Artykuły w czasopismach na temat „Reoxygenation”
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1
Hung, Tai-Ho, Jeremy N. Skepper, D. Stephen Charnock-Jones i Graham J. Burton. "Hypoxia-Reoxygenation". Circulation Research 90, nr 12 (28.06.2002): 1274–81. http://dx.doi.org/10.1161/01.res.0000024411.22110.aa.
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Greene, E. L., i M. S. Paller. "Xanthine oxidase produces O2-. in posthypoxic injury of renal epithelial cells". American Journal of Physiology-Renal Physiology 263, nr 2 (1.08.1992): F251—F255. http://dx.doi.org/10.1152/ajprenal.1992.263.2.f251.
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The hypothesis that posthypoxic renal injury is mediated by xanthine oxidase-derived oxygen free radical production was tested in an in vitro model of rat proximal tubule epithelial cells in primary culture subjected to 60 min of hypoxia and 30 min of reoxygenation. Hypoxia-reoxygenation-induced injury, measured as lactate dehydrogenase (LDH) release, was 54.0 +/- 7.1%. Inhibition of xanthine oxidase by 10(-4) M allopurinol attenuated injury (LDH release = 35.5 +/- 3.7%; P less than 0.01). Oxypurinol was similarly effective. Alternatively, cells were treated with 50 or 100 microM tungsten to inactivate xanthine oxidase. Tungsten prevented hypoxia-reoxygenation-induced superoxide radical production (basal = 97 +/- 8, hypoxia-reoxygenation = 172 +/- 12, and plus tungsten = 73 +/- 8 nmol/micrograms protein) and attenuated hypoxia-reoxygenation-induced injury (LDH release: basal = 18.8 +/- 3.0%, hypoxia-reoxygenation = 62.0 +/- 4.8%, plus 50 microM tungsten = 24.8 +/- 5.0%, and plus 100 microM tungsten = 6.0 +/- 0.7%). In addition, hypoxia and reoxygenation increased the ratio of xanthine oxidase to total activity (xanthine oxidase + xanthine dehydrogenase) from 73 to 100%. Therefore xanthine oxidase was responsible for hypoxia-reoxygenation-induced superoxide radical formation and hypoxia-reoxygenation-induced injury. Xanthine oxidase is likely to be the major source of oxygen free radicals during renal ischemia and reperfusion.
3
Seiler, K. S., J. P. Kehrer i J. W. Starnes. "Effect of perfusion pressure at reoxygenation on reflow and function in isolated rat hearts". American Journal of Physiology-Heart and Circulatory Physiology 262, nr 4 (1.04.1992): H1029—H1035. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1029.
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The effect of coronary perfusion pressure during reoxygenation on recovery of endocardial flow, arrhythmogenesis, and mechanical function was investigated in the isolated rat heart. Hearts were subjected to 30 min of substrate-free hypoxia followed by 30 min reoxygenation at either 80 or 150 cmH2O perfusion pressure. No flow areas were quantified by 0.3% phthalocyanine blue injection after 30 min of hypoxia, 30 min reoxygenation at 80 cmH2O, or 30 min reoxygenation at 150 cmH2O. After hypoxia, 31 +/- 2% of the myocardium was unperfused. After 80 cmH2O reoxygenation, 13 +/- 4% of the heart remained unperfused. Ten of 12 (83%) 80-cmH2O hearts were in sustained fibrillation after 10 min of reoxygenation. Reoxygenation at 150 cmH2O resulted in complete reperfusion of the myocardium. Fibrillation was absent in all hearts reoxygenated at this higher pressure. Functional recovery after 30 min reoxygenation (% of normoxic heart rate x left ventricular developed pressure) was significantly (P less than 0.05) higher in 150 cmH2O vs. 80 cmH2O (60 +/- 5 vs. 42 +/- 8%). Elevating perfusion pressure upon reoxygenation appears to counter the vascular compression caused by contracture and leads to a more rapid and homogeneous restoration of coronary flow during the transition from the hypoxic to the normoxic state.
4
Corno, Antonio F., i Michele Samaja. "The reoxygenation phenomenon". Journal of Thoracic and Cardiovascular Surgery 105, nr 2 (luty 1993): 373. http://dx.doi.org/10.1016/s0022-5223(19)33831-0.
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DEJONG, J. "Reperfusion/reoxygenation—Introduction". Journal of Molecular and Cellular Cardiology 19 (1987): S16. http://dx.doi.org/10.1016/s0022-2828(87)80055-x.
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Hempel, S. L., D. L. Haycraft, J. C. Hoak i A. A. Spector. "Reduced prostacyclin formation after reoxygenation of anoxic endothelium". American Journal of Physiology-Cell Physiology 259, nr 5 (1.11.1990): C738—C745. http://dx.doi.org/10.1152/ajpcell.1990.259.5.c738.
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Human umbilical vein endothelial cells subjected to 24 h of anoxia followed by reoxygenation released less prostacyclin (PGI2) in response to thrombin, calcium ionophore A23187, or arachidonic acid. This was associated with a substantial increase in stimulated platelet adherence. Increased lactate dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the high rate of release did not persist during the subsequent 23 h of reoxygenation. The changes in platelet adherence and PGI2 release partially resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced, suggesting that cyclooxygenase activity, but not prostacyclin synthase, is affected by reoxygenation. A decrease in arachidonic acid release from cellular lipids also occurred. The reduction in cyclooxygenase activity, but not arachidonic acid release, was prevented by the presence of ibuprofen during reoxygenation. Addition of catalase or superoxide dismutase during reoxygenation increased PGI2 release but did not completely overcome the reduction relative to control cultures. These findings suggest that the increase in platelet adherence during reoxygenation may be mediated in part by a change in cyclooxygenase activity. This is only partly overcome by extracellular oxygen species scavengers but is prevented by the presence of a reversible cyclooxygenase inhibitor during reoxygenation.
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Ihnken, Kai, Kiyozo Morita i Gerald D. Buckberg. "Delayed cardioplegic reoxygenation reduces reoxygenation injury in cyanotic immature hearts". Annals of Thoracic Surgery 66, nr 1 (lipiec 1998): 177–82. http://dx.doi.org/10.1016/s0003-4975(98)00320-8.
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Zhang, Yanmei, Gaoyong Chen, Shuping Zhong, Fuchun Zheng, Fenfei Gao, Yicun Chen, Zhanqin Huang i in. "N-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms". Oxidative Medicine and Cellular Longevity 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/912310.
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N-n-butyl haloperidol iodide (F2) has been shown to antagonize myocardial ischemia/reperfusion injury by blocking calcium channels. This study explores the biological functions of ERK pathway in cardiomyocytes hypoxia/reoxygenation injury and clarifies the mechanisms by which F2ameliorates cardiomyocytes hypoxia/reoxygenation injury through the extracellular-calcium-dependent and -independent ERK1/2-related pathways. In extracellularcalcium-containing hypoxia/reoxygenation cardiomyocytes, PKCαand ERK1/2 were activated, Egr-1 protein level and cTnI leakage increased, and cell viability decreased. The ERK1/2 inhibitors suppressed extracellular-calcium-containing-hypoxia/reoxygenation-induced Egr-1 overexpression and cardiomyocytes injury. PKCαinhibitor downregulated extracellularcalcium-containing-hypoxia/reoxygenation-induced increase in p-ERK1/2 and Egr-1 expression. F2downregulated hypoxia/reoxygenation-induced elevation of p-PKCα, p-ERK1/2, and Egr-1 expression and inhibited cardiomyocytes damage. The ERK1/2 and PKCαactivators antagonized F2’s effects. In extracellular-calcium-free-hypoxia/reoxygenation cardiomyocytes, ERK1/2 was activated, LDH and cTnI leakage increased, and cell viability decreased. F2and ERK1/2 inhibitors antagonized extracellular-calcium-free-hypoxia/reoxygenation-induced ERK1/2 activation and suppressed cardiomyocytes damage. The ERK1/2 activator antagonized F2’s above effects. F2had no effect on cardiomyocyte cAMP content or PKA and Egr-1 expression. Altogether, ERK activation in extracellular-calcium-containing and extracellular-calcium-free hypoxia/reoxygenation leads to cardiomyocytes damage. F2may ameliorate cardiomyocytes hypoxia/reoxygenation injury by regulating the extracellular-calcium-dependent PKCα/ERK1/2/Egr-1 pathway and through the extracellular-calcium-independent ERK1/2 activation independently of the cAMP/PKA pathway or Egr-1 overexpression.
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Doctor, R. B., i L. J. Mandel. "Minimal role of xanthine oxidase and oxygen free radicals in rat renal tubular reoxygenation injury." Journal of the American Society of Nephrology 1, nr 7 (styczeń 1991): 959–69. http://dx.doi.org/10.1681/asn.v17959.
