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1
Reading, Stacey A., and Maggie Yeomans. "Oxygen absorption by skin exposed to oxygen supersaturated water." Canadian Journal of Physiology and Pharmacology 90, no. 5 (May 2012): 515–24. http://dx.doi.org/10.1139/y2012-020.
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The present study tests the hypothesis that skin on the plantar surface of the foot absorbs oxygen (O2) when immersed in water that has a high dissolved O2 content. Healthy male and female subjects (24.2 ± 1.4 years) soaked each foot in tap water (1.7 ± 0.1 mg O2·L–1; 30.7 ± 0.3 °C) or O2-infused water (50.2 ± 1.7 mg O2·L–1; 32.1 ± 0.5 °C) for up to 30 min in 50 different experiments. Transcutaneous oximetry and near infrared spectroscopy were used to evaluate changes in skin PO2, oxygenated haemoglobin, and cytochrome oxidase aa3 that resulted from treatment. Compared with the tap water condition, tissue oxygenation index was 3.5% ± 1.3% higher in feet treated for 30 min with O2-infused water. This effect persisted after treatment, as skin PO2 was higher in feet treated with O2-infused water at 2 min (237 ± 9 vs. 112 ± 5 mm HG) and 15 min (131 ± 1 vs. 87 ± 4 mm HG) post-treatment. When blood flow to the foot was occluded for 5 min, feet resting in O2-infused water maintained a 3-fold higher O2 consumption rate than feet treated with tap water (9.1 ± 1.4 vs. 3.0 ± 1.0 µL·100 g–1·min–1). We estimate that skin absorbs 4.5 mL of O2·m–2·min–1 from O2-infused water. Thus, skin absorbs appreciable amounts of O2 from O2-infused water. This finding may prove useful and assist development of treatments targeting skin diseases with ischemic origin.
2
Mangum, C. P. "Oxygen transport in invertebrates." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 5 (May 1, 1985): R505—R514. http://dx.doi.org/10.1152/ajpregu.1985.248.5.r505.
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The distribution of the O2 carrying proteins suggests that the original transport system was a hemoglobin similar to the alpha-chain of hemoglobin A and packaged in a nucleated red blood cell. These molecules, which occur in large open fluid compartments, function as O2 stores for regular periods of hypoxia as well as carriers between sites of gas exchange. When the closed circulatory system first arose, the red blood cell was abandoned in favor of extracellular heme proteins, and the O2 storage function became less important. Alternative O2 carriers, hemerythrins, appear in the blood at about the same phylogenetic level as the intracellular hemoglobins, and their respiratory functions appear to be similar. The presence of hemoglobins instead of hemerythrins in the vertebrates may be an evolutionary accident. Still other O2 carriers, hemocyanins, arose separately in two specialized groups that left no descendants. Their O2 binding has all the adaptive features of vertebrate hemoglobin O2 binding, with unique features also. The respiratory function of the hemocyanins is largely limited to O2 transport, which makes a far greater contribution to aerobic metabolism than the O2 carriers found in simpler systems.
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Hochachka, P. W. "Metabolic suppression and oxygen availability." Canadian Journal of Zoology 66, no. 1 (January 1, 1988): 152–58. http://dx.doi.org/10.1139/z88-021.
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The aerobic metabolic rates of cells, tissues, and even whole organisms remain relatively constant down to very low values (O2-regulating response) or decline steadily with O2 availability (O2-conforming response). (O2-regulating systems attempt to make up the energy deficit arising when O2 uptake begins to decline by activating anaerobic metabolism; this process is termed the Pasteur effect and typically involves 5- to 15-fold increases in glucose utilization rates. O2 conformers do not make up the energy deficit and thus enter a metabolically arrested state as O2 availability declines. Current data suggest that O2 conformers can maintain coupled metabolism–membrane functions at metabolically arrested states while O2 regulators cannot, presumably because of more permeable membranes and thus higher energy-dependent ion pumping requirements. These fundamental differences in response to, and tolerance of, hypoxia may be related to qualitative or quantitative differences in inducible stress proteins during O2 deprivation.
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Hoffman, David L., and Paul S. Brookes. "Oxygen Sensitivity of Mitochondrial Reactive Oxygen Species Generation Depends on Metabolic Conditions." Journal of Biological Chemistry 284, no. 24 (April 14, 2009): 16236–45. http://dx.doi.org/10.1074/jbc.m809512200.
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The mitochondrial generation of reactive oxygen species (ROS) plays a central role in many cell signaling pathways, but debate still surrounds its regulation by factors, such as substrate availability, [O2] and metabolic state. Previously, we showed that in isolated mitochondria respiring on succinate, ROS generation was a hyperbolic function of [O2]. In the current study, we used a wide variety of substrates and inhibitors to probe the O2 sensitivity of mitochondrial ROS generation under different metabolic conditions. From such data, the apparent Km for O2 of putative ROS-generating sites within mitochondria was estimated as follows: 0.2, 0.9, 2.0, and 5.0 μm O2 for the complex I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein quinone oxidoreductase of β-oxidation, respectively. Differential effects of respiratory inhibitors on ROS generation were also observed at varying [O2]. Based on these data, we hypothesize that at physiological [O2], complex I is a significant source of ROS, whereas the electron transfer flavoprotein quinone oxidoreductase may only contribute to ROS generation at very high [O2]. Furthermore, we suggest that previous discrepancies in the assignment of effects of inhibitors on ROS may be due to differences in experimental [O2]. Finally, the data set (see supplemental material) may be useful in the mathematical modeling of mitochondrial metabolism.
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Kizaki, Z., and R. G. Thurman. "Stimulation of oxygen uptake by glucagon is oxygen dependent in perfused rat liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 2 (February 1, 1989): G369—G376. http://dx.doi.org/10.1152/ajpgi.1989.256.2.g369.
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Livers from well-fed female Sprague-Dawley rats (100-150 g) were perfused at flow rates of 4 or 8 ml.g liver-1.min-1 to deliver O2 to the organ at various rates. During perfusion at normal flow rates (4 ml.g-1.min-1), glucagon (10 nM) increased O2 uptake in perfused liver by approximately 40 mumol.g-1.h-1. In contrast, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 when livers were perfused at high flow rates. Increase in O2 uptake was directly proportional to flow rate and was blocked partially by infusion of phorbol myristate acetate (100 nM) before glucagon. Increase in O2 uptake due to elevated flow was not due to enhanced glucagon delivery, since infusion of 120 nM glucagon at normal flow rates only increased O2 uptake by approximately 40 mumol.g-1.h-1. On the other hand, when O2 tension in the perfusate was manipulated at normal flow rates, the stimulation of O2 uptake by glucagon increased proportional to the average O2 tension in the liver. Infusion of 8-bromo-adenosine 3',5'-cyclic monophosphate (BrcAMP; 25 microM) also increased O2 uptake more than twice as much at high compared with normal flow rates. In the presence of angiotensin II (5 nM), a hormone that increases intracellular calcium, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 at normal flow rates. Infusion of glucagon or BrcAMP into livers perfused at normal flow rates increased state 3 rates of O2 uptake of subsequently isolated mitochondria significantly by approximately 25%. In contrast, perfusion with glucagon or BrcAMP at high flow rates increased mitochondrial respiration by 50-60%. Glucagon addition acutely to suspensions of mitochondria, however, had no effect on O2 uptake. These data are consistent with reports that glucagon administration in vivo or treatment of intact cells with glucagon increases O2 uptake of subsequently isolated mitochondria, a phenomenon that can account for the observed increase in O2 uptake in livers perfused at high flow rates with glucagon. Furthermore, these results are consistent with the hypothesis that the effect of glucagon on mitochondria is O2 dependent in the perfused liver. This is most likely due to an effect of intracellular calcium on a mechanism mediated via cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)
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Nakagawa, Y., T. Matsumura, M. Goto, W. Qu, F. C. Kauffman, and R. G. Thurman. "Increase in oxygen uptake due to arachidonic acid is oxygen dependent in the perfused liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 5 (May 1, 1994): G953—G959. http://dx.doi.org/10.1152/ajpgi.1994.266.5.g953.
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The purpose of this study was to determine whether the effect of arachidonic acid on hepatic O2 uptake is O2 dependent and which region of the liver lobule it affects. In livers perfused at normal flow rates, infusion of arachidonate increased O2 uptake significantly by about 20-25 mumol.g-1.h-1. When the flow rate was doubled to make the hepatic O2 gradient shallower, the increase in O2 uptake due to arachidonate was two to three times larger (i.e., approximately 50 mumol.g-1.h-1). In livers perfused in the retrograde direction, maximal rates of O2 uptake were about twofold higher in upstream pericentral than in downstream periportal regions, and arachidonic acid nearly doubled O2 uptake in downstream areas without affecting rates in upstream regions. Thus it is concluded that arachidonate stimulates O2 uptake in an O2-dependent manner. This effect was sensitive to an inhibitor of the lipoxygenase, nordihydroguaiaretic acid, in perfused liver but not in isolated hepatocytes. In addition, conditioned medium from Kupffer cells incubated at high O2 tension stimulated parenchymal cell O2 uptake. Furthermore, arachidonate increased intracellular Ca2+ in isolated Kupffer cells in a dose-dependent manner. These findings suggest that eicosanoids produced by nonparenchymal cells participate in a hepatic O2 sensor mechanism involving Ca2+ that regulates O2 uptake by parenchymal cells in the liver.
