The rate of oxygen utilization by cells.

doi:10.1016/J.FREERADBIOMED.2011.05.024

Home
/
Papers
/
The rate of oxygen utilization by cells.

Journal Article•DOI•

The rate of oxygen utilization by cells.

Brett A. Wagner¹, Sujatha Venkataraman¹, Garry R. Buettner¹•Institutions (1)

University of Iowa¹

01 Aug 2011-Free Radical Biology and Medicine (Free Radic Biol Med)-Vol. 51, Iss: 3, pp 700-712

TL;DR: The discovery of oxygen is considered by some to be the most important scientific discovery of all time--from both physical-chemical/astrophysics and biology/evolution viewpoints.

read less

About: This article is published in Free Radical Biology and Medicine.The article was published on 2011-08-01 and is currently open access. It has received 284 citations till now. The article focuses on the topics: Oxygen & Apparent oxygen utilisation.

...read moreread less

Citations

PDF

Open Access

More filters

Journal Article•DOI•

Oxidative stress and autophagy: the clash between damage and metabolic needs

[...]

Giuseppe Filomeni¹, D De Zio¹, Francesco Cecconi¹•Institutions (1)

University of Rome Tor Vergata¹

01 Mar 2015-Cell Death & Differentiation

TL;DR: This review aims at providing novel insight into the regulatory pathways of autophagy in response to glucose and amino acid deprivation, as well as their tight interconnection with metabolic networks and redox homeostasis.

...read moreread less

Abstract: Autophagy is a catabolic process aimed at recycling cellular components and damaged organelles in response to diverse conditions of stress, such as nutrient deprivation, viral infection and genotoxic stress. A growing amount of evidence in recent years argues for oxidative stress acting as the converging point of these stimuli, with reactive oxygen species (ROS) and reactive nitrogen species (RNS) being among the main intracellular signal transducers sustaining autophagy. This review aims at providing novel insight into the regulatory pathways of autophagy in response to glucose and amino acid deprivation, as well as their tight interconnection with metabolic networks and redox homeostasis. The role of oxidative and nitrosative stress in autophagy is also discussed in the light of its being harmful for both cellular biomolecules and signal mediator through reversible posttranslational modifications of thiol-containing proteins. The redox-independent relationship between autophagy and antioxidant response, occurring through the p62/Keap1/Nrf2 pathway, is also addressed in order to provide a wide perspective upon the interconnection between autophagy and oxidative stress. Herein, we also attempt to afford an overview of the complex crosstalk between autophagy and DNA damage response (DDR), focusing on the main pathways activated upon ROS and RNS overproduction. Along these lines, the direct and indirect role of autophagy in DDR is dissected in depth.

...read moreread less

1,376 citations

Journal Article•DOI•

Live-Cell Super-Resolution Imaging with Synthetic Fluorophores

[...]

Sebastian van de Linde¹, Mike Heilemann, Markus Sauer¹•Institutions (1)

University of Würzburg¹

04 Apr 2012-Annual Review of Physical Chemistry

TL;DR: Synthetic fluorophores have a small size, are available in many colors spanning the whole spectrum, and can easily be chemically modified and used for stoichiometric labeling of proteins in live cells.

...read moreread less

Abstract: Super-resolution imaging methods now can provide spatial resolution that is well below the diffraction limit approaching virtually molecular resolution. They can be applied to biological samples and provide new and exciting views on the structural organization of cells and the dynamics of biomolecular assemblies on wide timescales. These revolutionary developments come with novel requirements for fluorescent probes, labeling techniques, and data interpretation strategies. Synthetic fluorophores have a small size, are available in many colors spanning the whole spectrum, and can easily be chemically modified and used for stoichiometric labeling of proteins in live cells. Because of their brightness, their photostability, and their ability to be operated as photoswitchable fluorophores even in living cells under physiological conditions, synthetic fluorophores have the potential to substantially accelerate the broad application of live-cell super-resolution imaging methods.

...read moreread less

248 citations

Journal Article•DOI•

Limitations of oxygen delivery to cells in culture: An underappreciated problem in basic and translational research

[...]

Trenton L. Place¹, Frederick E. Domann¹, Adam J. Case²•Institutions (2)

Roy J. and Lucille A. Carver College of Medicine¹, University of Nebraska Medical Center²

01 Dec 2017-Free Radical Biology and Medicine

TL;DR: This review aims to provide an overview of the physics, potential consequences, and alternative culture methods currently available to help circumvent this largely unrecognized problem ofconsumptive oxygen depletion (COD).

...read moreread less

239 citations

Journal Article•DOI•

Tumor cells have decreased ability to metabolize H2O2: Implications for pharmacological ascorbate in cancer therapy

[...]