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The role of xanthine oxidase and oxygen free radicals in postischemic reperfusion injury in the rat kidney remains controversial. Proximal tubules, the focal segment affected by ischemic renal injury, were isolated in bulk, assayed for xanthine oxidase activity, and subjected to 60 min of anoxia or hypoxia and 60 min of reoxygenation to evaluate the participation of xanthine oxidase and oxygen radicals in proximal tubule reoxygenation injury. The total xanthine oxidase in isolated rat proximal tubules was 1.1 mU/mg of protein, approximately 30% to 40% of the activity found in rat intestine and liver. Lactate dehydrogenase release, an indicator of irreversible cell damage, increased substantially during anoxia (39.8 +/- 2.3 versus 9.8 +/- 1.8% in controls) with an additional 8 to 12% release during reoxygenation. Addition of 0.2 mM allopurinol, a potent xanthine oxidase inhibitor, and dimethylthiourea, a hydroxyl radical scavenger, failed to protect against the reoxygenation lactate dehydrogenase release. Analysis of xanthine oxidase substrate levels after anoxia and flux rates during reoxygenation indicates that hypoxanthine and xanthine concentrations are in a 15-fold excess over the enzyme Km and 0.3 mU/mg of protein of xanthine oxidase activity exists during reoxygenation. Hypoxic tubule suspensions had a minimal lactate dehydrogenase release during hypoxia and failed to demonstrate accelerated injury upon reoxygenation. In conclusion, although xanthine oxidase is present and active during reoxygenation in isolated rat proximal tubules, oxygen radicals did not mediate reoxygenation injury.
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Agulló, Luis, David García-Dorado, Javier Inserte, Amaya Paniagua, Pasi Pyrhonen, Joan Llevadot i Jordi Soler-Soler. "l-Arginine limits myocardial cell death secondary to hypoxia-reoxygenation by a cGMP-dependent mechanism". American Journal of Physiology-Heart and Circulatory Physiology 276, nr 5 (1.05.1999): H1574—H1580. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1574.
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The objective of this study was to investigate the effect ofl-arginine supplementation on myocardial cell death secondary to hypoxia-reoxygenation. Isolated rat hearts ( n = 51) subjected to 40 min of hypoxia and 90 min of reoxygenation received 3 mMl-arginine and/or 1 μM 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ; a selective inhibitor of soluble guanylyl cyclase) throughout the experiment or during the equilibration, hypoxia, or reoxygenation periods. The incorporation ofl-[3H]arginine into myocytes during energy deprivation was investigated in isolated adult rat myocytes. The addition ofl-arginine to the perfusate throughout the experiment resulted in higher cGMP release ( P < 0.05), reduced lactate dehydrogenase release ( P < 0.05), and increased pressure-rate product ( P < 0.05) during reoxygenation. These effects were reproduced whenl-arginine was added only during equilibration, but addition ofl-arginine during hypoxia or reoxygenation had no effect. Addition of ODQ either throughout the experiment or only during reoxygenation reversed the beneficial effects of l-arginine.l-[3H]arginine was not significantly incorporated into isolated myocytes subjected to energy deprivation. We conclude thatl-arginine supplementation protects the myocardium against reoxygenation injury by cGMP-mediated actions. To be effective during reoxygenation,l-arginine must be added before anoxia.
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Siegmund, B., T. Klietz, P. Schwartz i H. M. Piper. "Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes". American Journal of Physiology-Heart and Circulatory Physiology 260, nr 2 (1.02.1991): H426—H435. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h426.
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Reoxygenation after 120-min substrate-free anoxia causes sudden hypercontracture in isolated rat cardiomyocytes. Reoxygenated-hypercontracted cardiomyocytes maintain their sarcolemmal integrity as indicated by the absence of enzyme release and reestablish a nearly normal free energy change of ATP hydrolysis within 15 min [Siegmund, B., A. Koop, T. Klietz, P. Schwartz, and H. M. Piper.Am J. Physiol. 258 (Heart Circ. Physiol. 27): H285-H291, 1990]. In the same model, it was now investigated whether a temporary contractile blockade by 20 mM 2,3-butanedione monoxime (BDM) can prevent reoxygenation-induced hypercontracture. When BDM was present during 120-min anoxia and the subsequent 15-min reoxygenation, hypercontracture could be prevented. The anoxic changes of high-energy phosphate contents, the free energy change of ATP hydrolysis, and the ultrastructure of the cells remained unaffected by the presence of BDM. When BDM was applied anoxically immediately before reoxygenation, it also prevented hypercontracture. Contracture still remained absent when BDM was washed out after the first 15 min of reoxygenation. These results demonstrate that a temporary contractile blockade (15 min) at the onset of reoxygenation prevents hypercontracture in anoxic-reoxygenated cardiomyocytes. This result, the energetic recovery, and the sarcolemmal integrity of cardiomyocytes in anoxia-reoxygenation demonstrate that reoxygenation-induced hypercontracture is not based on an already irreversible cell damage.
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Delcamp, T. J., C. Dales, L. Ralenkotter, P. S. Cole i R. W. Hadley. "Intramitochondrial [Ca2+] and membrane potential in ventricular myocytes exposed to anoxia-reoxygenation". American Journal of Physiology-Heart and Circulatory Physiology 275, nr 2 (1.08.1998): H484—H494. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h484.
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The aim of this study was to investigate the role of mitochondrial ionic homeostasis in promoting reoxygenation-induced hypercontracture in cardiac muscle. Mitochondrial membrane potential and intramitochondrial Ca2+ concentration ([Ca2+]) were measured using confocal imaging in guinea pig ventricular myocytes exposed to anoxia and reoxygenation. Anoxia produced a variable, but often profound, mitochondrial depolarization. Some cells mounted a recovery of their mitochondrial membrane potential during reoxygenation; the depolarization was sustained in other cells. Recovery of the mitochondrial membrane potential seemed essential to avoid reoxygenation-induced hypercontracture. Reoxygenation also caused a sizable elevation in intramitochondrial [Ca2+], the amplitude of which was correlated with the likelihood of a cell undergoing hypercontracture. A sustained Ca2+load analogous to that seen during reoxygenation was imposed on cardiac mitochondria through permeabilization of the plasma membrane. Elevation of intracellular [Ca2+] to 800 nM caused a substantial mitochondrial depolarization. We propose that the conditions seen in guinea pig ventricular myocytes during reoxygenation are well suited to produce Ca2+-dependent mitochondrial depolarization, which may play a significant role in promoting irreversible cell injury.
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Halsey, James H., Karl A. Conger, Julio H. Garcia i Eniko Sarvary. "The Contribution of Reoxygenation to Ischemic Brain Damage". Journal of Cerebral Blood Flow & Metabolism 11, nr 6 (listopad 1991): 994–1000. http://dx.doi.org/10.1038/jcbfm.1991.166.
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This study examined the hypothesis that the level of postischemic reperfusion affects the severity of the resulting neuronal necrosis. In rats, tissue Po2% was monitored as an index of flow (reoxygenation) at four cortical sites by chronically implanted platinum electrodes. Twenty minutes of total global cerebral ischemia was followed by 30 min of reoxygenation. The level of reoxygenation was controlled to maintain the Po2 nearly constant at one or more of the cortical electrodes. Tissue from within 400 μm of each of 19 electrode sites among seven rats was evaluated histologically. There was a positive correlation between reoxygenation level and severity of neuronal damage. Perineuronal lucent halo formation, probably representing astrocyte foot process swelling, was negatively correlated with reoxygenation level. This study demonstrates that ischemic neuronal damage was aggravated by increased reoxygenation but that perineuronal swelling, as evidenced by halo formation, was somewhat ameliorated.
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Welker, Alexis F., Élida G. Campos, Luciano A. Cardoso i Marcelo Hermes-Lima. "Role of catalase on the hypoxia/reoxygenation stress in the hypoxia-tolerant Nile tilapia". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, nr 9 (1.05.2012): R1111—R1118. http://dx.doi.org/10.1152/ajpregu.00243.2011.
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The specific contribution of each antioxidant enzyme to protection against the reoxygenation-associated oxidative stress after periods of hypoxia is not well understood. We assessed the physiological role of catalase during posthypoxic reoxygenation by the combination of two approaches. First, catalase activity of Nile tilapias ( Oreochromis niloticus ) was 90% suppressed by intraperitoneal injection of 3-amino-1,2,4-triazole (ATZ, 1g/kg). In ATZ-injected fish, liver GSH levels, oxidative stress markers, and activities of other antioxidant enzymes remained unchanged. Second, animals with depleted catalase activity (or those saline-injected) were subjected to a cycle of severe hypoxia (dissolved O2= 0.28 mg/l for 3 h) followed by reoxygenation (0.5 to 24 h). Hypoxia did not induce changes in the above-mentioned parameters, either in saline- or in ATZ-injected animals. Reoxygenation increased superoxide dismutase activity in saline-injected fish, whose levels were similar to ATZ-injected animals. The activities of glutathione S-transferase, selenium-dependent glutathione peroxidase, and total-GPX and the levels of GSH-eq, GSSG, and thiobarbituric acid reactive substances remained unchanged during reoxygenation in both saline- and ATZ-injected fish. The GSSG/GSH-eq ratio in ATZ-injected fish increased at 30 min of reoxygenation compared with saline-injected ones. Reoxygenation also increased carbonyl protein levels in saline-injected fish, whose levels were similar to the ATZ-injected group. Our work shows that inhibition of liver tilapia catalase causes a redox imbalance during reoxygenation, which is insufficient to induce further oxidative stress. This indicates the relevance of hepatic catalase for hypoxia/reoxygenation stress in tilapia fish.