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Puntarulo, S., and A. I. Cederbaum. "Effect of oxygen concentration on microsomal oxidation of ethanol and generation of oxygen radicals." Biochemical Journal 251, no. 3 (May 1, 1988): 787–94. http://dx.doi.org/10.1042/bj2510787.
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The iron-catalysed production of hydroxyl radicals, by rat liver microsomes (microsomal fractions), assessed by the oxidation of substrate scavengers and ethanol, displayed a biphasic response to the concentration of O2 (varied from 3 to 70%), reaching a maximal value with 20% O2. The decreased rates of hydroxyl-radical generation at lower O2 concentrations correlates with lower rates of production of H2O2, the precursor of hydroxyl radical, whereas the decreased rates at elevated O2 concentrations correlate with lower rates (relative to 20% O2) of activity of NADPH-cytochrome P-450 reductase, which reduces iron and is responsible for redox cycling of iron by the microsomes. The oxidation of aniline or aminopyrine and the cytochrome P-450/oxygen-radical-independent oxidation of ethanol also displayed a biphasic response to the concentration of O2, reaching a maximum at 20% O2, which correlates with the dithionite-reducible CO-binding spectra of cytochrome P-450. Microsomal lipid peroxidation increased as the concentration of O2 was raised from 3 to 7 to 20% O2, and then began to level off. This different pattern of malondialdehyde generation compared with hydroxyl-radical production probably reflects the lack of a role for hydroxyl radical in microsomal lipid peroxidation. These results point to the complex role for O2 in microsomal generation of oxygen radicals, which is due in part to the critical necessity for maintaining the redox state of autoxidizable components of the reaction system.
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Han, Jiuli, Lu Bai, Bingbing Yang, Yinge Bai, Shuangjiang Luo, Shaojuan Zeng, Hongshuai Gao, et al. "Highly Selective Oxygen/Nitrogen Separation Membrane Engineered Using a Porphyrin-Based Oxygen Carrier." Membranes 9, no. 9 (September 3, 2019): 115. http://dx.doi.org/10.3390/membranes9090115.
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Air separation is very important from the viewpoint of the economic and environmental advantages. In this work, defect-free facilitated transport membranes based on poly(amide-12-b-ethylene oxide) (Pebax-2533) and tetra(p-methoxylphenyl)porphyrin cobalt chloride (T(p-OCH3)PPCoCl) were fabricated in systematically varied compositions for O2/N2 separation. T(p-OCH3)PPCoCl was introduced as carriers that selectively and reversibly interacted with O2 and facilitated O2 transport in the membrane. The T(p-OCH3)PPCoCl had good compatibility with the Pebax-2533 via the hydrogen bond interaction and formed a uniform and thin selective layer on the substrate. The O2 separation performance of the thin film composite (TFC) membranes was improved by adding a small amount of the T(p-OCH3)PPCoCl and decreasing the feed pressure. At the pressure of 0.035 MPa, the O2 permeability and O2/N2 selectivity of the 0.6 wt % T(p-OCH3)PPCoCl/Pebax-2533 was more than 3.5 times that of the Pebax-2533 TFC membrane, which reached the 2008 Robeson upper bound. It provides a candidate membrane material for O2/N2 efficient separation in moderate conditions.
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Zhou, J., B. Delille, F. Brabant, and J. L. Tison. "Insights into oxygen transport and net community production in sea ice from oxygen, nitrogen and argon concentrations." Biogeosciences 11, no. 18 (September 18, 2014): 5007–20. http://dx.doi.org/10.5194/bg-11-5007-2014.
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Abstract. We present and compare the dynamics (i.e., changes in standing stocks, saturation levels and concentrations) of O2, Ar and N2 in landfast sea ice, collected in Barrow (Alaska), from February through June 2009. The comparison suggests that the dynamic of O2 in sea ice strongly depends on physical processes (gas incorporation and subsequent transport). Since Ar and N2 are only sensitive to the physical processes in the present study, we then discuss the use of O2 / Ar and O2 / N2 to correct for the physical contribution to O2 supersaturations, and to determine the net community production (NCP). We conclude that O2 / Ar suits better than O2 / N2, due to the relative abundance of O2, N2 and Ar, and the lower biases when gas bubble formation and gas diffusion are maximized. We further estimate NCP in the impermeable layers during ice growth, which ranged from −6.6 to 3.6 μmol O2 L−1 d−1, and the concentrations of O2 due to biological activity in the permeable layers during ice decay (3.8 to 122 μmol O2 L−1). We finally highlight the key issues to solve for more accurate NCP estimates in the future.
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Trushina, Aleksandra P., Veniamin G. Goldort, Sergei A. Kochubei, and Alexey V. Baklanov. "UV-photoexcitation of encounter complexes of oxygen O2–O2 as a source of singlet oxygen O2(1Δg) in gas phase." Chemical Physics Letters 485, no. 1-3 (January 2010): 11–15. http://dx.doi.org/10.1016/j.cplett.2009.11.058.
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Zhou, J., B. Delille, F. Brabant, and J. L. Tison. "Insights into oxygen transport and net community production in sea ice from oxygen, nitrogen and argon concentrations." Biogeosciences Discussions 11, no. 2 (February 4, 2014): 2045–81. http://dx.doi.org/10.5194/bgd-11-2045-2014.
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Abstract. We present the evolution of O2 standing stocks, saturation levels and concentrations in landfast sea ice, collected in Barrow (Alaska), from February to June 2009. The comparison of the standing stocks and saturation levels of O2 against those of N2 and Ar suggests that the dynamic of O2 in sea ice strongly depends on physical processes (gas incorporation and subsequent transport). We then discuss on the use of O2 / Ar and O2 / N2 to correct for the physical contribution and to determine the biological contribution (NCP) to O2 supersaturations. We conclude that O2 / Ar suits better than O2 / N2, because O2 / N2 is more sensitive due to the relative abundance of O2, N2 and Ar, and less biased when gas bubble formation and gas diffusion are maximized. We further estimate the NCP in the impermeable layers during ice growth and in the permeable layers during ice decay. Our results indicate that NCP contributed to a~release of carbon to the atmosphere in the upper ice layers, but to an uptake of carbon at sea ice bottom. Overall, seawater (rather than the atmosphere) may be the main supplier of carbon for sea ice microorganisms.
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Trimbee, Annette M., and E. E. Prepas. "Dependence of Lake Oxygen Depletion Rates on Maximum Oxygen Storage in a Partially Meromictic Lake in Alberta." Canadian Journal of Fisheries and Aquatic Sciences 45, no. 3 (March 1, 1988): 571–76. http://dx.doi.org/10.1139/f88-069.
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Areal rates of hypolimnetic oxygen depletion (AHOD) and winter oxygen depletion (AWOD) varied considerably from year to year in a partially meromictic lake (Narrow Lake) in central Alberta. AHOD ranged from 0.222 to 0.522 g O2∙m−2∙d−1 over four summers and AWOD ranged from 0.354 to 0.614 g O2∙m−2∙d−1 over three winters. AHOD was positively correlated with maximum storage of dissolved oxygen (O2) at the onset of summer thermal stratification (P < 0.05). Similarly, AWOD was higher in years when mixing was more complete and maximum O2 storage at freeze-up was higher. These results suggest that the prediction of O2 depletion rates for lakes with year-to-year variation in maximum O2 storage can be improved if maximum O2 storage after lake mixing is considered in addition to other factors known to influence O2 depletion rates such as lake productivity and morphometry.
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Murphy, Michael P. "How mitochondria produce reactive oxygen species." Biochemical Journal 417, no. 1 (December 12, 2008): 1–13. http://dx.doi.org/10.1042/bj20081386.
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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.
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Samsel, R. W., D. Cherqui, A. Pietrabissa, W. M. Sanders, M. Roncella, J. C. Emond, and P. T. Schumacker. "Hepatic oxygen and lactate extraction during stagnant hypoxia." Journal of Applied Physiology 70, no. 1 (January 1, 1991): 186–93. http://dx.doi.org/10.1152/jappl.1991.70.1.186.
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As O2 delivery falls, tissues must extract increasing amounts of O2 from blood to maintain a normal O2 consumption. Below a critical delivery threshold, increases in O2 extraction cannot compensate for the falling delivery, and O2 uptake falls in a supply-dependent fashion. Numerous studies have identified a critical delivery in whole animals, but the regional contributions to the critical O2 delivery are less fully understood. In the present study, we explored the limits of O2 extraction in the isolated liver, seeking to determine 1) the normal relationship between O2 consumption and delivery in the liver and 2) the relationship of hepatic lactate extraction to the drop in hepatic O2 consumption at low O2 deliveries. To answer these questions, using support dogs as a source for oxygenated metabolically stable blood, we studied eight pump-perfused canine livers. By lowering the blood flow in a model of stagnant hypoxia, we explored the relationship between O2 consumption and delivery over the entire physiological range of O2 delivery. The critical O2 delivery was 28 +/- 5 (SD) ml.kg-1.min-1; the livers extracted 68 +/- 9% of the delivered O2 before reaching supply dependence. This suggests that the liver has an O2 extraction capacity quite similar to the body as a whole and not different from other tissues that have been isolated. At high blood flows, the livers extracted approximately 10% of the lactate delivered by the blood, but the arteriovenous lactate differences were small. At low blood flows, however, the livers changed from lactate consumption to production. The O2 delivery coinciding with the dropoff in lactate extraction did not differ significantly from the critical O2 delivery. We conclude that reductions in lactate uptake by the liver do not precede the transition to O2 supply dependence.
