Mitochondrial electron transport chain, ROS generation and uncoupling (Review)
TL;DR: This review discusses the sites of ROS generation in each ETC complex, including sites IF and IQ in complex I, site IIF in complex II and site IIIQo in complex III, and the physiological and pathological regulation of ROS.
read more
Abstract: The mammalian mitochondrial electron transport chain (ETC) includes complexes I‑IV, as well as the electron transporters ubiquinone and cytochrome c. There are two electron transport pathways in the ETC: Complex I/III/IV, with NADH as the substrate and complex II/III/IV, with succinic acid as the substrate. The electron flow is coupled with the generation of a proton gradient across the inner membrane and the energy accumulated in the proton gradient is used by complex V (ATP synthase) to produce ATP. The first part of this review briefly introduces the structure and function of complexes I‑IV and ATP synthase, including the specific electron transfer process in each complex. Some electrons are directly transferred to O2 to generate reactive oxygen species (ROS) in the ETC. The second part of this review discusses the sites of ROS generation in each ETC complex, including sites IF and IQ in complex I, site IIF in complex II and site IIIQo in complex III, and the physiological and pathological regulation of ROS. As signaling molecules, ROS play an important role in cell proliferation, hypoxia adaptation and cell fate determination, but excessive ROS can cause irreversible cell damage and even cell death. The occurrence and development of a number of diseases are closely related to ROS overproduction. Finally, proton leak and uncoupling proteins (UCPS) are discussed. Proton leak consists of basal proton leak and induced proton leak. Induced proton leak is precisely regulated and induced by UCPs. A total of five UCPs (UCP1‑5) have been identified in mammalian cells. UCP1 mainly plays a role in the maintenance of body temperature in a cold environment through non‑shivering thermogenesis. The core role of UCP2‑5 is to reduce oxidative stress under certain conditions, therefore exerting cytoprotective effects. All diseases involving oxidative stress are associated with UCPs.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
TL;DR: This review explores the mutual connection of mitochondria and endoplasmic reticulum in mediating oxidative stress and autophagy through ROS and Ca2+ and aims to provide part of the theoretical basis for alleviating oxidative stress through Autophagy mediated by mitochondrial-endoplasmo-reticulum communication.
Unfolding the Interactions between Endoplasmic Reticulum Stress and Oxidative Stress
Gideon Ong,Susan E. Logue +1 more
TL;DR: In this paper , the authors evaluate the interplay between ER stress, oxidative stress, and UPR signaling networks, and assess how UPR signalling mediators can influence antioxidant responses.
Reactive Oxygen Species: Not Omnipresent but Important in Many Locations
TL;DR: In this article, it was shown that cells regulate their redox balance by strictly controlling ROS source activation as well as localization, amount, duration and location of ROS production, which strongly depends on the cell type and the source, amount and location.
Individual and combined effects of amoxicillin, enrofloxacin, and oxytetracycline on Lemna minor physiology
Marcelo Pedrosa Gomes,Júlio César Moreira de Brito,Daiane Cristina Rocha,Mário Antônio Navarro-Silva,Philippe Juneau +4 more
TL;DR: The results therefore indicate L. minor as a candidate for phytoremediation of service waters contaminated by AMX, ENR, and/or OXY, which prevented the overaccumulation of ROS by increasing catalase enzyme activity.
60
Oxidative cell death in cancer: mechanisms and therapeutic opportunities
Xiaoqin An,Wenfeng Yu,Jinbao Liu,Daolin Tang,Yang Li,Xin Chen +5 more
TL;DR: This review explores oxidative cell death mechanisms in cancer, highlighting the potential of targeting antioxidant proteins to induce cell death in cancer cells, offering a promising approach for cancer prevention and treatment.
60
References
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Karen Bedard,Karl-Heinz Krause +1 more
TL;DR: This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
Mitochondrial formation of reactive oxygen species.
TL;DR: This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments and discusses various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.
4.6K
Neurodegenerative diseases and oxidative stress.
TL;DR: Oxidative stress has been implicated in the progression of Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis and different strategies, including novel metal–protein attenuating compounds aimed at a variety of targets have shown promise in clinical studies.
3.8K
ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis
TL;DR: The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling.
Reactive oxygen species, cellular redox systems and apoptosis
Magdalena L. Circu,Tak Yee Aw +1 more
TL;DR: A full understanding of the redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders.
3.2K