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Murphy, J. G., T. W. Smith i J. D. Marsh. "Mechanisms of reoxygenation-induced calcium overload in cultured chick embryo heart cells". American Journal of Physiology-Heart and Circulatory Physiology 254, nr 6 (1.06.1988): H1133—H1141. http://dx.doi.org/10.1152/ajpheart.1988.254.6.h1133.
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We examined mechanisms by which Ca enters cultured myocardial cells during posthypoxic reoxygenation. Monolayer cultures of chick embryo ventricular cells were prepared from hearts 10 days in ovo. Cells were exposed to hypoxic conditions (PO2 less than 1.5 Torr), and 45Ca uptake during subsequent reoxygenation was then examined in the absence and presence of modulators of Ca channel-dependent Ca entry and Na-Ca exchange. Modulation of Ca entry by free radical-scavenging enzymes was also examined. Hypoxia for 120 min followed by reoxygenation increased Ca content from 1.9 to 6.1 nmol/mg protein (P less than 0.05) at 30 min. Verapamil (10(-5) M) added before reoxygenation reduced Ca overload to 3.1 +/- 0.2 nmol/mg protein (P less than 0.05), but both verapamil and BAY K 8644 were without effect on modulating Ca entry if added 30 min after reoxygenation. 24Na content of cells increased from 70 nmol/mg protein in control cells to 157 nmol/mg protein (P less than 0.05) after hypoxia and reoxygenation, favoring Ca entry via Na-Ca exchange. Dichlorobenzamil significantly ameliorated reoxygenation-induced Ca overload, as did catalase and superoxide dismutase. We conclude that reoxygenation-induced Ca overload is unlikely to occur via the Ca channel. It occurs in part via Na-Ca exchange and is substantially ameliorated by enzymatic O2 free radical scavengers.
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Schluter, K. D., P. Schwartz, B. Siegmund i H. M. Piper. "Prevention of the oxygen paradox in hypoxic-reoxygenated hearts". American Journal of Physiology-Heart and Circulatory Physiology 261, nr 2 (1.08.1991): H416—H423. http://dx.doi.org/10.1152/ajpheart.1991.261.2.h416.
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Reoxygenation after 60 min substrate-free hypoxic perfusion (modified Tyrode solution, 37 degrees C) caused isolated Langendorff hearts (from rats) to rapidly develop hypercontracture and sarcolemmal disruptions indicated by massive and sudden loss of enzymes ("oxygen paradox"). Reoxygenation (30 min) caused an augmented loss of creatine kinase by 25.8% (lactate dehydrogenase by 40.1%) of the initial total tissue activity. It was investigated whether a temporary contractile blockade by 2,3-butanedione monoxime (BDM; 20 mM) can prevent reoxygenation-induced injury. In the presence of BDM, reoxygenation no longer caused hypercontracture or increased enzyme release. Instead, ultrastructure recovered, and contents of creatine phosphate (CrP) were partially restored (60 min hypoxia: 0.4 mumol CrP/g dry wt; after subsequent 60 min reoxygenation in presence of BDM: 7.8 mumol CrP/g dry wt). When BDM was eluted after first 20 min of reoxygenation, an attenuated but distinct increase in enzyme release was still observed. When BDM was eluted after 60 min of reoxygenation, ultrastructure did not deteriorate and increase of enzyme release remained virtually absent. During first 30 min after removal of BDM, the increased loss of creatine kinase amounted to only 5.7% (lactate dehydrogenase to 6.9%) of the initial total tissue activity. The results demonstrate that the oxygen paradox can be prevented in the hypoxic-reoxygenated heart when the contractile apparatus is temporarily paralyzed during the initial phase of reoxygenation.
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Fu, Xinyu, i Yuan Xu. "Dynamic Metabolic Changes in Arabidopsis Seedlings under Hypoxia Stress and Subsequent Reoxygenation Recovery". Stresses 3, nr 1 (2.01.2023): 86–101. http://dx.doi.org/10.3390/stresses3010008.
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Hypoxic stress, caused by the low cellular oxygen in the events of flooding or waterlogging, limits crop productivity in many regions of the world. Hypoxic stress in plants is often dynamic and followed by a reoxygenation process that returns the oxygen level to normal. Although metabolic responses to hypoxia have been studied in many plants, less is known about the recovery processes following stress removal. To better understand the dynamic metabolic shift from a low-oxygen environment to a reoxygenated environment, we performed time-course measurements of metabolites in Arabidopsis seedlings at 0, 6, 12, and 24 h of reoxygenation recovery after 24 h of hypoxia stress (100% N2 environment). Among the 80 metabolic features characterized using GC-MS, 60% of them were significantly changed under hypoxia. The reoxygenation phase was accompanied by progressively fewer metabolic changes. Only 26% significantly changed metabolic features by the 24 h reoxygenation. Hypoxia-induced metabolic changes returned to normal levels at different speeds. For example, hypoxia-induced accumulation of lactate decreased to a basal level after 6 h of reoxygenation, whereas hypoxia-induced accumulation of alanine and GABA showed partial recovery after 24 h of reoxygenation. Some metabolites, such as gluconate, xylose, guanine, and adenosine, constantly increased during hypoxia reoxygenation. These dynamic metabolic changes demonstrate the flexibility and complexity of plant metabolism during hypoxia stress and subsequent reoxygenation recovery.
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Rymsa, B., J. F. Wang i H. de Groot. "O2-. release by activated Kupffer cells upon hypoxia-reoxygenation". American Journal of Physiology-Gastrointestinal and Liver Physiology 261, nr 4 (1.10.1991): G602—G607. http://dx.doi.org/10.1152/ajpgi.1991.261.4.g602.
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Primary cultures of rat liver Kupffer cells generated large amounts of superoxide anion radical (O2-.) when subjected to reoxygenation after a hypoxic period of at least 2 h. O2-. formation reached its maximum rate of approximately 25 nmol/10(6) cells within 1 h after reoxygenation. Two to four hours after reoxygenation, the number of injured cells began to increase and after 10 h approximately 60% of the cells were dead. During the period of O2-. release no significant difference in cell viability was observed between reoxygenated and hypoxically incubated cells, indicating a distinct time lag between O2-. release and onset of cell damage. Addition of diphenyliodonium, a specific inhibitor of the neutrophilic NADPH oxidase, to the Kupffer cells just before reoxygenation diminished both O2-. formation and cell injury up to 70%. Reoxygenation injury was completely prevented when superoxide dismutase and catalase were added immediately before reoxygenation. The results indicate that Kupffer cells subjected to hypoxia-reoxygenation generate a burst of reactive oxygen species and that this kind of "activation," probably by activating the NADPH oxidase, contributes to the self-destruction of the cells.
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Kusunoki, K., Y. Nakamura, T. Konishi i C. Kawai. "Effects of hypoxia and reoxygenation on maximum rate of early left ventricular filling". American Journal of Physiology-Heart and Circulatory Physiology 255, nr 6 (1.12.1988): H1311—H1316. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1311.
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Left ventricular early filling during hypoxia and reoxygenation was examined in isolated working rat hearts that contracted 300 times/min when perfused with Krebs-Henseleit solution at 37 degrees C. Left ventricular short-axial diameter (LVD = D) was measured with a pair of ultrasonic crystals. The maximum lengthening velocity of LVD [(dD/dt)max] decreased with hypoxia and recovered after reoxygenation (from a control of 20.3 +/- 6.7 to 7.3 +/- 1.7 mm/s after 15 min of hypoxia and to 16.3 +/- 8.1 mm/s after 15 min of reoxygenation; n = 7). However, (dD/dt)max/delta D (where delta D is systolic shortening) showed no significant change with either hypoxia or reoxygenation (from a control of 21.0 +/- 2.9 l/s to 22.2 +/- 2.7 l/s after 15 min of hypoxia and to 22.5 +/- 3.7 l/s after 15 min of reoxygenation; n = 7). Therefore, we concluded that the changes of (dD/dt)max with hypoxia and reoxygenation were caused by the changed systolic shortening and that left ventricular myocardial recoil, expressed by (dD/dt)max/delta D, showed no change with either hypoxia or reoxygenation.
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Lushchak, Volodymyr I., Ludmyla P. Lushchak, Alice A. Mota i Marcelo Hermes-Lima. "Oxidative stress and antioxidant defenses in goldfish Carassius auratus during anoxia and reoxygenation". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, nr 1 (1.01.2001): R100—R107. http://dx.doi.org/10.1152/ajpregu.2001.280.1.r100.
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The purpose of this work was to evaluate the response of the antioxidant system of goldfish Carassius auratus during anoxia and reoxygenation. The exposure of goldfish to 8 h of anoxia induced a 14% decrease in total glutathione levels in the kidney, although the liver, brain, and muscle were unaffected. Anoxia also resulted in increases in the activities of liver catalase, brain glucose-6-phosphate dehydrogenase, and brain glutathione peroxidase (by 38, 26, and 79%, respectively) and a decrease in kidney catalase activity (by 17.5%). After 14 h of reoxygenation, liver catalase and brain glutathione peroxidase activities remained higher than controls and several other tissue-specific changes occurred in enzyme activities. Superoxide dismutase activity was unaffected by anoxia and reoxygenation. The levels of conjugated dienes, as indicators of lipid peroxidation, increased by 114% in liver after 1 h of reoxygenation and by 75% in brain after 14 h of reoxygenation. Lipid peroxidation was unaffected in kidney and depressed during anoxia and reoxygenation (by 44–61%) in muscle. Regulation of the goldfish antioxidant system during anoxia may constitute a biochemical mechanism that minimizes oxidative stress following reoxygenation.