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Dean, Jay B., Daniel K. Mulkey, Richard A. Henderson, Stephanie J. Potter, and Robert W. Putnam. "Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons." Journal of Applied Physiology 96, no. 2 (February 2004): 784–91. http://dx.doi.org/10.1152/japplphysiol.00892.2003.
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Hyperoxia is a popular model of oxidative stress. However, hyperoxic gas mixtures are routinely used for chemical denervation of peripheral O2 receptors in in vivo studies of respiratory control. The underlying assumption whenever using hyperoxia is that there are no direct effects of molecular O2 and reactive O2 species (ROS) on brain stem function. In addition, control superfusates used routinely for in vitro studies of neurons in brain slices are, in fact, hyperoxic. Again, the assumption is that there are no direct effects of O2 and ROS on neuronal activity. Research contradicts this assumption by demonstrating that O2 has central effects on the brain stem respiratory centers and several effects on neurons in respiratory control areas; these need to be considered whenever hyperoxia is used. This mini-review summarizes the long-recognized, but seldom acknowledged, paradox of respiratory control known as hyperoxic hyperventilation. Several proposed mechanisms are discussed, including the recent hypothesis that hyperoxic hyperventilation is initiated by increased production of ROS during hyperoxia, which directly stimulates central CO2 chemoreceptors in the solitary complex. Hyperoxic hyperventilation may provide clues into the fundamental role of redox signaling and ROS in central control of breathing; moreover, oxidative stress may play a role in respiratory control dysfunction. The practical implications of brain stem O2 and ROS sensitivity are also considered relative to the present uses of hyperoxia in respiratory control research in humans, animals, and brain stem tissues. Recommendations for future research are also proposed.
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Tsan, M. F., C. Y. Lee, and J. E. White. "Interleukin 1 protects rats against oxygen toxicity." Journal of Applied Physiology 71, no. 2 (August 1, 1991): 688–97. http://dx.doi.org/10.1152/jappl.1991.71.2.688.
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We studied the effect of interleukin 1 alpha (IL-1) in the protection against O2 toxicity. Tracheal insufflation of IL-1 resulted in a dose-dependent protection against O2 toxicity. All control rats died within 3 days of O2 exposure. In contrast, 84, 71, and 20% of rats insufflated with 5, 1, and 0.2 microgram(s) IL-1 (150, 30, and 6 x 10(4) U), respectively, survived 100% O2 exposure for greater than 11 days. At 2.3 days after O2 exposure, control rats showed severe pulmonary injury, which insufflation of 5 microgram(s) IL-1 markedly attenuated. The protection against O2 toxicity was associated with a selective enhancement of pulmonary Mn-superoxide dismutase (Mn-SOD) activity in IL-1-insufflated rats. In rats insufflated with IL-1 that survived exposure to 100% O2 for 7 days, the activities of pulmonary Mn-SOD, Cu,Zn-SOD, catalase, and glutathione peroxidase were all increased. The increased pulmonary Mn-SOD activity demonstrated in IL-1-insufflated rats at 2.3 days after O2 exposure may contribute to the protection against acute O2 toxicity, and the markedly increased activities of all pulmonary antioxidant enzymes shown in rats insufflated with IL-1 that survived O2 exposure for 7 days may in part be responsible for the chronic adaptation of these rats to a 100% O2 environment.
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Rocha, N. A. S., B. C. S. Leão, M. F. Accorsi, and G. Z. Mingoti. "90 INTRACELLULAR REACTIVE OXYGEN SPECIES IN BOVINE EMBRYOS CULTURED IN VITRO WITH CATALASE UNDER VARIOUS OXYGEN TENSIONS." Reproduction, Fertility and Development 24, no. 1 (2012): 157. http://dx.doi.org/10.1071/rdv24n1ab90.
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The production of reactive oxygen species (ROS), such as superoxide anion (O2–), hydroxyl radical (OH–) hydrogen peroxide (H2O2) and organic peroxides, is a normal process that occurs in the cellular mitochondrial respiratory chain. The high oxygen tension in in vitro culture (IVC) conditions is believed to induce oxidative stress, as a result of increase in ROS intracellular production, that can be correlated with embryonic developmental failure. Supplementation with antioxidants during IVC appears to increase the resistance of bovine embryos to the oxidative stress and consequently improve embryo development. The aim of this study was to evaluate the effects of antioxidant (catalase) and oxygen tensions during IVC on the embryonic development and quantification of intracellular ROS. Cumulus–oocyte complexes (COC; n = 337) were in vitro matured (IVM) in TCM-199 supplemented with 0.2 mM pyruvate, 25 mM sodium bicarbonate, 75 μg mL–1 gentamicin, 10% FCS and hormones for 24 h at 38.5°C and 5% CO2 in air. Then they were fertilized and the presumptive zygotes were cultured in SOFaa medium without (control) or with 100 UI catalase (CAT) for 7 days at 38.5°C in one of 2 types of humified atmosphere: 5% CO2 in air (≈20% O2) or in gaseous mixture (7% O2, 5% CO2 and 88% N2). The cleavage rate was evaluated at 72 hours post-insemination (hpi) and the embryonic development at 168 hpi. At this time, the level of intracellular ROS was measured using the fluorescent probe 6-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (H2DCFDA; Molecular Probes, Invitrogen, Oakville, Canada), at 5 μM (Bain et al. 2011 Reprod. Fertil. Dev. 23, 561–575). Stained embryos were imaged immediately using an inverted microscope and analysed by Q-Capture Pro image software (QImaging, Surrey, BC, Canada). The signal intensity values of embryos were subtracted by the average of backgrounds in the images. Embryo development was analysed by chi-squared test and means of the intensity of fluorescence were compared by ANOVA followed by Tukey's test (P < 0.05). The cleavage rates were 84.04%a (control 20% O2), 77.55%a (CAT 20% O2), 77.03%a (control 7% O2) and 71.83%a (CAT 7% O2). The embryonic development rates were 40.43%a (control 20% O2), 33.67%a (CAT 20% O2), 20.27%b (control 7% O2) and 16.90%b (CAT 7% O2). The fluorescent intensity were 3.9 ± 0.4a (control 20% O2), 1.8 ± 0.2b (CAT 20% O2), 2.7 ± 0.2ab (control 7% O2) and 2.8 ± 0.2ab (CAT 7% O2). Although catalase did not significantly affect blastocyst frequencies (P > 0.05), embryo development was adversely affected by reduced O2 tension (P < 0.05). H2DCFDA staining indicated a significant (P < 0.05) reduction in the levels of intracellular ROS within embryos cultured with catalase under 20% O2 compared with the control group in the same O2 tension. Additionally, a consistent but insignificant reduction in intracellular ROS within embryos cultured under 7% O2 was found. We can conclude that supplementation with catalase to IVC medium at 20% O2 is suitable for lowering intracellular ROS levels in IVP bovine embryos, without lowering the rates of blastocysts production. This finding corroborates with theory that antioxidants are beneficial to embryo quality. Alta Genetics Brazil, Deoxi Biotecnologia.
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Gonzalez-Fernandez, J. M., and S. E. Atta. "Comparative facilitated transport of oxygen." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 1 (July 1, 1986): R1—R12. http://dx.doi.org/10.1152/ajpregu.1986.251.1.r1.
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Numerical solutions were obtained for a model of facilitated transport of O2. The dependence of the facilitated flow on the concentrations of O2 at the two boundaries of the transport path was studied. The numerical values of the parameters correspond to the adult Ascaris lumbricoides and to vertebrate red striated muscle. A global control principle is formulated. This states that for every fixed O2 concentration at the low concentration boundary there exists an O2 concentration at the high concentration boundary for which the facilitated flow is maximum. The collection of these maxima makes possible the existence of a global adjustment of the facilitated transport in contradistinction to the mere presence of a local maximum. The ranges of the pairs of boundary O2 concentrations thus defined and for which the facilitated flow is within 70% of its attainable maximum were found to coincide with the physiological ranges of boundary O2 concentrations for the Ascaris and vertebrate striated muscle. This phenomenon has the character of a graded compensatory mechanism to hypoxia. It is an intrinsic property of the carrier transport system and does not depend on sensors for hypoxia.
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Lewis, Daniel M., Kyung Min Park, Vitor Tang, Yu Xu, Koreana Pak, T. S. Karin Eisinger-Mathason, M. Celeste Simon, and Sharon Gerecht. "Intratumoral oxygen gradients mediate sarcoma cell invasion." Proceedings of the National Academy of Sciences 113, no. 33 (August 2, 2016): 9292–97. http://dx.doi.org/10.1073/pnas.1605317113.