Claire M. Doskey¹, Visarut Buranasudja¹, Brett A. Wagner¹, Justin G. Wilkes¹, Juan Du¹, Joseph J. Cullen², Joseph J. Cullen¹, Garry R. Buettner¹ - Show less +4 more•Institutions (2)

University of Iowa¹, Veterans Health Administration²

01 Dec 2016-Redox biology

TL;DR: It is hypothesize that sensitivity of tumor cells to P-AscH− compared to normal cells is due to their lower capacity to metabolize H2O2, and Catalase activity could present a promising indicator of which tumors may respond to the reducing agent.

...read moreread less

Abstract: Ascorbate (AscH−) functions as a versatile reducing agent At pharmacological doses (P-AscH−; [plasma AscH−] ≥≈20 mM), achievable through intravenous delivery, oxidation of P-AscH− can produce a high flux of H2O2 in tumors Catalase is the major enzyme for detoxifying high concentrations of H2O2 We hypothesize that sensitivity of tumor cells to P-AscH− compared to normal cells is due to their lower capacity to metabolize H2O2 Rate constants for removal of H2O2 (kcell) and catalase activities were determined for 15 tumor and 10 normal cell lines of various tissue types A differential in the capacity of cells to remove H2O2 was revealed, with the average kcell for normal cells being twice that of tumor cells The ED50 (50% clonogenic survival) of P-AscH− correlated directly with kcell and catalase activity Catalase activity could present a promising indicator of which tumors may respond to P-AscH−

...read moreread less

199 citations

Cites background from "The rate of oxygen utilization by c..."

...The metabolic rate of oxygen consumption by low passage MIA PaCa-2 cells is on the order of 40 amol cell s [43]....
[...]

Journal Article•DOI•

ROS and RNS signalling: adaptive redox switches through oxidative/nitrosative protein modifications.

[...]

N. T. Moldogazieva¹, Innokenty M. Mokhosoev¹, N.B. Feldman¹, Sergey V. Lutsenko¹•Institutions (1)

I.M. Sechenov First Moscow State Medical University¹

19 Apr 2018-Free Radical Research

TL;DR: Recent advances in investigation of mechanisms of protein redox modifications and adaptive redox switches such as MAPK/PI3K/PTEN, Nrf2/Keap1, and NF-κB/IκB, powerful regulators of numerous physiological processes, also implicated in various diseases are discussed.

...read moreread less

Abstract: Over the last decade, a dual character of cell response to oxidative stress, eustress versus distress, has become increasingly recognized. A growing body of evidence indicates that under physiological conditions, low concentrations of reactive oxygen and nitrogen species (RONS) maintained by the activity of endogenous antioxidant system (AOS) allow reversible oxidative/nitrosative modifications of key redox-sensitive residues in regulatory proteins. The reversibility of redox modifications such as Cys S-sulphenylation/S-glutathionylation/S-nitrosylation/S-persulphidation and disulphide bond formation, or Tyr nitration, which occur through electrophilic attack of RONS to nucleophilic groups in amino acid residues provides redox switches in the activities of signalling proteins. Key requirement for the involvement of the redox modifications in RONS signalling including ROS-MAPK, ROS-PI3K/Akt, and RNS-TNF-α/NF-kB signalling is their specificity provided by a residue microenvironment and reaction kinetics. Glutathione, glutathione peroxidases, peroxiredoxins, thioredoxin, glutathione reductases, and glutaredoxins modulate RONS level and cell signalling, while some of the modulators (glutathione, glutathione peroxidases and peroxiredoxins) are themselves targets for redox modifications. Additionally, gene expression, activities of transcription factors, and epigenetic pathways are also under redox regulation. The present review focuses on RONS sources (NADPH-oxidases, mitochondrial electron-transportation chain (ETC), nitric oxide synthase (NOS), etc.), and their cross-talks, which influence reversible redox modifications of proteins as physiological phenomenon attained by living cells during the evolution to control cell signalling in the oxygen-enriched environment. We discussed recent advances in investigation of mechanisms of protein redox modifications and adaptive redox switches such as MAPK/PI3K/PTEN, Nrf2/Keap1, and NF-κB/IκB, powerful regulators of numerous physiological processes, also implicated in various diseases.

...read moreread less

187 citations

1
2
3
4
…
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57

Collapse

References

PDF

Open Access

More filters

Book•

CRC Handbook of Chemistry and Physics

[...]

William M. Haynes¹•Institutions (1)

National Institute of Standards and Technology¹

01 Jan 1973

TL;DR: CRC handbook of chemistry and physics, CRC Handbook of Chemistry and Physics, CRC handbook as discussed by the authors, CRC Handbook for Chemistry and Physiology, CRC Handbook for Physics,

...read moreread less

Abstract: CRC handbook of chemistry and physics , CRC handbook of chemistry and physics , کتابخانه مرکزی دانشگاه علوم پزشکی تهران

...read moreread less

52,268 citations

Journal Article•DOI•

Superoxide Dismutase AN ENZYMIC FUNCTION FOR ERYTHROCUPREIN (HEMOCUPREIN)

[...]

