Mitochondrial ROS-induced ROS release: an update and review.
By D. Zorov, M. Juhaszova, Steven J. Sollott. Biochimica et Biophysica Acta, 2006
1,049 citations recorded by the source corpus.
Unstable mitochondrial membrane potential and redox transitions can occur following insults including ischemia/reperfusion injury and toxin exposure, with negative consequences for mitochondrial integrity and cellular survival. These transitions can involve mechanisms such as the recently described process, "Reactive Oxygen Species (ROS)-induced ROS-release" (RIRR), and be generated by circuits where the mitochondrial permeability transition (MPT) pore and the inner membrane anion channel (IMAC) are involved. The exposure to excessive oxidative stress results in an increase in ROS reaching a threshold level that triggers the opening of one of the requisite mitochondrial channels. In turn, this leads to the simultaneous collapse of the mitochondrial membrane potential and a transient increased ROS generation by the electron transfer chain. Generated ROS can be released into cytosol and trigger RIRR in neighboring mitochondria. This mitochondrion-to-mitochondrion ROS-signaling constitutes a positive feedback mechanism for enhanced ROS production leading to potentially significant mitochondrial and cellular injury. This review and update considers a variety of RIRR mechanisms (involving MPT, IMAC and episodes of mitochondrial transient hyperpolarization). RIRR 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.
Subfields: Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/d98370ec31ff4ca35ca8b2fc51fd86138703763d
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In Molecular Biology
- Michael R Hamblin
- M. Juhaszova
- D. Zorov
- Steven J. Sollott
- Y. Bae
- Young-Mi Go
- Hyunjin Oh
- Young Do Yoo
In Pathology and Forensic Medicine
Citations in the corpus
- Regulation of reactive oxygen species generation in cell signaling (2011, background): “Oxidative stress-induced ROS production among external stimuli is significantly implicated in neighboring mitochondrial damage and cell death and this phenomenon is called “ROSinduced ROS release (RIRR)” (Zorov et al., 2000; 2006).”
- Superoxide Dismutases: Role in Redox Signaling, Vascular Function, and Diseases (2011, neutral): “In addition to being a major site of ROS production, mitochondria are a target for ROS/RNS and compromised by severe and/or prolonged oxidative stress (256).”
- Redox compartmentalization in eukaryotic cells. (2008, background): “This can trigger “ROS-induced ROS release” in neighboring mitochondria [25].”
- Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “However, these inhibitors as well as others including cyclosporine A, cyanide, myxothiazol, nigericin, and oligomycin did not block RIRR associated with transient mitochondrial hyperpolarizations (mitochondrial membrane potential flickers described above) (FIGURE 9) (493).”
- Mechanisms and Mitochondrial Redox Signaling in Photobiomodulation (2018, background): “another damaging feedback loop to increase cellular damage (51).”
- Mitochondrial membrane potential (2017, background): “However, the correct interpretation of “mitochondrial hyperpolarization” is complex and susceptible to artifacts due to difficulties inherent in measurements of the membrane potential that are usually performed by using fluorescent probes [52].”