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Hypoxia is a critical factor in the progression and metastasis of many cancers, including soft tissue sarcomas. Frequently, oxygen (O2) gradients develop in tumors as they grow beyond their vascular supply, leading to heterogeneous areas of O2 depletion. Here, we report the impact of hypoxic O2 gradients on sarcoma cell invasion and migration. O2 gradient measurements showed that large sarcoma mouse tumors (>300 mm3) contain a severely hypoxic core [≤0.1% partial pressure of O2 (pO2)] whereas smaller tumors possessed hypoxic gradients throughout the tumor mass (0.1–6% pO2). To analyze tumor invasion, we used O2-controllable hydrogels to recreate the physiopathological O2 levels in vitro. Small tumor grafts encapsulated in the hydrogels revealed increased invasion that was both faster and extended over a longer distance in the hypoxic hydrogels compared with nonhypoxic hydrogels. To model the effect of the O2 gradient accurately, we examined individual sarcoma cells embedded in the O2-controllable hydrogel. We observed that hypoxic gradients guide sarcoma cell motility and matrix remodeling through hypoxia-inducible factor-1α (HIF-1α) activation. We further found that in the hypoxic gradient, individual cells migrate more quickly, across longer distances, and in the direction of increasing O2 tension. Treatment with minoxidil, an inhibitor of hypoxia-induced sarcoma metastasis, abrogated cell migration and matrix remodeling in the hypoxic gradient. Overall, we show that O2 acts as a 3D physicotactic agent during sarcoma tumor invasion and propose the O2-controllable hydrogels as a predictive system to study early stages of the metastatic process and therapeutic targets.
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Chen, Yifan, Pritmohinder S. Gill, and William J. Welch. "Oxygen availability limits renal NADPH-dependent superoxide production." American Journal of Physiology-Renal Physiology 289, no. 4 (October 2005): F749—F753. http://dx.doi.org/10.1152/ajprenal.00115.2005.
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Renal oxygen tension is substantially lower in the medulla than in the cortex and is reduced in hypertensive rats, a model of oxidative stress. Expression of NADPH oxidase, the primary source for superoxide anion (O2−·) in the kidney, is elevated in hypertension. Because molecular oxygen (O2) is required for O2−· formation, we tested the hypothesis that renal NADPH oxidase activity is limited by low O2. O2−· production by rat kidney tissue or cultured cells exposed to levels of Po2 that mimics those in the kidney was assessed by lucigenin-enhanced chemiluminescence. NADPH-dependent O2−· production by kidney homogenates decreased reversibly by 60–90% after graded reductions of ambient O2 from 10 to 0% (76 to 2 mmHg Po2). The NADPH-dependent O2−· production by the kidney homogenate was reduced by decreasing Po2 below ∼30 mmHg. The response of tissue homogenates to low Po2 was not different between normotensive and hypertensive rats. Similarly, NADPH-dependent O2−· production was lower during 2% O2 compared with 10% O2 in rat proximal tubule cells (−57 ± 1%), vascular smooth muscle (−42 ± 5%), cardiomyocytes (−57 ± 1%), and mouse inner medulla collecting duct cells (−58 ± 3%). We conclude that O2−· production by NADPH oxidase is dependent on availability of O2. Therefore, O2−· generation may be limited in the kidney, both in the normal renal medulla and in the cortex of hypertensive kidneys.
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Gray, Mark E., Jamie R. K. Marland, Camelia Dunare, Ewen O. Blair, James Meehan, Andreas Tsiamis, Ian H. Kunkler, et al. "In vivo validation of a miniaturized electrochemical oxygen sensor for measuring intestinal oxygen tension." American Journal of Physiology-Gastrointestinal and Liver Physiology 317, no. 2 (August 1, 2019): G242—G252. http://dx.doi.org/10.1152/ajpgi.00050.2019.
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Recent advances in the fields of electronics and microfabrication techniques have led to the development of implantable medical devices for use within the field of precision medicine. Monitoring visceral surface tissue O2 tension ([Formula: see text]) by means of an implantable sensor is potentially useful in many clinical situations, including the perioperative management of patients undergoing intestinal resection and anastomosis. This concept could provide a means by which treatment could be tailored to individual patients. This study describes the in vivo validation of a novel, miniaturized electrochemical O2 sensor to provide real-time data on intestinal [Formula: see text]. A single O2 sensor was placed onto the serosal surface of the small intestine of anesthetized rats that were exposed to ischemic (superior mesenteric artery occlusion) and hypoxemic (alterations in inspired fractional O2 concentrations) insults. Control experiments demonstrated that the sensors can function and remain stable in an in vivo environment. Intestinal [Formula: see text] decreased following superior mesenteric artery occlusion and with reductions in inspired O2 concentrations. These results were reversible after reinstating blood flow or by increasing inspired O2 concentrations. We have successfully developed an anesthetized rat intestinal ischemic and hypoxic model for validation of a miniaturized O2 sensor to provide real-time measurement of intestinal [Formula: see text]. Our results support further validation of the sensors in physiological conditions using a large animal model to provide evidence of their use in clinical applications where monitoring visceral surface tissue O2 tension is important. NEW & NOTEWORTHY This is the first report of real-time continuous measurements of intestinal oxygen tension made using a microfabricated O2 sensor. Using a developed rodent model, we have validated this sensor's ability to accurately measure dynamic and reversible changes in intestinal oxygenation that occur through ischemic and hypoxemic insults. Continuous monitoring of local intestinal oxygenation could have value in the postoperative monitoring of patients having undergone intestinal surgery.
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Osaka, Masahiko, Ken Kurosaki, and Shinsuke Yamanaka. "Oxygen potential of (Pu0.91Am0.09)O2−x." Journal of Nuclear Materials 357, no. 1-3 (October 2006): 69–76. http://dx.doi.org/10.1016/j.jnucmat.2006.05.044.
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Otobe, Haruyoshi, Mitsuo Akabori, Yasuo Arai, and Kazuo Minato. "Oxygen Potentials of (Am0.5Np0.5)O2−x." Journal of the American Ceramic Society 92, no. 1 (January 2009): 174–78. http://dx.doi.org/10.1111/j.1551-2916.2008.02828.x.
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Schumacker, P. T., N. Chandel, and A. G. Agusti. "Oxygen conformance of cellular respiration in hepatocytes." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 4 (October 1, 1993): L395—L402. http://dx.doi.org/10.1152/ajplung.1993.265.4.l395.
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Cellular respiratory rates are normally determined by metabolic activity, but become rate limited by O2 availability if the cell O2 tension (PO2) falls below a critical value (typically 1–10 Torr). An ability to reduce metabolic activity and energy demand in response to a falling O2 availability might confer an increased resistance to a diminished O2 supply. Isolated rat hepatocytes were studied in primary culture under controlled O2 tensions. Cells were obtained by collagenase digestion and seeded into nutritive media in control and experimental spinner flasks at identical cell densities. Cells subjected to rapid reduction in PO2 (100⇢0 Torr over < 40 min) exhibited undiminished O2 uptake until PO2 fell below 10 Torr. By contrast, when cell PO2 was reduced over several hours, significant decreases in O2 uptake became evident at O2 tensions as high as 70 Torr. These decreases were associated with a reduction in ATP concentration and an increase in NAD(P)H, compared with rapidly deoxygenated cells at the same PO2. No loss in cell viability was detected after 24 h at reduced PO2. The decrease in respiratory rate was associated with an increased rate of lactic acid production relative to normoxic controls. Restoration of normoxia was associated with an immediate return of O2 uptake to control levels. These results demonstrate that hepatocytes are capable of reversibly decreasing metabolic activity and O2 demand during sustained moderate reductions in PO2, via a mechanism that appears to involve an inhibition of mitochondrial function other than O2 supply limitation. This response may alter cellular susceptibility to physiological stresses including hypoxia.
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López-Barneo, José, Raquel del Toro, Konstantin L. Levitsky, María D. Chiara, and Patricia Ortega-Sáenz. "Regulation of oxygen sensing by ion channels." Journal of Applied Physiology 96, no. 3 (March 2004): 1187–95. http://dx.doi.org/10.1152/japplphysiol.00929.2003.
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O2 sensing is of critical importance for cell survival and adaptation of living organisms to changing environments or physiological conditions. O2-sensitive ion channels are major effectors of the cellular responses to hypoxia. These channels are preferentially found in excitable neurosecretory cells (glomus cells of the carotid body, cells in the neuroepithelial bodies of the lung, and neonatal adrenal chromaffin cells), which mediate fast cardiorespiratory adjustments to hypoxia. O2-sensitive channels are also expressed in the pulmonary and systemic arterial smooth muscle cells where they participate in the vasomotor responses to low O2 tension (particularly in hypoxic pulmonary vasoconstriction). The mechanisms underlying O2 sensing and how the O2 sensors interact with the ion channels remain unknown. Recent advances in the field give different support to the various current hypotheses. Besides the participation of ion channels in acute O2 sensing, they also contribute to the gene program developed under chronic hypoxia. Gene expression of T-type calcium channels is upregulated by hypoxia through the same hypoxiainducible factor-dependent signaling pathway utilized by the classical O2-regulated genes. Alteration of acute or chronic O2 sensing by ion channels could participate in the pathophysiology of human diseases, such as sudden infant death syndrome or primary pulmonary hypertension.