Joe M. McCord¹, Irwin Fridovich¹•Institutions (1)

Duke University¹

25 Nov 1969-Journal of Biological Chemistry

TL;DR: The demonstration that O2·- can reduce ferricytochrome c and tetranitromethane, and that superoxide dismutase, by competing for the superoxide radicals, can markedly inhibit these reactions, is demonstrated.

...read moreread less

12,468 citations

"The rate of oxygen utilization by c..." refers background in this paper

...Superoxide dismutase (SOD) catalyzes the removal of O2, producing oxygen and hydrogen peroxide (Reaction (4)) [17]:...
[...]

Journal Article•DOI•

How mitochondria produce reactive oxygen species.

[...]

Michael P. Murphy

01 Jan 2009-Biochemical Journal

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

...read moreread less

Abstract: The production of ROS (reactive oxygen species) by mammalian mitochondria is important because it underlies oxidative damage in many pathologies and contributes to retrograde redox signalling from the organelle to the cytosol and nucleus. Superoxide (O2•−) is the proximal mitochondrial ROS, and in the present review I outline the principles that govern O2•− production within the matrix of mammalian mitochondria. The flux of O2•− is related to the concentration of potential electron donors, the local concentration of O2 and the second-order rate constants for the reactions between them. Two modes of operation by isolated mitochondria result in significant O2•− production, predominantly from complex I: (i) when the mitochondria are not making ATP and consequently have a high Δp (protonmotive force) and a reduced CoQ (coenzyme Q) pool; and (ii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix. For mitochondria that are actively making ATP, and consequently have a lower Δp and NADH/NAD+ ratio, the extent of O2•− production is far lower. The generation of O2•− within the mitochondrial matrix depends critically on Δp, the NADH/NAD+ and CoQH2/CoQ ratios and the local O2 concentration, which are all highly variable and difficult to measure in vivo. Consequently, it is not possible to estimate O2•− generation by mitochondria in vivo from O2•−-production rates by isolated mitochondria, and such extrapolations in the literature are misleading. Even so, the description outlined here facilitates the understanding of factors that favour mitochondrial ROS production. There is a clear need to develop better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