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Shimizu, S., Y. Eguchi, W. Kamiike, Y. Akao, H. Kosaka, J. Hasegawa, H. Matsuda i Y. Tsujimoto. "Involvement of ICE family proteases in apoptosis induced by reoxygenation of hypoxic hepatocytes". American Journal of Physiology-Gastrointestinal and Liver Physiology 271, nr 6 (1.12.1996): G949—G958. http://dx.doi.org/10.1152/ajpgi.1996.271.6.g949.
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Cell death due to reoxygenation after hypoxia was characterized in primary cultured hepatocytes. Fluorescence and electron microscopic analyses of reoxygenated hepatocytes revealed morphological characteristics of apoptosis, including chromatin condensation, nuclear fragmentation, and formation of apoptotic bodies. Few necrotic hepatocytes, defined by loss of plasma membrane integrity, mitochondrial swelling, and formation of large vacuoles, were observed. Activation of interleukin-1 beta-converting enzyme (ICE)-like and CPP32/Yama-like proteases, which are known to drive apoptosis, was observed during reoxygenation, and addition of their respective inhibitors inhibited the induction of apoptosis, indicating the involvement of ICE family proteases in apoptosis by reoxygenation. Production of oxygen radicals was enhanced by reoxygenation of hypoxic cells, and reoxygenation-induced apoptosis was inhibited by oxygen radical scavengers, suggesting a role for reactive oxygen species as a triggering factor in cell death. Electrophoretic analysis revealed the presence of 50-kb DNA fragments but not oligonucleosomal DNA fragments in reoxygenation-induced apoptotic hepatocytes.
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Andrade Jr., Dahir Ramos de, Dahir Ramos de Andrade i Sânia Alves dos Santos. "Study of rat hepatocytes in primary culture submitted to hypoxia and reoxygenation: action of the cytoprotectors prostaglandin E1, superoxide dismutase, allopurinol and verapamil". Arquivos de Gastroenterologia 46, nr 4 (grudzień 2009): 333–40. http://dx.doi.org/10.1590/s0004-28032009000400016.
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CONTEXT: Exposure of hepatocytes to pathological conditions in a microenvironment of hypoxia and reoxygenation is very frequent in hepatic diseases. Several substances present perspectives for cytoprotective action on hepatocyte submitted to reoxygenation after hypoxia and simple hypoxia. OBJECTIVE: We research therapeutic options for hepatocytes submitted to hypoxia and hypoxia + reoxygenation injury. METHODS: Primary culture of rat hepatocytes was submitted to hypoxia (2 hours) plus reoxygenation (2 hours) and simple hypoxia (4 hours) in the presence or the absence of cytoprotectors. The hepatocyte lesion was evaluated by functional criteria through percentage of lactate dehydrogenase released and cell viability. The effects of the cytoprotectors prostaglandin E1 3 ηg/mL, superoxide dismutase 80 μg/mL, allopurinol 20 μM and verapamil 10-4 M were studied in this model of injury. RESULTS: Reoxygenation after hypoxia induced more significant lesion in cultured hepatocytes compared to simple hypoxia, detected by analysis of functional criteria. There was a significant reduction of percentage of lactate dehydrogenase released and a significant increase of percentage of cell viability in the hypoxia + reoxygenation + cytoprotectors groups compared to hypoxia + reoxygenation groups. Prostaglandin E1, superoxide dismutase and verapamil also protected the group submitted to simple hypoxia, when evaluated by functional criteria. CONCLUSIONS: We conclude that reoxygenation after hypoxia significantly increased the lesion of cultured rat hepatocytes when compared to simple hypoxia. Prostaglandin E1, superoxide dismutase, allopurinol and verapamil acted as cytoprotectors to the rat cultured hepatocytes submitted to hypoxia + reoxygenation in vitro. The substances prostaglandin E1, superoxide dismutase and verapamil protected hepatocytes submitted to simple hypoxia on the basis of all the criteria studied in this experimental model.
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Basnakian, Alexei G., Norishi Ueda, Xiaoman Hong, Valentin E. Galitovsky, Xiaoyan Yin i Sudhir V. Shah. "Ceramide synthase is essential for endonuclease-mediated death of renal tubular epithelial cells induced by hypoxia-reoxygenation". American Journal of Physiology-Renal Physiology 288, nr 2 (luty 2005): F308—F314. http://dx.doi.org/10.1152/ajprenal.00204.2004.
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Ceramide is known to play a role in the cell signaling pathway involved in apoptosis. Most studies suggest that enhanced ceramide generation is the result of hydrolysis of sphingomyelin by sphingomyelinases. However, the role of ceramide synthase in enhanced ceramide generation has not been previously examined in hypoxia-reoxygenation injury. In the present study, we demonstrated that 60-min hypoxia of rat renal tubular epithelial NRK-52E cells in a gas chamber with 95% N2-5% CO2 with glucose deprivation resulted in a significant increase in ceramide generation. The ceramide level further increased after reoxygenation for 60 min. Exposure of cells to hypoxia-reoxygenation resulted in a significant increase in ceramide synthase activity without any significant change in acid or neutral sphingomyelinase. The hypoxia-reoxygenation of NRK-52E cells was also associated with the release of endonuclease G (EndoG) from mitochondria to cytoplasm measured by Western blot analysis and endonuclease activity assay. It further led to the fragmentation of DNA and cell death. A specific inhibitor of ceramide synthase, fumonisin B1 (50 μM), suppressed hypoxia-reoxygenation-induced ceramide generation and provided protection against hypoxia-reoxygenation-induced EndoG release, DNA fragmentation, and cell death. Taken together, our data suggest that hypoxia-reoxygenation results in an activation of ceramide synthase rather than sphingomyelinase and that ceramide synthase-dependent ceramide generation is a key modulator of EndoG-mediated cytotoxicity in hypoxia-reoxygenation injury to renal tubular epithelial cells.
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Hempel, S. L., D. A. Wessels i A. A. Spector. "Effect of glutathione on endothelial prostacyclin synthesis after anoxia". American Journal of Physiology-Cell Physiology 264, nr 6 (1.06.1993): C1448—C1457. http://dx.doi.org/10.1152/ajpcell.1993.264.6.c1448.
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We previously observed decreased prostacyclin (PGI2) formation after reoxygenation of anoxic endothelium. In the present study, the effects of glutathione on endothelial prostaglandin (PG) H synthase activity after reoxygenation were explored. Intracellular glutathione content decreased 70% after 24 h of anoxia; reoxygenation did not produce any additional decrease in glutathione content. Intracellular glutathione was maintained in the reduced state by the endothelium even during the oxidant stress caused by reoxygenation or the addition of peroxide. Glutathione depletion produced by DL-buthionine-(S,R)-sulfoximine (BSO), 1,3-bis(chloroethyl)1-nitrosourea (BCNU), or incubation in a sulfhydryl-free medium resulted in increased sensitivity of PGH synthase to the effects of added H2O2. However, glutathione depletion resulting from BSO or culture in sulfhydryl-free medium during anoxia did not increase the sensitivity of PGH synthase to reoxygenation. In addition, anoxia did not make the endothelium more sensitive to H2O2. Glutathione peroxidase and glutathione reductase activities were preserved after anoxia-reoxygenation. When glutathione reductase was inhibited with BCNU during reoxygenation, PGI2 release was decreased further. These findings demonstrate that, although anoxia decreases endothelial glutathione content, the endothelium is able to utilize its remaining glutathione to protect against additional oxidant stress because glutathione peroxidase and glutathione reductase retain their activity.
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Okada, Takayuki, Hajime Otani, Yue Wu, Shiori Kyoi, Chiharu Enoki, Hiroyoshi Fujiwara, Tomohiko Sumida, Reiji Hattori i Hiroji Imamura. "Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation". American Journal of Physiology-Heart and Circulatory Physiology 289, nr 6 (grudzień 2005): H2310—H2318. http://dx.doi.org/10.1152/ajpheart.00462.2005.
