Cellular adaptation to oxygen deficiency beyond the Nobel award

López‐Barneo, José; Simon, M. Celeste

doi:10.1038/s41467-020-14469-9

Cited by 19 publications

(9 citation statements)

References 20 publications

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“…Hypoxia is defined as the decreased availability of oxygen in cells and tissues. Low oxygen levels trigger a series of responses that are related to many physiological and pathophysiological scenarios [ 53 ]. The counterintuitive observation that hypoxia induced the production of ROS was called the ROS paradox in hypoxia [ 54 , 55 ].…”

Section: Ros In Acute Hypoxiamentioning

confidence: 99%

Generation of Reactive Oxygen Species by Mitochondria

2021

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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.

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Section: Ros In Acute Hypoxiamentioning

confidence: 99%

Generation of Reactive Oxygen Species by Mitochondria

2021

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“…Unicellular organisms show high adaptability to a wide range of [O 2 ] in the medium through manipulation of their own anaerobic/aerobic metabolism ( Bunn and Poyton, 1996 ; Johnson, 2019 ; López-Barneo and Simon, 2020 ), using detoxifying enzymes ( Sies, 1993 ; Inupakutika et al, 2016 ; Lyall et al, 2020 ) or uncoupling proteins (UCPs) ( Jarmuszkiewicz et al, 2010 ; Busiello et al, 2015 ; Demine et al, 2019 ; Nicholls, 2021 ).…”

Section: Unicellular Eukaryotesmentioning

confidence: 99%

Thriving in Oxygen While Preventing ROS Overproduction: No Two Systems Are Created Equal

et al. 2022

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From 2.5 to 2.0 billion years ago, atmospheric oxygen concentration [O2] rose thousands of times, leading to the first mass extinction. Reactive Oxygen Species (ROS) produced by the non-catalyzed partial reduction of O2 were highly toxic eliminating many species. Survivors developed different strategies to cope with ROS toxicity. At the same time, using O2 as the final acceptor in respiratory chains increased ATP production manifold. Thus, both O2 and ROS were strong drivers of evolution, as species optimized aerobic metabolism while developing ROS-neutralizing mechanisms. The first line of defense is preventing ROS overproduction and two mechanisms were developed in parallel: 1) Physiological uncoupling systems (PUS), which increase the rate of electron fluxes in respiratory systems. 2) Avoidance of excess [O2]. However, it seems that as avoidance efficiency improved, PUSs became less efficient. PUS includes branched respiratory chains and proton sinks, which may be proton specific, the mitochondrial uncoupling proteins (UCPs) or unspecific, the mitochondrial permeability transition pore (PTP). High [O2] avoidance also involved different strategies: 1) Cell association, as in biofilms or in multi-cellularity allowed gas-permeable organisms (oxyconformers) from bacterial to arthropods to exclude O2. 2) Motility, to migrate from hypoxic niches. 3) Oxyregulator organisms: as early as in fish, and O2-impermeable epithelium excluded all gases and only exact amounts entered through specialized respiratory systems. Here we follow the parallel evolution of PUS and O2-avoidance, PUS became less critical and lost efficiency. In regard, to proton sinks, there is fewer evidence on their evolution, although UCPs have indeed drifted in function while in some species it is not clear whether PTPs exist.

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“…Any circumstance or pathology that could mean an interruption in the caption and distribution of oxygen can trigger this response. For example, oxygen concentration decreases with geographic altitude, which triggers a systemic adaptive response [152].…”

Section: Mechanisms For Physiological Adaptation To Hypoxiamentioning

confidence: 99%

Cellular senescence or stemness: hypoxia flips the coin

Otero-Albiol

Carnero

2021

J Exp Clin Cancer Res

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Cellular senescence is a complex physiological state whose main feature is proliferative arrest. Cellular senescence can be considered the reverse of cell immortalization and continuous tumor growth. However, cellular senescence has many physiological functions beyond being a putative tumor suppressive trait. It remains unknown whether low levels of oxygen or hypoxia, which is a feature of every tissue in the organism, modulate cellular senescence, altering its capacity to suppress the limitation of proliferation. It has been observed that the lifespan of mammalian primary cells is increased under low oxygen conditions. Additionally, hypoxia promotes self-renewal and pluripotency maintenance in adult and embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs) and cancer stem cells (CSCs). In this study, we discuss the role of hypoxia facilitating senescence bypass during malignant transformation and acquisition of stemness properties, which all contribute to tumor development and cancer disease aggressiveness.

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Cellular adaptation to oxygen deficiency beyond the Nobel award

Cited by 19 publications

References 20 publications

Generation of Reactive Oxygen Species by Mitochondria

Generation of Reactive Oxygen Species by Mitochondria

Thriving in Oxygen While Preventing ROS Overproduction: No Two Systems Are Created Equal

Cellular senescence or stemness: hypoxia flips the coin

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