...read moreread less

6,371 citations

"The rate of oxygen utilization by c..." refers background in this paper

...[61] Antunes, F.; Cadenas, E. Estimation of H2O2 gradients across biomembranes....
[...]
...Rat hepatocytes (fresh) Primary, rat (SC) 200 12 fmol min−1 cell−1 Fick's law [71] Rat hepatocytes (fresh) Primary, rat (on scaffold) 200 12 fmol min−1 cell−1 Fick's law [71] Rat hepatocytes Rat hepatocytes 350 0.35 nmol s−1 (106 cells)−1 Clark electrode with real-time numerical averaging [49] Rat hepatocytes Rat hepatocytes 430 0.43 nmol s−1 (106 cells)−1 Clark electrode [51] Porcine hepatocytes Day 4 after seeding Day 15 after seeding 900 300 0.9 nmol s−1 (106 cells)−1 0.3 nmol s−1 (106 cells)−1 Clark electrode with real-time numerical averaging [49] Synaptosomes Rat brain, no treatment (65 amol s−1 ng-protein−1) 3.92 nmol min−1 (mg protein)−1 Clark electrode [80] Sf9 insect cells Spodoptera frugiperda, ovarian 33 2.0 fmol min−1 cell−1 Fick's law (G2)b [71] Hi-5 insect cells Trichoplusia ni, ovarian 105 6.3 fmol min−1 cell−1 Fick's law (G2)b [71] FS-4 Human diploid foreskin cells (SC) 14 0.05 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient (G3)c [48] HLM Liver (AC) 102 0.37 mmol h−1 (109 cells)−1 Use modified Cartesian diver [48,81] LIR Liver (AC) 83 0.30 mmol h−1 (109 cells)−1 Use modified Cartesian diver [48,81] Skin fibroblast Human (AC) 18 0.064 mmol h−1 (109 cells)−1 Use modified Cartesian diver [48,81] 143B Human osteosarcoma (AC) 16.3 16.32±0.53fpmol O2 s−1 (106 cells)−1 Oxygen monitor with Clark electrode [72] 143Bρ0 Human osteosarcoma with knockout mitochondria (AC) 5.6 5.62±0.40fpmol O2 s−1 (106 cells)−1 Oxygen monitor with Clark electrode [72] Detroit 6 From bone marrow of lung cancer patients (AC) 120 0.43 mmol h−1 (109 cells)−1 [82] MCN Leukemia (AC) 61 0.22 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient [82] Conjunctiva Human eye cells (AC) 78 0.28 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient [82] Lung To Human embryonic lung cells (AC) 67 0.24 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient [82] Intestine 407 Human (AC) 111 0.40 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient [82] MAF-E Adult Fallopian tube (AC) 106 0.38 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient [82] Red blood cells Human (adult) 4×10−5 Contribution estimated from the rate of autoxidation of oxyhemoglobin to form superoxide; H2O2 is generated at a rate of 3.9± 0.6 nmol·h−1·gHb−1 This corresponds to about 50 superoxide radicals being produced each second in an RBC. [83] Red blood cells Rabbit 0.02 (1.5±0.2)×10−15 L RBC−1 h−1 Gilson differential recording respirometer, 38 °C [84] Lymphoblastoid (Namalioa) Human (AC) 15 0.053 mmol h−1 (109 cells)−1 Based on oxygen demand by cells and mass transfer coefficient [85] J774A.1 Murine macrophages (AC) 31 1.87 nmol min−1 (106 cells)−1 EPR oximetry [86] J774A.1 Murine macrophages (AC) 6.2 6.18±0.33fpmol O2 s−1 (106 cells)−1 Oxygen monitor with Clark electrode [72] CHO Chinese hamster ovary cells (SC) 74 4.43 nmol min−1 (106 cells)−1 EPR oximetry (G4)d [86] CHO Chinese hamster ovary cells (SC) 88 3.2×10−13 mol cell−1 h−1 (5.3 nmol min−1 (106 cells)−1) Microtiter plate with oxygen sensor [87] CHO Chinese hamster ovary cells (SC) 86 0.31 pmol cell−1 h−1 Using a respirometer [73] CHO Chinese hamster ovary cells (SC) 8.0 0.50 fmol min−1 cell−1 Fick's law (G1)a [71] CHO Chinese hamster ovary cells (SC) 63 3.8×107 molecules of O2 s−1 cell−1 EPR oximetry [47] CCD Kidney cortex collecting duct cells 25 1.48 nmol min−1 (106 cells)−1 EPR oximetry [86] AG08472 Vascular endothelial cells of the pig thoracic aorta (AC) 17 1±0.15 nmol min−1 (106 cells)−1 (when measured at 22 °C), 0.64 (at 4 °C) Optical method using oxygen quenchers [88] AG08473 SMC of cells of the pig thoracic aorta (AC) 44 2.64±0.14 nmol min−1 (106 cells)−1 Optical method using oxygen quenchers [88] 704 B.A ....
[...]
...This superoxide is thought to be primarily produced by the reaction of dioxygenwith the semiquinone radical (CoQ•−) of coenzyme Q (ubiquinone) of the electron transport chain [7,11–16]: CoQ •− þ O2↔ CoQ þ O•−2 : ð3Þ Superoxide dismutase (SOD) catalyzes the removal of O2•−, producing oxygen and hydrogen peroxide (Reaction (4)) [17]: O•−2 + O •− 2 + 2H þ→H2O2 + O2: ð4Þ Superoxide and hydrogen peroxide can be initiators or contributors to pathology....
[...]
...A small fraction undergoes one-electron reduction to form superoxide, estimated to ≈1% or less of the rate of oxygen consumption (OCR) [7–10]; the actual univalent reduction of dioxygen in the electron transport chain of the mitochondrion in vivo is thought to be much less than this [7]....
[...]
...In metabolic processes that produce ATP only a small fraction, on the order of 1% or less, of the oxygen utilization results in the production of O2 and H2O2[7,9,10]....
[...]

Journal Article•DOI•

The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology

[...]

Karen Bedard¹, Karl-Heinz Krause•Institutions (1)

University of Geneva¹

01 Jan 2007-Physiological Reviews

TL;DR: This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.

...read moreread less

Abstract: For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phag...

...read moreread less

5,873 citations

"The rate of oxygen utilization by c..." refers background in this paper

...There is a family of NADPH-oxidases that serve a variety of functions [66]....
[...]

Journal Article•DOI•

Mitochondrial formation of reactive oxygen species.

[...]

Julio F. Turrens¹•Institutions (1)

University of South Alabama¹

01 Oct 2003-The Journal of Physiology

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.

...read moreread less

Abstract: The reduction of oxygen to water proceeds via one electron at a time. In the mitochondrial respiratory chain, Complex IV (cytochrome oxidase) retains all partially reduced intermediates until full reduction is achieved. Other redox centres in the electron transport chain, however, may leak electrons to oxygen, partially reducing this molecule to superoxide anion (O2−•). Even though O2−• is not a strong oxidant, it is a precursor of most other reactive oxygen species, and it also becomes involved in the propagation of oxidative chain reactions. Despite the presence of various antioxidant defences, the mitochondrion appears to be the main intracellular source of these oxidants. 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. We also discuss various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.

...read moreread less

4,282 citations