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Activation of p38 mitogen-activated protein (MAP) kinase (MAPK) has been implicated in the mechanism of cardiomyocyte (CMC) protection and injury. The p38 MAPK controversy may be related to differential effects of this kinase on apoptosis and necrosis. We have hypothesized that p38 MAPK-mediated F-actin reorganization promotes apoptotic cell death, whereas it protects from osmotic stress-induced necrotic cell death. Cultured neonatal rat CMCs were subjected to 2 h of simulated ischemia followed by reoxygenation. p38 MAPK activity measured by phosphorylation of MAP kinase-activated protein (MAPKAP) kinase 2 was increased during simulated ischemia and reoxygenation. This was associated with translocation of heat shock protein 27 (HSP27) from the cytosolic to the cytoskeletal fraction and F-actin reorganization. Cytochrome c release from mitochondria, caspase-3 activation, and DNA fragmentation were increased during reoxygenation. Robust lactate dehydrogenase (LDH) release was observed under hyposmotic (140 mosM) reoxygenation. The p38 MAPK inhibitor SB-203580 abrogated activation of p38 MAPK, translocation of HSP27, and F-actin reorganization and prevented cytochrome c release, caspase-3 activation, and DNA fragmentation. Conversely, SB-203580 enhanced LDH release during hyposmotic reoxygenation. The F-actin disrupting agent cytochalasin D inhibited F-actin reorganization and prevented cytochrome c release, caspase-3 activation, and DNA fragmentation, whereas it enhanced LDH release during hyposmotic reoxygenation. When CMCs were incubated under the isosmotic condition for the first 15 min of reoxygenation, SB-203580 and cytochalasin D increased ATP content of CMCs and prevented LDH release after the conversion to the hyposmotic condition. These results suggest that F-actin reorganization mediated by activation of p38 MAPK plays a differential role in apoptosis and protection against osmotic stress-induced necrosis during reoxygenation in neonatal rat CMCs; however, the sarcolemmal fragility caused by p38 MAPK inhibition can be reversed during temporary blockade of physical stress during reoxygenation.
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Corno, Antonio F., Giuseppina Milano, Michele Samaja i Ludwig K. von Segesser. "Myocardial Damage Induced by Uncontrolled Reoxygenation". Asian Cardiovascular and Thoracic Annals 8, nr 1 (marzec 2000): 34–37. http://dx.doi.org/10.1177/021849230000800109.
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To evaluate myocardial impairment induced by uncontrolled reoxygenation, the effects of hypoxia-reoxygenation were compared with ischemia-reperfusion in isolated rat hearts. After stabilization, 2 groups (n = 8) of Langendorff-perfused rat hearts were exposed to 40 minutes of ischemia (10% of baseline flow) or hypoxia (10% of baseline oxygen content) followed by a sudden return to baseline conditions (reperfusion or reoxygenation). The O2 content was identical for the two groups during baseline conditions, O2 shortage, and O2 readmission. Metabolic (lactate production) and functional parameters (heart rate, peak systolic pressure, left ventricular developed pressure, maximal contraction and relaxation rates, end-diastolic pressure, coronary perfusion pressure) were recorded at the end of stabilization, after O2 deficiency, and after 2 minutes of reoxygenation. Systolic function was significantly depressed after ischemia (p < 0.0001) but completely recovered to baseline values after 2 minutes of reperfusion. In contrast, systolic function was less severely depressed after hypoxia but failed to return to baseline after 2 minutes of reoxygenation. Diastolic function, unchanged during ischemia-reperfusion, remained significantly impaired during hypoxia-reoxygenation.
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Matheis, G., M. P. Sherman, G. D. Buckberg, D. M. Haybron, H. H. Young i L. J. Ignarro. "Role of L-arginine-nitric oxide pathway in myocardial reoxygenation injury". American Journal of Physiology-Heart and Circulatory Physiology 262, nr 2 (1.02.1992): H616—H620. http://dx.doi.org/10.1152/ajpheart.1992.262.2.h616.
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In view of the recent findings that NO reacts with superoxide anion to generate hydroxyl radical, the present study was conducted to ascertain the role of endogenous NO in mediating myocardial reoxygenation injury in the hypoxic piglet on cardiopulmonary bypass. Anesthetized piglets were made hypoxic (PaO2 = 20-30 mmHg) for up to 120 min, followed by reoxygenation on cardiopulmonary bypass for 30 min. Reoxygenation caused rapidly developing myocardial injury characterized by decreased contractility (expressed as end-systolic elastance) and increased lipid peroxidation (measured as conjugated dienes). Systemic venous and coronary sinus blood content of NO decreased significantly during hypoxia and increased substantially above prehypoxic levels during reoxygenation on cardiopulmonary bypass. Administration of either the antioxidants mercaptopropionyl glycine and catalase or the NO synthase inhibitor, NG-nitro-L-arginine methyl ester, to the extracorporeal circuit afforded similar and nearly complete protection against myocardial reoxygenation injury. The protective effects of NG-nitro-L-arginine methyl ester were nullified by adding an excess of L-arginine to the pump circuit, suggesting that the L-arginine-NO pathway is involved in myocardial reoxygenation injury.
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Inauen, W., D. N. Granger, C. J. Meininger, M. E. Schelling, H. J. Granger i P. R. Kvietys. "Anoxia-reoxygenation-induced, neutrophil-mediated endothelial cell injury: role of elastase". American Journal of Physiology-Heart and Circulatory Physiology 259, nr 3 (1.09.1990): H925—H931. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h925.
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The aim of this study was to assess the role of neutrophilic elastase in anoxia-reoxygenation-induced, neutrophil-mediated injury to microvascular endothelium. Cultured bovine microvascular endothelial cells were grown to confluence and labeled with 51Cr. The endothelial cells were exposed to a 30-min period of anoxia and subsequently reoxygenated. Endothelial cell injury, quantitated as 51Cr release and cell detachment, was determined 8 h after reoxygenation. Addition of neutrophils upon reoxygenation enhanced the anoxia-reoxygenation-induced increase in 51Cr release and cell detachment. The neutrophil-mediated injury was associated with elastase release from the neutrophils. Four agents were used to inhibit neutrophilic elastase activity: Eglin C, methoxysuccunyl-Ala2-Pro-Val-CH2Cl, L658,758, and a monoclonal antibody against neutrophilic elastase. All elastase inhibitors attenuated the neutrophil-mediated endothelial cell detachment but not 51Cr release. Addition of purified human neutrophilic elastase, at a level that mimicked the release from neutrophils, increased cell detachment in endothelial cells exposed to anoxia-reoxygenation but did not affect 51Cr release. Our results indicate that elastase plays an important role in anoxia-reoxygenation-induced, neutrophil-mediated endothelial cell dysfunction.
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Foresti, Roberta, Helen Goatly, Colin J. Green i Roberto Motterlini. "Role of heme oxygenase-1 in hypoxia-reoxygenation: requirement of substrate heme to promote cardioprotection". American Journal of Physiology-Heart and Circulatory Physiology 281, nr 5 (1.11.2001): H1976—H1984. http://dx.doi.org/10.1152/ajpheart.2001.281.5.h1976.
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Heme oxygenase-1 (HO-1) catalyzes the enzymatic degradation of heme to carbon monoxide, bilirubin, and iron. All three products possess biological functions; bilirubin, in particular, is a potent free radical scavenger of which its antioxidant property is enhanced at low oxygen tension. Here, we investigated the effect of severe hypoxia and reoxygenation on HO-1 expression in cardiomyocytes and determined whether HO-1 and its product, bilirubin, have a protective role against reoxygenation damage. Hypoxia caused a time-dependent increase in both HO-1 expression and heme oxygenase activity, which gradually declined during reoxygenation. Reoxygenation of hypoxic cardiomyocytes produced marked injury; however, incubation with hemin or bilirubin during hypoxia considerably reduced the damage at reoxygenation. The protective effect of hemin is attributable to increased availability of substrate for heme oxygenase activity, because hypoxic cardiomyocytes generated very little bilirubin when incubated with medium alone but produced substantial bile pigment in the presence of hemin. Interestingly, incubation with hemin also maintained high heme oxygenase activity levels during the reoxygenation period. Reactive oxygen species generation was enhanced after hypoxia, and hemin and bilirubin were capable once again to attenuate this effect. These results indicate that the HO-1-bilirubin pathway can effectively defend hypoxic cardiomyocytes against reoxygenation injury and highlight the issue of heme availability in the cytoprotective action afforded by HO-1.
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Rognlien, Anne Gro W., Embjørg J. Wollen, Monica Atneosen-Åsegg, Rajikala Suganthan, Magnar Bjørås i Ola Didrik Saugstad. "Neonatal Ogg1/Mutyh knockout mice have altered inflammatory gene response compared to wildtype mice in the brain and lung after hypoxia-reoxygenation". Journal of Perinatal Medicine 47, nr 1 (19.12.2018): 114–24. http://dx.doi.org/10.1515/jpm-2018-0172.
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Abstract Background 8-Oxoguanine DNA-glycosylase 1 (OGG1) and mutY DNA glycosylase (MUTYH) are crucial in the repair of the oxidative DNA lesion 7,8-dihydro-8-oxoguanine caused by hypoxia-reoxygenation injury. Our objective was to compare the gene expression changes after hypoxia-reoxygenation in neonatal Ogg1-Mutyh double knockout mice (OM) and wildtype mice (WT), and study the gene response in OM after hyperoxic reoxygenation compared to normoxic. Methods Postnatal day 7 mice were subjected to 2 h of hypoxia (8% O2) followed by reoxygenation in either 60% O2 or air, and sacrificed right after completed reoxygenation (T0h) or after 72 h (T72h). The gene expression of 44 a priori selected genes was examined in the hippocampus/striatum and lung. Results We found that OM had an altered gene response compared to WT in 21 genes in the brain and 24 genes in the lung. OM had a lower expression than WT of inflammatory genes in the brain at T0h, and higher expression at T72h in both the brain and lung. In the lung of OM, five genes were differentially expressed after hyperoxic reoxygenation compared to normoxic. Conclusion For the first time, we report that Ogg1 and Mutyh in combination protect against late inflammatory gene activation in the hippocampus/striatum and lung after neonatal hypoxia-reoxygenation.