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Sircar, S. S. "The oxygen-carrying flask: a representational transform of the oxygen dissociation curve of hemoglobin." Advances in Physiology Education 266, no. 6 (June 1994): S33. http://dx.doi.org/10.1152/advances.1994.266.6.s33.
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The teaching of oxygen transport by hemoglobin is supported by a graphic depiction of the sigmoid O2 dissociation curve of hemoglobin. However, a reconstruction of the same curve into an alternate paradigm, the "O2-carrying flask," affords a visual demonstration of the significance of its sigmoid shape and the implications of its shifts, which should be useful in elucidating certain aspects of O2 transport to undergraduate students of physiology. This article provides a mathematical justification for the flask design.
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Whipp, B. J., H. B. Rossiter, and S. A. Ward. "Exertional oxygen uptake kinetics: a stamen of stamina?" Biochemical Society Transactions 30, no. 2 (April 1, 2002): 237–47. http://dx.doi.org/10.1042/bst0300237.
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The fundamental pulmonary O2 uptake (o2) response to moderate, constant-load exercise can be characterized as (do2/dt)(τ) + Δo2 (t) = Δo2SS where Δo2SS is the steady-state response, and τ is the time constant, with the o2 kinetics reflecting intramuscular O2 uptake (o2) kinetics, to within 10%. The role of phosphocreatine (FCr) turnover in o2 control can be explored using 31P-MR spectroscopy, simultaneously with o2. Although τo2 and τPCr vary widely among subjects (approx. 20–65 s), they are not significantly different from each other, either at the on- or off-transient. A caveat to interpreting the ‘well-fit’ exponential is that numerous units of similar Δo2SS but with a wide τ distribution can also yield a o2 response with an apparent single τ. This τ is, significantly, inversely correlated with lactate threshold and o2max (but is poorly predictive; a frail stamen, therefore), consistent with τ not characterizing a compartment with uniform kinetics. At higher intensities, the fundamental kinetics become supplemented with a slowly-developing phase, setting o2 on a trajectory towards maximum o2. This slow component is also demonstrable in Δ[PCr]: the decreased efficiency thereby reflecting a predominantly high phosphate-cost of force production rather than a high O2-cost of phosphate production. We also propose that the O2-deficit for the slow-component is more likely to reflect shifting Δo2SS rather than a single one with a single τ.
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Poole, DC. "Current concepts of oxygen transport during exercise." Equine and Comparative Exercise Physiology 1, no. 1 (February 2004): 5–22. http://dx.doi.org/10.1079/ecp20036.
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AbstractThis brief review examines the athletic potential of mammals in general and the horse in particular as it relates to oxygen (O2) transport and utilization. The horse has been bred selectively for over six millennia based upon its ability to run fast. Whereas this has optimized cardiovascular and muscle function and the capacity to deliver and utilize O2, it has resulted in lung failure during intense exercise. Horses in their athletic prime are considered and attention is focused on their maximal capacities as related to O2 transport, irrespective of age per se. Following a few comments on the history of O2, this review moves from established principles of O2 transport at the integrative organ level to the microcirculation and the processes and principles that govern O2 offloading, where much remains to be discovered. Four principal questions are addressed: (1) as an athlete, what are the most outstanding physiological characteristics of the horse? (2) what anatomical and physiological capacities facilitate this superlative performance and such prodigious O2 fluxes (i.e. maximal VO2)? (3) do cardiovascular dynamics or intramuscular energetic processes limit VO2 kinetics (i.e. the speed at which VO2 increases at the onset of exercise)? VO2 kinetics determine the size of the O2 deficit and as such represent an important determinant of muscle metabolism and fatigue; and (4) what determines the efficacy of muscle microcirculatory O2 exchange?
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Midden, W. Robert, and Thomas A. Dahl. "Biological inactivation by single oxygen: distinguishing O2(1Δg) and O2(1Σg+)." Biochimica et Biophysica Acta (BBA) - General Subjects 1117, no. 2 (September 1992): 216–22. http://dx.doi.org/10.1016/0304-4165(92)90082-6.
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Todd, M. M., B. Wu, M. Maktabi, B. J. Hindman, and D. S. Warner. "Cerebral blood flow and oxygen delivery during hypoxemia and hemodilution: role of arterial oxygen content." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 5 (November 1, 1994): H2025—H2031. http://dx.doi.org/10.1152/ajpheart.1994.267.5.h2025.
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To determine the role of arterial O2 content (CaO2) in the cerebral blood flow (CBF) responses to hypoxemia and hemodilution, CaO2 was progressively reduced from approximately 18 to approximately 6 ml O2/dl in normocapnic, normothermic, pentobarbital-anesthetized rabbits. This was done either by reducing PaO2 (hypoxemia, minimum PaO2 approximately 26 mmHg) or arterial hematocrit (isovolemic hemodilution with hetastarch, minimum hematocrit approximately 14%) while CBF was measured with radioactive microspheres. As CaO2 decreased, CBF increased in both groups but was greater in hypoxemic animals at CaO2 values < or = 9 ml O2/dl. For example, at a CaO2 approximately 6 ml O2/dl, CBF in hypoxemic animals was 110 +/- 38 ml.100 g-1.min-1 (means +/- SD) compared with 82 +/- 22 ml.100 g-1.min-1 in hemodiluted animals (means +/- SD). While calculated cerebral O2 delivery (cerebral DO2) was well maintained in hypoxemic animals, it decreased significantly during hemodilution (from 7.95 +/- 2.92 baseline to 5.08 +/- 1.10 ml O2/dl.100 g-1.min-1 at the lowest CaO2 value). This decrease in cerebral DO2 was offset by an increase in oxygen extraction ratio during hemodilution. By contrast, the small increase in oxygen extraction ratio seen with hypoxemia did not achieve significance. These results suggest that there are different adaptive responses to acute hypoxemia or hemodilution . They also imply that at similar CBF and CaO2 values, tissue O2 availability may be greater during hemodilution than during hypoxemia.
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Smith, K. M., and D. A. Newnham. "Near-infrared absorption cross sections and integrated absorption intensities of molecular oxygen (O2, O2-O2, and O2-N2)." Journal of Geophysical Research: Atmospheres 105, no. D6 (March 1, 2000): 7383–96. http://dx.doi.org/10.1029/1999jd901171.
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Vadapalli, Arjun, Roland N. Pittman, and Aleksander S. Popel. "Estimating oxygen transport resistance of the microvascular wall." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 2 (August 1, 2000): H657—H671. http://dx.doi.org/10.1152/ajpheart.2000.279.2.h657.
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The problem of diffusion of O2 across the endothelial surface in precapillary vessels and its utilization in the vascular wall remains unresolved. To establish a relationship between precapillary release of O2 and vascular wall consumption, we estimated the intravascular flux of O2 on the basis of published in vivo measurements. To interpret the data, we utilized a diffusion model of the vascular wall and computed possible physiological ranges for O2 consumption. We found that many flux values were not consistent with the diffusion model. We estimated the mitochondrial-based maximum O2 consumption of the vascular wall (Mmt) and a possible contribution to O2 consumption of nitric oxide production by endothelial cells (MNO). Many values of O2 consumption predicted from the diffusion model exceeded Mmt + MNO. In contrast, reported values of O2consumption for endothelial and smooth muscle cell suspensions and vascular strips in vitro do not exceed Mmt. We conjecture that most of the reported values of intravascular O2 flux are overestimated, and the likely source is in the experimental estimates of convective O2 transport at upstream and downstream points of unbranched vascular segments.
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Nunn, J. F., K. Makita, and B. Royston. "Validation of oxygen consumption measurements during artificial ventilation." Journal of Applied Physiology 67, no. 5 (November 1, 1989): 2129–34. http://dx.doi.org/10.1152/jappl.1989.67.5.2129.
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We describe a system for the absolute calibration of indirect calorimeters, under the conditions of artificial ventilation and increased inspired O2 concentration, in which butane, at a measured flow rate, is burned downstream of an artificial lung. One milliliter of butane requires 6.4 ml O2 for its combustion, and the respiratory quotient is 0.615. With the closed-circuit O2-replenishment method there was no significant systematic error in the measurement of either O2 consumption or CO2 output and a random error with a SD of 8.3 ml/min for O2 consumption and 6.3 ml/min for CO2 output. There were no significant differences in the errors with inspired O2 concentrations between 23.8 and 59.5% and O2 consumptions between 89 and 366 ml/min.
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Raddatz, E., M. Servin, and P. Kucera. "Oxygen uptake during early cardiogenesis of the chick." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1224—H1230. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1224.
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Oxidative metabolism of the isolated embryonic heart of the chick has been determined using a spectrophotometric technique allowing global as well as localized micromeasurements of the O2 uptake. Entire hearts, excised from embryos of 10 somites (primordia fused, stage 10 HH) and 40 somites (S shaped, stage 20 HH) were placed in a special chamber under controlled metabolic conditions where they continued to beat spontaneously and regularly. During the 32 h of development, the O2 consumption of the whole heart increased from 0.9 +/- 0.1 to 5.3 +/- 0.8 nmol O2/h. These values corrected for protein content were, however, comparable (0.45 nmol O2.h-1.micrograms-1). At stage 10-12, the O2 uptake varied along the cardiac tube (from 0.74 to 1.0 nmol O2.h-1.mm-2). From stage 10 to 20, the O2 uptake per unit area of ventricle wall increased from 0.7 +/- 0.2 to 1.8 +/- 0.2 nmol O2.h-1.mm-2, and the O2 uptake per myocardial volume during one cardiac cycle varied from 7 to 2.5 nmol O2/cm3. These results indicate that, despite an intense morphogenesis, the cardiac tissue has a rather low and stable oxidative metabolism, although the O2 requirement of the whole heart increases significantly. Moreover, the normalized suprabasal aerobic energy expenditure decreases throughout early cardiogenesis. The functional integrity of the isolated embryonic heart combined with the experimental possibilities of the microtechnique make the preparation appropriate for studying the changes in cardiac metabolism during development.
