scholarly journals Generation of Reactive Oxygen Species by Mitochondria

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 415
Author(s):  
Pablo Hernansanz-Agustín ◽  
José Antonio Enríquez
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Molecular Level ◽  
Reactive Oxygen ◽  
Level Of Detail ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Transport Chain ◽  
Chemical Products

Reactive oxygen species (ROS) are series of chemical products originated from one or several electron reductions of oxygen. ROS are involved in physiology and disease and can also be both cause and consequence of many biological scenarios. Mitochondria are the main source of ROS in the cell and, particularly, the enzymes in the electron transport chain are the major contributors to this phenomenon. Here, we comprehensively review the modes by which ROS are produced by mitochondria at a molecular level of detail, discuss recent advances in the field involving signalling and disease, and the involvement of supercomplexes in these mechanisms. Given the importance of mitochondrial ROS, we also provide a schematic guide aimed to help in deciphering the mechanisms involved in their production in a variety of physiological and pathological settings.

Possible role of free oxidation processes in the regulation of reactive oxygen species production in plant mitochondria

2003 ◽  
Vol 31 (6) ◽  
pp. 1316-1317 ◽  
Author(s):  
V.N. Popov
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Plant Mitochondria ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Oxidation Processes ◽  
Transport Chain ◽  
Electron Reduction ◽  
Species Production

The non-coupled substrate oxidation mediated by components of the electron transport chain that are not coupled to energy accumulation (such as plant alternative oxidase and rotenone-insensitive NADH dehydrogenases) and uncoupled respiration are peculiar features of plant mitochondria. The physiological significance of such energy-wasting oxidation processes is still debated. It is proposed that non-coupled oxidation could regulate the level of reduction of components of the electron transport chain and the rate of one-electron reduction of oxygen, thereby affecting the rate of formation of reactive oxygen species.

scholarly journals Impact of High Light on Reactive Oxygen Species Production within Photosynthetic Biological Membranes

2015 ◽  
Vol 6 (2) ◽  
pp. 50 ◽  
Author(s):  
Vetoshkina D. V. ◽  
Borisova-Mubarakshina M. M. ◽  
Naydov I. A. ◽  
Kozuleva M. A. ◽  
Ivanov B. N.
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Reactive Oxygen ◽  
Photosynthetic Electron Transport ◽  
Lipid Phase ◽  
H2o2 Production ◽  
Oxygen Species ◽  
Photosynthetic Electron Transport Chain ◽  
Transport Chain

In this study we describe the mechanisms of reactive oxygen species (ROS) production in the photosynthetic electron transport chain of higher plants chloroplasts under illumination. We implement an improved method for the measurement of hydrogen peroxide (H2O2) production in lipid phase of photosynthetic membranes of chloroplasts. Total rate of H2O2 production and the production within the thylakoid membrane under operation of photosynthetic electron transport chain is evaluated. Obtained data show that even in the presence of an efficient electron acceptor, methyl viologen, an increase in light intensity leads to an increase in H2O2 production mainly within the thylakoid membranes. The role of H2O2 produced within the photosynthetic biological membrane is discussed.

scholarly journals A Chemogenomic Screen in Saccharomyces cerevisiae Uncovers a Primary Role for the Mitochondria in Farnesol Toxicity and Its Regulation by the Pkc1 Pathway

2006 ◽  
Vol 282 (7) ◽  
pp. 4868-4874 ◽  
Author(s):  
Gregory D. Fairn ◽  
Kendra MacDonald ◽  
Christopher R. McMaster
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Electron Transport ◽  
Signaling Pathway ◽  
Electron Transport Chain ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Oxygen Species ◽  
Transport Chain

The isoprenoid farnesol has been shown to preferentially induce apoptosis in cancerous cells; however, the mode of action of farnesol-induced death is not established. We used chemogenomic profiling using Saccharomyces cerevisiae to probe the core cellular processes targeted by farnesol. This screen revealed 48 genes whose inactivation increased sensitivity to farnesol. The gene set indicated a role for the generation of oxygen radicals by the Rieske iron-sulfur component of complex III of the electron transport chain as a major mediator of farnesol-induced cell death. Consistent with this, loss of mitochondrial DNA, which abolishes electron transport, resulted in robust resistance to farnesol. A genomic interaction map predicted interconnectedness between the Pkc1 signaling pathway and farnesol sensitivity via regulation of the generation of reactive oxygen species. Consistent with this prediction (i) Pkc1, Bck1, and Mkk1 relocalized to the mitochondria upon farnesol addition, (ii) inactivation of the only non-essential and non-redundant member of the Pkc1 signaling pathway, BCK1, resulted in farnesol sensitivity, and (iii) expression of activated alleles of PKC1, BCK1, and MKK1 increased resistance to farnesol and hydrogen peroxide. Sensitivity to farnesol was not affected by the presence of the osmostabilizer sorbitol nor did farnesol affect phosphorylation of the ultimate Pkc1-responsive kinase responsible for controlling the cell wall integrity pathway, Slt2. The data indicate that the generation of reactive oxygen species by the electron transport chain is a primary mechanism by which farnesol kills cells. The Pkc1 signaling pathway regulates farnesol-mediated cell death through management of the generation of reactive oxygen species.

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