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Dhaliwal, H., L. A. Kirshenbaum, A. K. Randhawa i P. K. Singal. "Correlation between antioxidant changes during hypoxia and recovery on reoxygenation". American Journal of Physiology-Heart and Circulatory Physiology 261, nr 3 (1.09.1991): H632—H638. http://dx.doi.org/10.1152/ajpheart.1991.261.3.h632.
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Changes in myocardial antioxidants due to different durations of hypoxia at normal or lower temperatures were correlated with the recovery of structure and function on reoxygenation. Hearts perfused with substrate-free hypoxic buffer at 37 degrees C for 5 or 10 min and at 22 degrees C for 10 min showed a significant depression in the contractile function and rise in resting tension. Reoxygenation of these hearts at 37 degrees C for 20 min resulted in a recovery of these functions. On reoxygenation, hearts made hypoxic for 10 min at 37 degrees C showed poor recovery of the contractile function, increase in malondialdehyde content and a dramatic increase in the creatine phosphokinase activity in the coronary effluent. Addition of catalase to the perfusion medium markedly improved function recovery of these hearts. Hypoxia at 37 degrees C for 5 min or at 22 degrees C for 10 min with or without reoxygenation had no effect on superoxide dismutase (SOD) or glutathione peroxidase (GSHPx) activities. These antioxidants were depressed in hearts made hypoxic for 10 min at 37 degrees C with no further change on reoxygenation. Neither SOD nor GSHPx was detected in the coronary effluent during hypoxia or reoxygenation. Hypoxia at 37 or 22 degrees C for 10 min caused significant ultrastructural changes, and on reoxygenation 37 degrees C hypoxic hearts showed exacerbation, whereas the 22 degrees C hypoxic hearts showed recovery. These data support the hypothesis that reduced antioxidant reserve during hypoxia may contribute to the oxidative injury on reoxygenation, suggesting that maintenance of endogenous antioxidant levels during hypoxia may be important for recovery.
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Surova, O. V., V. E. Dosenko, V. S. Nagibin, L. V. Tumanovskaya i A. A. Moybenko. "SECOND ANOXIA-REOXYGENATION DOES NOT CAUSE THE APOPTOTIC CELL DEATH OF NEONATAL CARDIOMYOCYTES: POSSIBLE ROLE OF CHANGES OF mRNA EXPRESSION OF CYTOPROTECTIVE GENES". Fiziolohichnyĭ zhurnal 55, nr 1 (4.02.2009): 19–26. http://dx.doi.org/10.15407/fz55.01.019.
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The cells death and genes expression in neonatal cardiomyocytes culture at two anoxia-reoxygenation modeling were investigated. The primary culture of neonatal cardiomyocytes was undergone 30 min of anoxia followed by 24 h (A-R1) and the second anoxia-reoxygenation – 30 min and 60 min respectively (A-R2). The percentages of living, necrotic, apoptotic and autophagic cells were determined by staining with bis-benzimide, propidium iodide and monodansylcadaverine. Anoxia-reoxygenation significantly influenced the ratio of living, necrotic, apoptotic and autophagic cells both at its first A-R1 and second A-R2 episodes. It was shown that the main mechanism of cell death after the both periods of anoxia-reoxygenation is necrosis. The changes of mRNA levels of genes of heat shock proteins HSP70 and HSP90, antiapoptotic protein Bcl2 and key regulator of au-tophagy FRAP in cardiomyocytes culture were established. The data obtained allow to make suggestion that in 24 h after the first episode of anoxia-reoxygenation A-R1 the overexpression of heat shock proteins starts the cascade of reactions that causes the necrotic cell death prevalent and the blocking of apoptotic program at second anoxia-reoxygenation A-R2.
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Zhu, Kaiyi, Jia Guo, Xiaoxue Yu, Que Wang, Chao Yan, Quan Qiu, Weiqing Tang i in. "Polypeptide Globular Adiponectin Ameliorates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Necroptosis". Journal of Immunology Research 2021 (8.07.2021): 1–14. http://dx.doi.org/10.1155/2021/1815098.
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Adiponectin is a small peptide secreted and a key component of the endocrine system and immune system. Although globular adiponectin protects myocardial ischemia/reperfusion-induced cardiomyocyte injury, the protective mechanisms remain largely unresolved. Using a neonatal rat ventricular myocyte hypoxia/reoxygenation model, we investigated the role of its potential mechanisms of necroptosis in globular adiponectin-mediated protection in hypoxia/reoxygenation-induced cardiomyocyte injury as compared to apoptosis. We found that globular adiponectin treatment attenuated cardiomyocyte injury as indicated by increased cell viability and reduced lactate dehydrogenase release following hypoxia/reoxygenation. Immunofluorescence staining and Western blotting demonstrated that both necroptosis and apoptosis were triggered by hypoxia/reoxygenation and diminished by globular adiponectin. Necrostatin-1 (RIP1-specific inhibitor) and Z-VAD-FMK (pan-caspase inhibitor) only mimicked the inhibition of necroptosis and apoptosis, respectively, by globular adiponectin in hypoxia/reoxygenation-treated cardiomyocytes. Globular adiponectin attenuated reactive oxygen species production, oxidative damage, and p38MAPK and NF-κB signaling, all important for necroptosis and apoptosis. Collectively, our study suggests that globular adiponectin inhibits hypoxia/reoxygenation-induced necroptosis and apoptosis in cardiomyocytes probably by reducing oxidative stress and interrupting p38MAPK signaling.
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Caraceni, P., A. Gasbarrini, D. H. Van Thiel i A. B. Borle. "Oxygen free radical formation by rat hepatocytes during postanoxic reoxygenation: scavenging effect of albumin". American Journal of Physiology-Gastrointestinal and Liver Physiology 266, nr 3 (1.03.1994): G451—G458. http://dx.doi.org/10.1152/ajpgi.1994.266.3.g451.
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Free radical formation and reoxygenation injury were studied in rat hepatocytes perfused with Krebs-Henseleit bicarbonate buffer containing 1% or no albumin. After 2, 2.5, or 3 h of anoxia followed by 1 h reoxygenation in the absence of albumin, free radical formation assessed by low-level chemiluminescence and cell injury measured by lactate dehydrogenase (LDH) release and by trypan blue uptake increased proportionately. Chemiluminescence increased 4- to 7-fold, LDH release and trypan blue uptake increased 1.5- to 2-fold, compared with the end of anoxia. With 1% albumin, there was no increase in free radical formation during reoxygenation, and LDH release returned to control levels. There was a linear relation between the increase in chemiluminescence and the rise in LDH release (r2 = 0.83) and the increase in trypan blue uptake (r2 = 0.80), suggesting that free radical formation during reoxygenation is responsible for the cell injury. These experiments demonstrate that freshly isolated hepatocytes produce oxygen free radicals detectable by low-level chemiluminescence and that reoxygenation injury occurs after a relatively short period of anoxia (2-3 h). Albumin acts as a free radical scavenger, suppresses the release of reactive oxygen species, and significantly reduces reoxygenation injury.
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Ladilov, Y., S. Haffner, C. Balser-Schäfer, H. Maxeiner i H. M. Piper. "Cardioprotective effects of KB-R7943: a novel inhibitor of the reverse mode of Na+/Ca2+exchanger". American Journal of Physiology-Heart and Circulatory Physiology 276, nr 6 (1.06.1999): H1868—H1876. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1868.
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The novel inhibitor of the reverse mode of the Na+/Ca2+exchanger (NCE) KB-R7943 (KB) was tested in isolated rat cardiomyocytes exposed to 80 min of simulated ischemia [substrate-free anoxia, extracellular pH (pHo) of 6.4] and 15 min of reoxygenation (pHo 7.4). At pHo 6.4, 20 μmol/l KB was required for complete inhibition of the reverse mode of NCE. Treatment with 20 μmol/l KB only during anoxia did not influence the onset of rigor contracture and intracellular pH (pHi) (monitored with 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein) but significantly reduced the cytosolic accumulation of Ca2+ (monitored with fura 2) and Na+ (monitored with sodium-binding benzofuran isophthalate). During reoxygenation, cardiomyocytes developed hypercontracture. This was significantly reduced by anoxic KB treatment. To investigate this protection against reoxygenation-induced injury in the whole heart, we exposed Langendorff-perfused rat hearts to 110 min of anoxia (pHo 6.4) and 50 min of reoxygenation (pHo 7.4). Application of 20 μmol/l KB during anoxia significantly reduced the reoxygenation-induced enzyme release. We conclude that KB offers significant protection of cardiomyocytes against Ca2+ and Na+ overload during anoxia and hypercontracture or enzyme release on reoxygenation.