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Aaron, E. A., B. D. Johnson, C. K. Seow, and J. A. Dempsey. "Oxygen cost of exercise hyperpnea: measurement." Journal of Applied Physiology 72, no. 5 (May 1, 1992): 1810–17. http://dx.doi.org/10.1152/jappl.1992.72.5.1810.
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To quantitate the O2 cost of maximal exercise hyperpnea, we required eight healthy adult subjects to mimic, at rest, the important mechanical components of submaximal and maximal exercise hyperpnea. Expired minute ventilation (VE), transpulmonary and transdiaphragmatic (Pdi) pressures, and end-expiratory lung volume (EELV) were measured during exercise at 70 and 100% of maximal O2 uptake. At rest, subjects were given visual feedback of their exercise transpulmonary pressure-tidal volume loop (WV), breathing frequency, and EELV, which they mimicked repeatedly for 5 min per trial over several trials, while hypocapnia was prevented. The change in total body O2 uptake (VO2) was measured and presumed to represent the O2 cost of the hyperpnea. In 61 mimicking trials with VE of 115–167 l/min and WV of 124–544 J/min, VE, WV, duty cycle of the breath, and expiratory gastric pressure (Pga) integrated with respect to time (integral of Pga.dt/min) were not different from those observed during maximum exercise. integral of Pdi.dt/min was 14% less and EELV was 6% greater during maximum exercise than during mimicking. The O2 cost measurements within a subject were reproducible over 3–12 trials (coefficient of variation +/- 10% range 5–16%). The O2 costs of hyperpnea correlated highly and positively with VE and WV and less, but significantly, with integral of Pdi.dt and integral of Pga.dt. The O2 cost of VE rose out of proportion to the increasing hyperpnea, so that between 70 and 100% of maximal VO2 delta VO2/delta VE increased 40–60% (1.8 +/- 0.2 to 2.9 +/- 0.1 ml O2/l VE) as VE doubled.(ABSTRACT TRUNCATED AT 250 WORDS)
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Minaev, Boris. "Photochemistry and Spectroscopy of Singlet Oxygen in Solvents. Recent Advances which Support the Old Theory." Chemistry & Chemical Technology 10, no. 4s (December 25, 2016): 519–30. http://dx.doi.org/10.23939/chcht10.04si.519.
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Molecular oxygen is a paramagnetic gas with the triplet O2( ) ground state which exhibits just sluggish chemical reactivity in the absence of radical sources. In contrast, the excited metastable singlet oxygen O2( ) is highly reactive; it can oxygenate organic molecules in a wide range of specific reactions which differ from those of the usual triplet oxygen of the air. This makes the singlet oxygen an attractive reagent for new synthesis and even for medical treatments in photodynamic therapy. As an important intermediate O2( ) has attracted great attention of chemists during half-century studies of its reactivity and spectroscopy, but unusual properties of singlet oxygen makes it difficult to unravel all mysterious features. The semiempirical theory of spin-orbit coupling in dioxygen and in collision complexes of O2 with diamagnetic molecules proposed in 1982 year has explained and predicted many photochemical and spectral properties of dioxygen produced by the dye sensitization in solvents. Recent experiments with direct laser excitation of O2 in solvents provide a complete support of the old theory. The present review scrutinizes the whole story of development and experimental verification of this theory.
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Hoogakker, B. A. A., D. J. R. Thornalley, and S. Barker. "Millennial changes in North Atlantic oxygen concentrations." Biogeosciences Discussions 12, no. 15 (August 13, 2015): 12947–73. http://dx.doi.org/10.5194/bgd-12-12947-2015.
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Abstract. Glacial–interglacial changes in bottom water oxygen concentrations [O2] in the deep Northeast Atlantic have been linked to decreased ventilation relating to changes in ocean circulation and the biological pump (Hoogakker et al., 2015). In this paper we discuss seawater [O2] changes in relation to millennial climate oscillations in the North Atlantic ocean over the last glacial cycle, using bottom water [O2] reconstructions from 2 cores: (1) MD95-2042 from the deep northeast Atlantic (Hoogakker et al., 2015), and (2) ODP 1055 from the intermediate northwest Atlantic. Deep northeast Atlantic core MD95-2042 shows decreased bottom water [O2] during millennial scale cool events, with lowest bottom water [O2] of 170, 144, and 166 ± 17 μmol kg−1 during Heinrich ice rafting events H6, H4 and H1. Importantly, at intermediate core ODP 1055 bottom water [O2] was lower during parts of Marine Isotope Stage 4 and millennial cool events, with lowest values of 179 and 194 μmol kg−1 recorded during millennial cool events C21 and a cool event following Dansgaard–Oeschger event 19. Our reconstructions agree with previous model simulations suggesting that glacial cold events may be associated with lower seawater [O2] across the North Atlantic below ~1 km (Schmittner et al., 2007), although in our reconstructions the changes are less dramatic. The decreases in bottom water [O2] during North Atlantic Heinrich events and earlier cold events at the deep site can be linked to water mass changes in relation to ocean circulation changes, and possibly productivity changes. At the intermediate depth site a strong North Atlantic Intermediate Water cell precludes water mass changes as a cause for decreased bottom water [O2]. Instead we propose that the lower bottom [O2] there can be linked to productivity changes through increased export of organic material from the surface ocean.
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Yamada, Y., A. Ito, K. Kuono, H. Yoshida, and Y. Kobayashi. "Laser deposition of iron in oxygen atmosphere." Proceedings in Radiochemistry 1, no. 1 (September 1, 2011): 429–33. http://dx.doi.org/10.1524/rcpr.2011.0078.
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AbstractIron oxide films were produced by pulsed laser deposition (PLD) of 57Fe metal in an oxygen atmosphere and their compositions were studied by Mössbauer spectroscopy. The effects of gas-phase reactions were investigated by varying the pressure of O2 gas or an O2/Ar gas mixture. When PLD was performed in a high-pressure O2 atmosphere, the main product in the film was trivalent iron oxide particles. When the O2 pressure was reduced, hematite Fe2O3 became dominant in the film, while wüstite FeO was produced at very low O2 pressures. PLD in an O2/Ar gas mixture produced films of trivalent iron oxide particles and hematite solid, but wüstite was not produced. Increasing the substrate temperature during deposition induced annealing of the films, reducing the lattice defect density. X-ray diffraction patterns were obtained to confirm the assignments, and the surface morphologies of the films were investigated by scanning electron microscopy.
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Torres Filho, Ivo P., Bruce D. Spiess, Roland N. Pittman, R. Wayne Barbee, and Kevin R. Ward. "Experimental analysis of critical oxygen delivery." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (March 2005): H1071—H1079. http://dx.doi.org/10.1152/ajpheart.00884.2004.
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Systemic variables were evaluated with respect to O2 delivery to test the hypothesis that critical O2 delivery and critical Hb can be estimated by multiple variables collected simultaneously. Rats were subjected to transfusion with either fresh or stored blood and then subjected to stepwise isovolemic hemodilution. Critical levels were measured by the dual-regression method from plots of systemic variables against O2 delivery and Hb. Delivery was calculated from cardiac index and arterial O2 content. We found that 1) after hemodilution, O2 delivery changed in a nonlinear relationship with Hb; 2) critical delivery calculated using 30 different systemic variables was not statistically different from each other; 3) critical delivery and critical Hb were correlated but were not different between animals receiving fresh or stored blood; and 4) similar critical levels were found using a single variable from several animals and using several variables from the same subject. The best variables to estimate critical delivery were lactate, bicarbonate, base excess, O2 extraction ratio, expired CO2, pulse pressure, cardiac index, and systolic pressure. The data suggest that a multivariable analysis of critical delivery may help determine the physiological oxygenation boundary at the whole body level. This may assist in finding therapeutic triggers on an individual basis using systemic markers of the transition from aerobic to anaerobic metabolism.
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Gutierrez, G., A. R. Warley, and D. R. Dantzker. "Oxygen delivery and utilization in hypothermic dogs." Journal of Applied Physiology 60, no. 3 (March 1, 1986): 751–57. http://dx.doi.org/10.1152/jappl.1986.60.3.751.
