scholarly journals An Oxygen Paradox: Catalytic Use of Oxygen in Radical Photopolymerization

2019 ◽  
Vol 58 (47) ◽  
pp. 16811-16814 ◽  
Author(s):  
Liwen Zhang ◽  
Chenyu Wu ◽  
Kenward Jung ◽  
Yun Hau Ng ◽  
Cyrille Boyer
Keyword(s):  
Oxygen Paradox

scholarly journals Increasing Oxygen Partial Pressures Induce a Distinct Transcriptional Response in Human PBMC: A Pilot Study on the “Normobaric Oxygen Paradox”

2021 ◽  
Vol 22 (1) ◽  
pp. 458
Author(s):  
Deborah Fratantonio ◽  
Fabio Virgili ◽  
Alessandro Zucchi ◽  
Kate Lambrechts ◽  
Tiziana Latronico ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Stress Response ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Oxidative Stress Response ◽  
Molecular Characteristics ◽  
Nuclear Factor ◽  
Normobaric Oxygen ◽  
Oxygen Paradox

The term “normobaric oxygen paradox” (NOP), describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as oxygen shortage, and resulting in up-regulation of the Hypoxia-inducible factor 1α (HIF-1α) transcription factor activity. The molecular characteristics of this response have not been yet fully characterized. Herein, we report the activation time trend of oxygen-sensitive transcription factors in human peripheral blood mononuclear cells (PBMCs) obtained from healthy subjects after one hour of exposure to mild (MH), high (HH) and very high (VHH) hyperoxia, corresponding to 30%, 100%, 140% O2, respectively. Our observations confirm that MH is perceived as a hypoxic stress, characterized by the activation of HIF-1α and Nuclear factor (erythroid-derived 2)-like 2 (NRF2), but not Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB). Conversely, HH is associated to a progressive loss of NOP response and to an increase in oxidative stress leading to NRF2 and NF-kB activation, accompanied by the synthesis of glutathione (GSH). After VHH, HIF-1α activation is totally absent and oxidative stress response, accompanied by NF-κB activation, is prevalent. Intracellular GSH and Matrix metallopeptidase 9 (MMP-9) plasma levels parallel the transcription factors activation pattern and remain elevated throughout the observation time. In conclusion, our study confirms that, in vivo, the return to normoxia after MH is sensed as a hypoxic trigger characterized by HIF-1α activation. On the contrary, HH and VHH induce a shift toward an oxidative stress response, characterized by NRF2 and NF-κB activation in the first 24 h post exposure.

The normobaric oxygen paradox: A novel way to administer oxygen as an adjuvant treatment for cancer?

2011 ◽  
Vol 76 (4) ◽  
pp. 467-470 ◽  
Author(s):  
D. De Bels ◽  
F. Corazza ◽  
P. Germonpré ◽  
C. Balestra
Keyword(s):  
Adjuvant Treatment ◽  
Normobaric Oxygen ◽  
Oxygen Paradox

Progress in understanding the molecular oxygen paradox – function of mitochondrial reactive oxygen species in cell signaling

2017 ◽  
Vol 398 (11) ◽  
pp. 1209-1227 ◽  
Author(s):  
Nidhi Kuksal ◽  
Julia Chalker ◽  
Ryan J. Mailloux
Keyword(s):  
Reactive Oxygen Species ◽  
Molecular Oxygen ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Antioxidant Systems ◽  
Oxygen Species ◽  
Oxygen Paradox ◽  
Secondary Messenger ◽  
Cell Structures ◽  
By Products

AbstractThe molecular oxygen (O2) paradox was coined to describe its essential nature and toxicity. The latter characteristic of O2is associated with the formation of reactive oxygen species (ROS), which can damage structures vital for cellular function. Mammals are equipped with antioxidant systems to fend off the potentially damaging effects of ROS. However, under certain circumstances antioxidant systems can become overwhelmed leading to oxidative stress and damage. Over the past few decades, it has become evident that ROS, specifically H2O2, are integral signaling molecules complicating the previous logos that oxyradicals were unfortunate by-products of oxygen metabolism that indiscriminately damage cell structures. To avoid its potential toxicity whilst taking advantage of its signaling properties, it is vital for mitochondria to control ROS production and degradation. H2O2elimination pathways are well characterized in mitochondria. However, less is known about how H2O2production is controlled. The present review examines the importance of mitochondrial H2O2in controlling various cellular programs and emerging evidence for how production is regulated. Recently published studies showing how mitochondrial H2O2can be used as a secondary messenger will be discussed in detail. This will be followed with a description of how mitochondria use S-glutathionylation to control H2O2production.

Is there an oxygen paradox in skeletal muscle?