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Kimura, Chiwaka, Masahiro Oike i Yushi Ito. "Hypoxia-induced alterations in Ca2+mobilization in brain microvascular endothelial cells". American Journal of Physiology-Heart and Circulatory Physiology 279, nr 5 (1.11.2000): H2310—H2318. http://dx.doi.org/10.1152/ajpheart.2000.279.5.h2310.
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To investigate the possible cellular mechanisms of the ischemia-induced impairments of cerebral microcirculation, we investigated the effects of hypoxia/reoxygenation on the intracellular Ca2+ concentration ([Ca2+]i) in bovine brain microvascular endothelial cells (BBEC). In the cells kept in normal air, ATP elicited Ca2+ oscillations in a concentration-dependent manner. When the cells were exposed to hypoxia for 6 h and subsequent reoxygenation for 45 min, the basal level of [Ca2+]i was increased from 32.4 to 63.3 nM, and ATP did not induce Ca2+ oscillations. Hypoxia/reoxygenation also inhibited capacitative Ca2+entry (CCE), which was evoked by thapsigargin (Δ[Ca2+]i-CCE: control, 62.3 ± 3.1 nM; hypoxia/reoxygenation, 17.0 ± 1.8 nM). The impairments of Ca2+ oscillations and CCE, but not basal [Ca2+]i, were restored by superoxide dismutase and the inhibitors of mitochondrial electron transport, rotenone and thenoyltrifluoroacetone (TTFA). By using a superoxide anion (O2 −)-sensitive luciferin derivative MCLA, we confirmed that the production of O2 − was induced by hypoxia/reoxygenation and was prevented by rotenone and TTFA. These results indicate that hypoxia/reoxygenation generates O2 − at mitochondria and impairs some Ca2+mobilizing properties in BBEC.
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Hardy, L., J. B. Clark, V. M. Darley-Usmar, D. R. Smith i D. Stone. "Reoxygenation-dependent decrease in mitochondrial NADH:CoQ reductase (Complex I) activity in the hypoxic/reoxygenated rat heart". Biochemical Journal 274, nr 1 (15.02.1991): 133–37. http://dx.doi.org/10.1042/bj2740133.
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Reoxygenation of the hypoxic myocardium results in a number of processes, including an O2-dependent increase in total tissue Ca2+ and cell lysis in which mitochondrial electron transport plays a key role. In the present study we have isolated mitochondria from perfused rat hearts subjected to hypoxia and found no change in their respiratory function relative to controls. In contrast, mitochondria isolated immediately after reoxygenation of hypoxic-perfused hearts exhibited a specific and significant decrease in NADH:CoQ reductase (Complex I; EC 1.6.5.3) activity, as measured both polarographically and spectrophotometrically. Isolated cardiomyocytes subjected to a similar protocol of hypoxia/reoxygenation also exhibited a specific decrease in Complex I activity. Myocardial perfusion with media containing Ruthenium Red protected against the reoxygenation-dependent loss of Complex I activity. These observations taken together suggest that mitochondrial Ca2+ uptake on reoxygenation is implicated in the mechanism of the specific loss of Complex I activity.
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Mark, Karen S., i Thomas P. Davis. "Cerebral microvascular changes in permeability and tight junctions induced by hypoxia-reoxygenation". American Journal of Physiology-Heart and Circulatory Physiology 282, nr 4 (1.04.2002): H1485—H1494. http://dx.doi.org/10.1152/ajpheart.00645.2001.
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Cerebral microvessel endothelial cells that form the blood-brain barrier (BBB) have tight junctions (TJ) that are critical for maintaining brain homeostasis and low permeability. Both integral (claudin-1 and occludin) and membrane-associated zonula occluden-1 and -2 (ZO-1 and ZO-2) proteins combine to form these TJ complexes that are anchored to the cytoskeletal architecture (actin). Disruptions of the BBB have been attributed to hypoxic conditions that occur with ischemic stroke, pathologies of decreased perfusion, and high-altitude exposure. The effects of hypoxia and posthypoxic reoxygenation in cerebral microvasculature and corresponding cellular mechanisms involved in disrupting the BBB remain unclear. This study examined hypoxia and posthypoxic reoxygenation effects on paracellular permeability and changes in actin and TJ proteins using primary bovine brain microvessel endothelial cells (BBMEC). Hypoxia induced a 2.6-fold increase in [14C]sucrose, a marker of paracellular permeability. This effect was significantly reduced (∼58%) with posthypoxic reoxygenation. After hypoxia and posthypoxic reoxygenation, actin expression was increased (1.4- and 2.3-fold, respectively). Whereas little change was observed in TJ protein expression immediately after hypoxia, a twofold increase in expression was seen with posthypoxic reoxygenation. Furthermore, immunofluorescence studies showed alterations in occludin, ZO-1, and ZO-2 protein localization during hypoxia and posthypoxic reoxygenation that correlate with the observed changes in BBMEC permeability. The results of this study show hypoxia-induced changes in paracellular permeability may be due to perturbation of TJ complexes and that posthypoxic reoxygenation reverses these effects.
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ERNSTER, LARS. "Biochemistry of reoxygenation injury". Critical Care Medicine 16, nr 10 (październik 1988): 947–53. http://dx.doi.org/10.1097/00003246-198810000-00005.
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Sharikabad, Mohammad N., Kirsten M. Østbye, Torstein Lyberg i Odd Brørs. "Effect of extracellular Mg2+ on ROS and Ca2+ accumulation during reoxygenation of rat cardiomyocytes". American Journal of Physiology-Heart and Circulatory Physiology 280, nr 1 (1.01.2001): H344—H353. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h344.
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The effects of Mg2+ on reactive oxygen species (ROS) and cell Ca2+ during reoxygenation of hypoxic rat cardiomyocytes were studied. Oxidation of 2′,7′-dichlorodihydrofluorescein (DCDHF) to dichlorofluorescein (DCF) and of dihydroethidium (DHE) to ethidium (ETH) within cells were used as markers for intracellular ROS levels and were determined by flow cytometry. DCDHF/DCF is sensitive to H2O2 and nitric oxide (NO), and DHE/ETH is sensitive to the superoxide anion (O2 −·), respectively. Rapidly exchangeable cell Ca2+ was determined by 45Ca2+uptake. Cells were exposed to hypoxia for 1 h and reoxygenation for 2 h. ROS levels, determined as DCF fluorescence, were increased 100–130% during reoxygenation alone and further increased 60% by increasing extracellular Mg2+concentration to 5 mM at reoxygenation. ROS levels, measured as ETH fluorescence, were increased 16–24% during reoxygenation but were not affected by Mg2+. Cell Ca2+ increased three- to fourfold during reoxygenation. This increase was reduced 40% by 5 mM Mg2+, 57% by 10 μM 3,4-dichlorobenzamil (DCB) (inhibitor of Na+/Ca2+ exchange), and 75% by combining Mg2+ and DCB. H2O2 (25 and 500 μM) reduced Ca2+ accumulation by 38 and 43%, respectively, whereas the NO donor S-nitroso- N-acetyl-penicillamine (1 mM) had no effect. Mg2+ reduced hypoxia/reoxygenation-induced lactate dehydrogenase (LDH) release by 90%. In conclusion, elevation of extracellular Mg2+ to 5 mM increased the fluorescence of the H2O2/NO-sensitive probe DCF without increasing that of the O2 −·-sensitive probe ETH, reduced Ca2+ accumulation, and decreased LDH release during reoxygenation of hypoxic cardiomyocytes. The reduction in LDH release, reflecting the protective effect of Mg2+, may be linked to the effect of Mg2+ on Ca2+ accumulation and/or ROS levels.
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Martou, Glyka, Catherine A. O’Blenes, Ning Huang, Sandra E. McAllister, Peter C. Neligan, Homa Ashrafpour, Cho Y. Pang i Joan E. Lipa. "Development of an in vitro model for study of the efficacy of ischemic preconditioning in human skeletal muscle against ischemia-reperfusion injury". Journal of Applied Physiology 101, nr 5 (listopad 2006): 1335–42. http://dx.doi.org/10.1152/japplphysiol.00278.2006.
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Ischemia-reperfusion (I/R) injury causes skeletal muscle infarction and ischemic preconditioning (IPC) augments ischemic tolerance in animal models. To date, this has not been demonstrated in human skeletal muscle. This study aimed to develop an in vitro model to investigate the efficacy of simulated IPC in human skeletal muscle. Human skeletal muscle strips were equilibrated in oxygenated Krebs-Henseleit-HEPES buffer (37°C). Aerobic and reperfusion phases were simulated by normoxic incubation and reoxygenation, respectively. Ischemia was simulated by hypoxic incubation. Energy store, cell viability, and cellular injury were assessed using ATP, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2 H-tetrazolium bromide (MTT), and lactate dehydrogenase (LDH) assays, respectively. Morphological integrity was assessed using electron microscopy. Studies were designed to test stability of the preparation ( n = 5–11) under normoxic incubation over 24 h; the effect of 1, 2, 3, 4, or 6 h hypoxia followed by 2 h of reoxygenation; and the protective effect of hypoxic preconditioning (HPC; 5 min of hypoxia/5 min of reoxygenation) before 3 h of hypoxia/2 h of reoxygenation. Over 24 h of normoxic incubation, muscle strips remained physiologically intact as assessed by MTT, ATP, and LDH assays. After 3 h of hypoxia/2 h of reoxygenation, MTT reduction levels declined to 50.1 ± 5.5% ( P < 0.05). MTT reduction levels in HPC (82.3 ± 10.8%) and normoxic control (81.3 ± 10.2%) groups were similar and higher ( P < 0.05) than the 3 h of hypoxia/2 h of reoxygenation group (45.2 ± 5.8%). Ultrastructural morphology was preserved in normoxic and HPC groups but not in the hypoxia/reoxygenation group. This is the first study to characterize a stable in vitro model of human skeletal muscle and to demonstrate a protective effect of HPC in human skeletal muscle against hypoxia/reoxygenation-induced injury.