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Hypothermia produces a decrease in metabolic rate that may be beneficial under conditions of reduced O2 delivery (Do2). Another effect of hypothermia is to increase the affinity of hemoglobin for O2, which can adversely affect the release of O2 to the tissues. To determine the overall effect of hypothermia on the ability of the peripheral tissues to extract O2 from blood, we compared the response to hypoxemia of hypothermic dogs (n = 8) and of normothermic controls (n = 8). The animals were anesthetized, mechanically ventilated, and paralyzed to prevent shivering. The inspired concentration of O2 was progressively reduced until the dogs died. The core temperatures of the control and hypothermic dogs were 37.7 +/- 0.3 and 30.5 +/- 0.1 degree C, respectively (P less than 0.01). The O2 consumption (VO2) of the control dogs was significantly greater than that of the hypothermic dogs (P less than 0.05), being 4.7 +/- 0.4 and 3.2 +/- 0.3 ml X min-1 X kg-1, respectively. Hypothermia produced a left shift of the oxyhemoglobin dissociation curve (ODC) to a PO2 at which hemoglobin is half-saturated with O2 of 19.8 +/- 0.7 Torr (control = 32.4 +/- 0.7 Torr, P less than 0.01). The O2 delivery at which the VO2 becomes supply dependent (DO2crit) was 8.5 ml X min-1 X kg-1 for control and 6.2 ml X min-1 X kg-1 for hypothermia. The hypothermic dogs maintained their base-line VO2′s at lower arterial PO2′s than control.(ABSTRACT TRUNCATED AT 250 WORDS)
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Bender, Renar J., Jeffrey K. Brecht, Steven A. Sargent, and Donald J. Huber. "Mango Tolerance to Reduced Oxygen Levels in Controlled Atmosphere Storage." Journal of the American Society for Horticultural Science 125, no. 6 (November 2000): 707–13. http://dx.doi.org/10.21273/jashs.125.6.707.
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`Haden' and `Tommy Atkins' mangoes (Mangifera indica L.) were stored in air, 2, 3, 4 or 5 kPa O2 plus N2, or 25 kPa CO2 plus air for 14 days at 15 °C or 21 days at 12 °C, respectively, then in air for 5 days at 20 °C to determine their tolerance to reduced O2 levels for storage times encountered in typical marine shipments. All low O2 treatments reduced mature green mango respiration (CO2 production), however, elevated ethanol production occurred in 2 and 3 kPa O2 storage, with the levels two to three times higher in `Tommy Atkins' than `Haden'. In contrast, `Haden' fruit at the onset of the climacteric also accumulated ethanol in 4 kPa O2 and produced 10 to 20-fold more ethanol in 2 and 3 kPa O2 than preclimacteric fruit. While there were no visible injury symptoms, off flavor developed in mature green fruit at 2 kPa O2 and in ripening initiated fruit at 2 and 3 kPa O2. Ethanol production was not affected by storage in 25 kPa CO2. Ethylene production was reduced slightly by low O2, however, `Haden' fruit also showed a residual inhibitory effect on ethylene production after 2 or 3 kPa O2 storage, while `Tommy Atkins' fruit stored in 2 kPa O2 produced a burst of ethylene upon transfer to air at 20 °C. Fruit firmness, total sugars, and starch levels did not differ among the treatments, but 2, 3 or 4 kPa O2 and 25 kPa CO2 maintained significantly higher acidity than 5 kPa O2 or air. The epidermal ground color responded differently to low O2 and high CO2 in the two mango cultivars. Only 2 kPa O2 maintained `Haden' color better than air, while all low O2 levels maintained `Tommy Atkins' color equally well and better than air. High CO2 was more effective than low O2 in maintaining `Haden' color, but had about the same effect as low O2 on `Tommy Atkins'. Results indicate that preclimacteric `Haden' and `Tommy Atkins' mango fruit are able to tolerate 3 kPa O2 for 2 or 3 weeks at 12 to 15 °C and that tolerance to low O2 decreases as mangoes ripen. Results also show that low O2 and high CO2 affect mango ripening differentially.
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Hoogakker, B. A. A., D. J. R. Thornalley, and S. Barker. "Millennial changes in North Atlantic oxygen concentrations." Biogeosciences 13, no. 1 (January 15, 2016): 211–21. http://dx.doi.org/10.5194/bg-13-211-2016.
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Abstract. Glacial–interglacial changes in bottom water oxygen concentrations [O2] in the deep northeast Atlantic have been linked to decreased ventilation relating to changes in ocean circulation and the biological pump (Hoogakker et al., 2015). In this paper we discuss seawater [O2] changes in relation to millennial climate oscillations in the North Atlantic over the last glacial cycle, using bottom water [O2] reconstructions from 2 cores: (1) MD95-2042 from the deep northeast Atlantic (Hoogakker et al., 2015) and (2) ODP (Ocean Drilling Program) Site 1055 from the intermediate northwest Atlantic. The deep northeast Atlantic core MD95-2042 shows decreased bottom water [O2] during millennial-scale cool events, with lowest bottom water [O2] of 170, 144, and 166 ± 17 µmol kg−1 during Heinrich ice rafting events H6, H4, and H1. Importantly, at intermediate depth core ODP Site 1055, bottom water [O2] was lower during parts of Marine Isotope Stage 4 and millennial cool events, with the lowest values of 179 and 194 µmol kg−1 recorded during millennial cool event C21 and a cool event following Dansgaard–Oeschger event 19. Our reconstructions agree with previous model simulations suggesting that glacial cold events may be associated with lower seawater [O2] across the North Atlantic below ∼ 1 km (Schmittner et al., 2007), although in our reconstructions the changes are less dramatic. The decreases in bottom water [O2] during North Atlantic Heinrich events and earlier cold events at the two sites can be linked to water mass changes in relation to ocean circulation changes and possibly productivity changes. At the intermediate depth site a possible strong North Atlantic Intermediate Water cell would preclude water mass changes as a cause for decreased bottom water [O2]. Instead, we propose that the lower bottom [O2] there can be linked to productivity changes through increased export of organic material from the surface ocean and its subsequent remineralization in the water column and the sediment.
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Kedem, J., B. A. Acad, and H. R. Weiss. "Pacing during reperfusion elevates regional myocardial oxygen consumption." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 3 (September 1, 1990): H872—H878. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h872.
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Reperfusion after 2 h of coronary artery occlusion has been shown to result in depressed coronary blood flow to the reperfused region and elevated regional myocardial extraction. This suggests that reperfused myocardium, even after 4 h of reperfusion, possesses limited flow and O2 consumption reserves. We studied the capacity of reperfused myocardium to elevate regional blood flow and regional O2 consumption in response to sustained increased O2 demand, produced by atrial pacing. Two groups of anesthetized open-chest dogs were subjected to 2 h of left anterior descending coronary artery occlusion followed by 4 h of reperfusion. One group was subjected to atrial pacing (40% increase in heart rate) during the entire 4-h reperfusion period. Regional O2 saturation was measured by microspectrophotometry in samples of reperfused and nonoccluded subepicardium and subendocardium, which were taken at the end of the reperfusion period. In the paced group, regional blood flow (radiolabeled microspheres) to reperfused myocardium was significantly higher than to corresponding regions of unpaced hearts (110 +/- 22 vs. 40 +/- 9 ml.min-1 x 100 g-1 in the subendocardium). In the control group, O2 extraction of reperfused subendocardium was significantly higher than that measured in the corresponding nonoccluded region (11.0 +/- 0.9 vs. 8.0 +/- 0.6 ml O2/100 ml). Pacing did not elevate O2 extraction of reperfused myocardium (8.7 +/- 0.6 vs. 8.3 +/- 0.7 ml O2/100 ml). Myocardial O2 consumption was significantly elevated in all regions of the paced heart. It is concluded that reperfused myocardium possesses significant unutilized O2 supply and consumption reserves.
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Bender, P. R., B. M. Groves, R. E. McCullough, R. G. McCullough, S. Y. Huang, A. J. Hamilton, P. D. Wagner, A. Cymerman, and J. T. Reeves. "Oxygen transport to exercising leg in chronic hypoxia." Journal of Applied Physiology 65, no. 6 (December 1, 1988): 2592–97. http://dx.doi.org/10.1152/jappl.1988.65.6.2592.
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Residence at high altitude could be accompanied by adaptations that alter the mechanisms of O2 delivery to exercising muscle. Seven sea level resident males, aged 22 +/- 1 yr, performed moderate to near-maximal steady-state cycle exercise at sea level in normoxia [inspired PO2 (PIO2) 150 Torr] and acute hypobaric hypoxia (barometric pressure, 445 Torr; PIO2, 83 Torr), and after 18 days' residence on Pikes Peak (4,300 m) while breathing ambient air (PIO2, 86 Torr) and air similar to that at sea level (35% O2, PIO2, 144 Torr). In both hypoxia and normoxia, after acclimatization the femoral arterial-iliac venous O2 content difference, hemoglobin concentration, and arterial O2 content, were higher than before acclimatization, but the venous PO2 (PVO2) was unchanged. Thermodilution leg blood flow was lower but calculated arterial O2 delivery and leg VO2 similar in hypoxia after vs. before acclimatization. Mean arterial pressure (MAP) and total peripheral resistance in hypoxia were greater after, than before, acclimatization. We concluded that acclimatization did not increase O2 delivery but rather maintained delivery via increased arterial oxygenation and decreased leg blood flow. The maintenance of PVO2 and the higher MAP after acclimatization suggested matching of O2 delivery to tissue O2 demands, with vasoconstriction possibly contributing to the decreased flow.
