeability transition (MPT) in cardiac myocytes based on the observation of increased ROS production at sites of spontaneously deenergized mitochondria. We devised 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, ΔΨ. This ROS accumulation reproducibly triggered abrupt (and sometimes reversible) mitochondrial depolarization. This phenomenon was ascribed to MPT induction because (a) bongkrekic acid prevented it and (b) mitochondria became permeable for calcein (∼620 daltons) concurrently with depolarization. These photodynamically produced “triggering” ROS caused the MPT induction, as the ROS scavenger Trolox prevented it. The time required for triggering ROS to induce the MPT was dependent on intrinsic cellular ROS-scavenging redox mechanisms, particularly glutathione. MPT induction caused by triggering ROS coincided with a burst of mitochondrial ROS generation, as measured by dichlorofluorescein fluorescence, which we have termed mitochondrial “ROS-induced ROS release” (RIRR). This MPT induction/RIRR phenomenon in cardiac myocytes often occurred synchronously and reversibly among long chains of adjacent mitochondria demonstrating apparent cooperativity. The observed link between MPT and RIRR could be a fundamental phenomenon in mitochondrial and cell biology.

Subfields: Biophysics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/4db68a0f684b37f3a51801976d94f4df2741b5ea

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biophysics

In Molecular Biology

In Physiology

Citations in the corpus

Role of Phenolic Compounds in Human Disease: Current Knowledge and Future Prospects (2021, background): “After the occurrences of ROS-triggering of the mPTP followed by additional stimulation of ROS production, the phenomenon of ROS-induced ROS release (RIRR) [49] was named.”
Superoxide Flashes in Single Mitochondria (2008, neutral): “Recent studies have demonstrated massive increases in localized ROS production during metabolic stress (Romashko et al., 1998), photostimulation ( Zorov et al., 2000 ), and excessive elevations in intracellular ROS or Ca2+”
NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart (2010, background): “Because mitochondrial dysfunction facilitates electron leakage, thereby inducing ROS-induced ROS release (24), down-regulation of Nox4 may reduce oxidative stress not only by reducing its own O2 −”
Biological chemistry of reactive oxygen and nitrogen and radiation-induced signal transduction mechanisms (2003, background): “Hence, apparent modulation of oxidative stress suggested by changes in fluorescence of DCFH2 might reflect apoptotic pathways rather than real changes in ROS or RNS.”
New concepts in reactive oxygen species and cardiovascular reperfusion physiology. (2004, background): “An important additional concept is the notion of ROSinduced ROS release described by Zorov et al. [ 30 ].”
Role of ROS and RNS Sources in Physiological and Pathological Conditions (2016, background): “Oligodendrocytes are responsible for axon myelination, a protective layer required for propagation of action potentials and maintenance of intracellular communication.”
Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. (2004, neutral): “[3,5]) including cardiac myocytes [15,28,42].”
Mitochondrial calcium signalling and cell death: approaches for assessing the role of mitochondrial Ca2+ uptake in apoptosis. (2006, background): “A similar mechanism may be supported by the ROS that are produced and released from the mitochondria to the cytosol during mitochondrial membrane permeabilization [23] and promote the IP3R-mediated Ca2+ release [24].”
Mitochondrial ROS-induced ROS release: an update and review. (2006, background): “In contrast to the conventional belief (based on data obtained in in vitro models using isolated mitochondria) that Ca is an obligatory factor involved in MPT induction which is delayed by cyclosporine A, neither of these two were found to be direct MPT effectors in an in situ model (in isolated car”
Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Indeed, the term ROSinduced ROS release was coined by Sollott and colleagues (179) to describe the phenomenon during induction of the mitochondrial permeability transition in cardiac myocytes.”
Mechanisms and Mitochondrial Redox Signaling in Photobiomodulation (2018, background): “Activation of these channels in turn leads to the simultaneous collapse of MMP and increased ROS generation by the electron transport chain (50).”