1988 ◽  
Vol 16 (6) ◽  
pp. 1050-1050 ◽  
Author(s):  
NASRIN SHAMSADEEN ◽  
C. J. DUNCAN
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Paradox

Nitrogen loss and oxygen paradox in full-scale biofiltration for drinking water treatment

2007 ◽  
Vol 41 (7) ◽  
pp. 1455-1464 ◽  
Author(s):  
X YU ◽  
Z QI ◽  
X ZHANG ◽  
P YU ◽  
B LIU ◽  
...  
Keyword(s):  
Drinking Water ◽  
Water Treatment ◽  
Nitrogen Loss ◽  
Drinking Water Treatment ◽  
Full Scale ◽  
Oxygen Paradox

Yet another oxygen paradox

2005 ◽  
Vol 99 (4) ◽  
pp. 1245-1246 ◽  
Author(s):  
Thomas Clanton
Keyword(s):  
Oxygen Paradox

Free radical metabolites in myocardium during ischemia and reperfusion

1991 ◽  
Vol 261 (4) ◽  
pp. L81-L86 ◽  
Author(s):  
Enno K. Ruuge ◽  
Alexander N. Ledenev ◽  
Vladimir L. Lakomkin ◽  
Alexander A. Konstantinov ◽  
Marina Yu. Ksenzenko
Keyword(s):  
Electron Paramagnetic Resonance ◽  
Free Radical ◽  
Low Temperature ◽  
Coenzyme Q ◽  
Heart Tissue ◽  
Paramagnetic Species ◽  
Spectral Parameters ◽  
Paramagnetic Resonance ◽  
Oxygen Paradox ◽  
Electron Paramagnetic

Low-temperature electron paramagnetic resonance (EPR) spectroscopy and spin traps were used to measure paramagnetic species generation in rat hearts and isolated mitochondria. The hearts were freeze-clamped at 77 K during control perfusion by the Langendorff procedure, after 20–30 min of normothermic ischemia or 10–30 s of reperfusion with oxygenated perfusate. All EPR spectra measured at 4.5–50 K exhibited signals of both mitochondrial free radical centers and FeS proteins. The analysis of spectral parameters measured at 243 K showed that free radicals in heart tissue were semiquinones of coenzyme Q10 and flavins. The appearance of a typical “doublet” signal at g = 1.99 in low-temperature spectra indicated that a part of ubisemiquinones formed a complex with a high potential FeS protein of succinate dehydrogenase. Ischemia decreased the free radical species in myocardium ≈50%; the initiation of reflow of perfusate resulted in quick increase of the EPR signal. Mitochondria isolated from hearts during control perfusion and after 20–30 min of ischemia were able to produce superoxide radicals in both the NADH-coenzyme Q10 reductase and the bc1 segments of the respiratory chain. The rate of oxyradical generation was significantly higher in mitochondria isolated from ischemic heart. electron paramagnetic resonance; oxygen paradox; oxyradicals; rat heart; semiquinones

The Protective Effect of Lowered Temperature on the Oxygen Paradox in the Rat Heart

Pathobiology ◽  
1996 ◽  
Vol 64 (4) ◽  
pp. 217-221
Author(s):  
R.J. Harding ◽  
C.J. Duncan
Keyword(s):  
Protective Effect ◽  
Rat Heart ◽  
Oxygen Paradox

Sarcolemmal integrity and metabolic competence of cardiomyocytes under anoxia-reoxygenation

1990 ◽  
Vol 258 (2) ◽  
pp. H285-H291 ◽  
Author(s):  
B. Siegmund ◽  
A. Koop ◽  
T. Klietz ◽  
P. Schwartz ◽  
H. M. Piper
Keyword(s):  
Lactate Dehydrogenase ◽  
Cell Injury ◽  
Atp Hydrolysis ◽  
Isolated Cardiomyocytes ◽  
Adult Rat ◽  
Mechanical Constraints ◽  
Oxygen Paradox ◽  
Energetic State ◽  
Sarcolemmal Integrity ◽  
Partial Oxygen

In tissue, mechanical cell-to-cell interactions may contribute to cardiomyocyte injury in anoxia-reoxygenation. In the present study, the disturbance of energy metabolism and cell injury were investigated in isolated cardiomyocytes, free of external mechanical constraints. Cardiomyocytes from adult rat, attached to culture dishes, were exposed to 120 min of anoxia and 15 min of reoxygenation in a substrate-free modified Tyrode solution. The energetic state of the cells in anoxia-reoxygenation was characterized by the free-energy change of ATP hydrolysis (delta GATP), amounting to 57 kJ/mol ATP in normoxia. After 120 min of anoxia, all cells were contracted to 65% of their length and delta GATP decreased to 41 kJ/mol. No lactate dehydrogenase was released. Reoxygenation caused a partial oxygen paradox: immediate hypercontracture of the cells, but no release of lactate dehydrogenase. delta GATP recovered to 51 kJ/mol within 15 min. The results demonstrate that anoxic cardiomyocytes can be energy depleted without losing sarcolemmal integrity. They can undergo hypercontracture, elicited by reoxygenation, and yet an almost normal delta GATP can be reestablished.

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