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Wang, Shiow Y., and Hongjun Jiao. "367 Scavenging Capacity of Active Oxygen Species in Blackberry." HortScience 35, no. 3 (June 2000): 455E—455. http://dx.doi.org/10.21273/hortsci.35.3.455e.
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The effect of blackberries (Rubus sp.) genotypes on antioxidant activities against superoxide radicals (O2–), hydrogen peroxide (H2O2), hydroxyl radicals (OH), and singlet oxygen (O,), was evaluated. The results were expressed as percent inhibition of active oxygen species production in the presence of fruit juice. The active oxygen radical absorbance capacity (ORAC) value referred to the net protection in the presence of fruit juice, and was expressed as micromoles of α-tocopherol, ascorbate, α-tocopherol, and β-carotene equivalents per 10 g of fresh weight for O2–, H2O2, OH, and O2, respectively. Among the different cultivars, juice of Hull' blackberry had the highest oxygen species, superoxide radicals (O2–), hydrogen peroxide (H2O2), hydroxyl radicals (OH), and singlet oxygen (O2,) scavenging capacity. Different antioxidants have their functional scavenging capacity against active oxygen species. There were interesting and marked differences among the different antioxidants in their abilities to inhibit the different active oxygen species. β-carotene had by far the highest scavenging activity against O2– but had absolutely no effect on H2O2. Ascorbic acid was the best at inhibiting H2O2 free radical activity. For OH, there was a wide range of scavenging capacities with α-tocopherol the highest and ascorbic acid the lowest. Glutathione had higher O2– scavenging capacity compared to the other antioxidants.
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Linsey, G. A., and D. C. Lasenby. "Comparison of Summer and Winter Oxygen Consumption Rates in a Temperate Dimictic Lake." Canadian Journal of Fisheries and Aquatic Sciences 42, no. 10 (October 1, 1985): 1634–39. http://dx.doi.org/10.1139/f85-204.
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In a temperate dimictic lake in southern Ontario, the winter rate of oxygen loss determined from oxygen profiles differed considerably from the summer hypolimnetic rate, although the sediment oxygen demand (SOD) and water column oxygen demand (WOD) did not change significantly (SOD: winter = 0.018 mg O2∙L−1∙d−1, summer = 0.020 mg O2∙L−1∙d−1; WOD: winter = 0.032 mg O2∙L−1∙d−1, summer = 0.027 mg O2∙L−1∙d−1). In summer, the sum of SOD and WOD (0.047 mg O2∙L−1∙d−1) closely approximated the hypolimnetic deficit (0.040 mg O2∙L−1∙d−1), but in winter, SOD plus WOD (0.050 mg O2∙L−1∙d−1) greatly overestimated the observed consumption rate (0.003 mg O2∙L−1∙d−1). Measurement of primary production and an estimate of rainwater influx revealed that both could be significant sources of oxygen input during winter. Although both WOD and SOD were found to vary significantly between 10 sampling sites, a central station yielded seasonal mean values that closely approximated those obtained from combining the data from all stations.
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Kasil, Abdelsalam, Sebastien Giraud, Pierre Couturier, Akbar Amiri, Jerome Danion, Gianluca Donatini, Xavier Matillon, Thierry Hauet, and Lionel Badet. "Individual and Combined Impact of Oxygen and Oxygen Transporter Supplementation during Kidney Machine Preservation in a Porcine Preclinical Kidney Transplantation Model." International Journal of Molecular Sciences 20, no. 8 (April 23, 2019): 1992. http://dx.doi.org/10.3390/ijms20081992.
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Marginal kidney graft preservation in machine perfusion (MP) is well-established. However, this method requires improvement in order to mitigate oxidative stress during ischemia-reperfusion, by using oxygenation or an O2 carrier with anti-oxidant capacities (hemoglobin of the marine worm; M101). In our preclinical porcine (pig related) model, kidneys were submitted to 1h-warm ischemia, followed by 23 h hypothermic preservation in Waves® MP before auto-transplantation. Four groups were studied: W (MP without 100%-O2), W-O2 (MP with 100%-O2; also called hyperoxia), W-M101 (MP without 100%-O2 + M101 2 g/L), W-O2 + M101 (MP with 100%-O2 + M101 2 g/L) (n = 6/group). Results: Kidneys preserved in the W-M101 group showed lower resistance, compared to our W group. During the first week post-transplantation, W-O2 and W-M101 groups showed a lower blood creatinine and better glomerular filtration rate. KIM-1 and IL-18 blood levels were lower in the W-M101 group, while blood levels of AST and NGAL were lower in groups with 100% O2. Three months after transplantation, fractional excretion of sodium and the proteinuria/creatinuria ratio remained higher in the W group, creatininemia was lower in the W-M101 group, and kidney fibrosis was lower in M101 groups. We concluded that supplementation with M101 associated with or without 100% O2 improved the Waves® MP effect upon kidney recovery and late graft outcome.
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Baskerville, Tracey A., Graeme A. Deuchar, Christopher McCabe, Craig A. Robertson, William M. Holmes, Celestine Santosh, and I. Mhairi Macrae. "Influence of 100% and 40% Oxygen on Penumbral Blood Flow, Oxygen Level, and T*2-Weighted MRI in a Rat Stroke Model." Journal of Cerebral Blood Flow & Metabolism 31, no. 8 (May 11, 2011): 1799–806. http://dx.doi.org/10.1038/jcbfm.2011.65.
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Accurate imaging of the ischemic penumbra is a prerequisite for acute clinical stroke research. T*2 magnetic resonance imaging (MRI) combined with an oxygen challenge (OC) is being developed to detect penumbra based on changes in blood deoxyhemoglobin. However, inducing OC with 100% O2 induces sinus artefacts on human scans and influences cerebral blood flow (CBF), which can affect T*2 signal. Therefore, we investigated replacing 100% O2 OC with 40% O2 OC (5 minutes 40% O2 versus 100% O2) and determined the effects on blood pressure (BP), CBF, tissue pO2, and T*2 signal change in presumed penumbra in a rat stroke model. Probes implanted into penumbra and contralateral cortex simultaneously recorded pO2 and CBF during 40% O2 ( n = 6) or 100% O2 ( n = 8) OC. In a separate MRI study, T*2 signal change to 40% O2 ( n = 6) and 100% O2 ( n = 5) OC was compared. Oxygen challenge (40% and 100% O2) increased BP by 8.2% and 18.1%, penumbra CBF by 5% and 15%, and penumbra pO2 levels by 80% and 144%, respectively. T*2 signal significantly increased by 4.56% ± 1.61% and 8.65% ± 3.66% in penumbra compared with 2.98% ± 1.56% and 2.79% ± 0.66% in contralateral cortex and 1.09% ± 0.82% and −0.32% ± 0.67% in ischemic core, respectively. For diagnostic imaging, 40% O2 OC could provide sufficient T*2 signal change to detect penumbra with limited influence in BP and CBF.
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Zhang, Yong Feng, Xiang Yun Chen, Quan Zhou, Qian Cheng Zhang, and Chun Ping Li. "Combustion Kinetic Analysis of Lignite in Different Oxygen Concentration." Advanced Materials Research 884-885 (January 2014): 37–40. http://dx.doi.org/10.4028/www.scientific.net/amr.884-885.37.
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Combustion behavior of indigenous lignite in oxygen-enriched conditions was investigated by using thermogravimetric analyzer (TGA). Combustion tests were carried out in different oxygen concentration (21%O2/79%N2, 30%O2/70%N2, 40%O2/60%N2, 50%O2/50%N2, 60%O2/40%N2, 70%O2/30%N2). Then get the characteristic temperatures. . The model-fitting mathematical approach was used to evaluated the kinetic triplet (f (α),E,A) through Gorbatchev method. The combustion stages were divided into the early combustion stage and the later combustion stage. The calculation showed that the kinetics parameters higher in the early combustion stage than that in the later combustion stage.
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Chung, Youngran. "Oxygen reperfusion is limited in the postischemic hypertrophic myocardium." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 5 (May 2006): H2075—H2084. http://dx.doi.org/10.1152/ajpheart.00619.2005.
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Studies have shown that hypertrophied hearts are unusually vulnerable to ischemia. Compromised O2 supply has been postulated as a possible explanation for this phenomenon on the basis of elongated O2 diffusion distance and altered coronary vasculature found in hypertrophied myocardium. To examine the postulate, perfused heart experiments followed the metabolic and functional responses of hypertrophic myocardium to ischemia. 1H/31P NMR was used to measure cellular oxygenation and energy level during ischemia-reperfusion. The left ventricles from spontaneously hypertensive rats (SHR) were enlarged by 48%. With this moderate degree of hypertrophy, cellular O2 and energy levels were normal during baseline perfusion. After an ischemic episode, however, cellular O2 was severely deprived in the SHR hearts compared with the normal hearts. Depressed postischemic O2 reperfusion correlated well with depressed energetic and functional recovery. The results from the current study thus demonstrate a critical relationship between reperfused O2 level and functional recovery in hypertrophic myocardium. The role of reperfused O2, however, is time dependent. During early reperfusion, factor(s) other than O2 appear to limit functional recovery. It is when the mechanical function of the heart approaches a new steady state that O2 becomes a dominant factor. Meanwhile, the finding of a normal O2 level in preischemic SHR hearts defies the notion of preexisting hypoxia as a primer of ischemic damage.