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Sharikabad, Mohammad Nouri, Jan Magnus Aronsen, Espen Haugen, Janne Pedersen, Anne-Sophie W. Møller, Halvor Kjeang Mørk, Hans C. D. Aass, Ole M. Sejersted, Ivar Sjaastad i Odd Brørs. "Cardiomyocytes from postinfarction failing rat hearts have improved ischemia tolerance". American Journal of Physiology-Heart and Circulatory Physiology 296, nr 3 (marzec 2009): H787—H795. http://dx.doi.org/10.1152/ajpheart.00796.2008.
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Altered myocardial Ca2+ and Na+ handling in congestive heart failure (CHF) may be expected to decrease the tolerance to ischemia by augmenting reperfusion Ca2+ overload. The aim of the present study was to investigate tolerance to hypoxia-reoxygenation by measuring enzyme release, cell death, ATP level, and cell Ca2+ and Na+ in cardiomyocytes from failing rat hearts. CHF was induced in Wistar rats by ligation of the left coronary artery during isoflurane anesthesia, after which cardiac failure developed within 6 wk. Isolated cardiomyocytes were cultured for 24 h and subsequently exposed to 4 h of hypoxia and 2 h of reoxygenation. Cell damage was measured as lactate dehydrogenase (LD) release, cell death as propidium iodide uptake, and ATP by firefly luciferase assay. Cell Ca2+ and Na+ were determined with radioactive isotopes, and free intracellular Ca2+ concentration ([Ca2+]i) with fluo-3 AM. CHF cells showed less increase in LD release and cell death after hypoxia-reoxygenation and had less relative reduction in ATP level after hypoxia than sham cells. CHF cells accumulated less Na+ than sham cells during hypoxia (117 vs. 267 nmol/mg protein). CHF cells maintained much lower [Ca2+]i than sham cells during hypoxia (423 vs. 1,766 arbitrary units at 4 h of hypoxia), and exchangeable Ca2+ increased much less in CHF than in sham cells (1.4 vs. 6.7 nmol/mg protein) after 120 min of reoxygenation. Ranolazine, an inhibitor of late Na+ current, significantly attenuated both the increase in exchangeable Ca2+ and the increase in LD release in sham cells after reoxygenation. This supports the suggestion that differences in Na+ accumulation during hypoxia cause the observed differences in Ca2+ accumulation during reoxygenation. Tolerance to hypoxia and reoxygenation was surprisingly higher in CHF than in sham cardiomyocytes, probably explained by lower hypoxia-mediated Na+ accumulation and subsequent lower Ca2+ accumulation in CHF after reoxygenation.
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Fan, Jin, Yuwen Liu, Jian Yin, Qingqing Li, Yiming Li, Jun Gu, Weihua Cai i Guoyong Yin. "Oxygen-Glucose-Deprivation/Reoxygenation-Induced Autophagic Cell Death Depends on JNK-Mediated Phosphorylation of Bcl-2". Cellular Physiology and Biochemistry 38, nr 3 (2016): 1063–74. http://dx.doi.org/10.1159/000443057.
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Background/Aims: The purpose of this study was to investigate the role of autophagy in oxygen-glucose-deprivation/reoxygenation (OGD/R) injury in rat neurons. Methods and results: Cortical neurons were isolated from Sprague-Dawley rats and identified by immunofluorescence. The cortical neurons were randomly assigned to one of four groups: control group (I), experimental group (OGD/R group, II), JNK inhibitor pretreatment group (III) and JNK inhibitor pretreatment + OGD/R group (IV). Neuronal cell viability significantly decreased after 6h and 12h of reoxygenation in Group IV (P < 0.05). Electron microscopy showed the presence of many autophagic vacuoles and the formation of autolysosomes in the neurons; the number of autophagic vacuoles decreased transiently at 6h, while a new autophagic flux and a large number of empty autophagic vacuoles were observed at 12h. In Group IV, a large number of autophagic vacuoles were present at 0.5h and 2h of reoxygenation, which gradually decreased with increasing reoxygenation time. No significant differences in the expression of the LC3II protein were detected between the Group II and IV prior to 6h of reoxygenation, and LC3II expression showed an overall rise-decline pattern. However, LC3II protein expression increased in Group II at 12h of reoxygenation, whereas a continuous decline was observed in Group IV. The levels of phosphorylated JNK and Bcl-2 and the expression of Beclin-1 increased gradually as the reoxygenation time going in Group II, whereas they increased at 12h of reoxygenation in Group IV (P < 0.05). In addition, progressive dissociation of the Bcl-2/Beclin-1 complex was observed in the Group II, while JNK inhibitor suppressed this dissociation. Conclusion: The regulation of the JNK/Bcl-2/Beclin-1 signaling pathway may be one of the mechanisms underlying the OGD/R-induced autophagic cell death of neurons.
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Sun, He-Ying, Ning-Ping Wang, Faraz Kerendi, Michael Halkos, Hajime Kin, Robert A. Guyton, Jakob Vinten-Johansen i Zhi-Qing Zhao. "Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload". American Journal of Physiology-Heart and Circulatory Physiology 288, nr 4 (kwiecień 2005): H1900—H1908. http://dx.doi.org/10.1152/ajpheart.01244.2003.
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We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by hypoxic postconditioning (Postcon) is associated with a reduction in the generation of reactive oxygen species (ROS) and intracellular Ca2+ overload. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h of hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned after the 3-h index hypoxia by three cycles of 5 min of reoxygenation and 5 min of rehypoxia applied before 6 h of reoxygenation. Relative to sham control and hypoxia alone, the generation of ROS (increased lucigenin-enhanced chemiluminescence, SOD-inhibitable cytochrome c reduction, and generation of hydrogen peroxide) was significantly augmented after immediate reoxygenation as was the production of malondialdehyde, a product of lipid peroxidation. Concomitant with these changes, intracellular and mitochondrial Ca2+ concentrations, which were detected by fluorescent fluo-4 AM and X-rhod-1 AM staining, respectively, were elevated. Cell viability assessed by propidium iodide staining was decreased consistent with increased levels of lactate dehydrogenase after reoxygenation. Postcon treatment at the onset of reoxygenation reduced ROS generation and malondialdehyde concentration in media and attenuated cardiomyocyte death assessed by propidium iodide and lactate dehydrogenase. Postcon treatment was associated with a decrease in intracellular and mitochondrial Ca2+ concentrations. These data suggest that Postcon treatment reduces reoxygenation-induced injury in cardiomyocytes and is potentially mediated by attenuation of ROS generation, lipid peroxidation, and intracellular and mitochondrial Ca2+ overload.
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Borle, A. B., i R. T. Stanko. "Pyruvate reduces anoxic injury and free radical formation in perfused rat hepatocytes". American Journal of Physiology-Gastrointestinal and Liver Physiology 270, nr 3 (1.03.1996): G535—G540. http://dx.doi.org/10.1152/ajpgi.1996.270.3.g535.
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The effects of 5 mM pyruvate on anoxic injury, superoxide (O2-.) and hydrogen peroxide (H2O2) generation, and lactate dehydrogenase (LDH) release during reoxygenation after 2.5 h anoxia were studied in perfused rat hepatocytes. When pyruvate was present during anoxia and reoxygenation, there was little anoxic injury, and the generation of free radicals and LDH release during reoxygenation were reduced 50-60%. When Pyruvate was added during reoxygenation, there was no decrease in O2-. or LDH release, although H2O2 formation was depressed. Free radical formation and anoxic/reperfusion injury were significantly reduced when pyruvate was added during the anoxic period only. Pyruvate reduced the deleterious effects of 10 microM antimycin A by preventing the increase in O2-. formation and LDH release evoked by the inhibitor. These results indicate that pyruvate protected hepatocytes against anoxic injury and that its protective action occurred principally during anoxia and not during reoxygenation. Pyruvate appeared to act at a mitochondrial site, since it reduced the deleterious effects of antimycin A.
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Freiberg, Rachel A., Ester M. Hammond, Mary Jo Dorie, Scott M. Welford i Amato J. Giaccia. "DNA Damage during Reoxygenation Elicits a Chk2-Dependent Checkpoint Response". Molecular and Cellular Biology 26, nr 5 (1.03.2006): 1598–609. http://dx.doi.org/10.1128/mcb.26.5.1598-1609.2006.
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ABSTRACT Due to the abnormal vasculature of solid tumors, tumor cell oxygenation can change rapidly with the opening and closing of blood vessels, leading to the activation of both hypoxic response pathways and oxidative stress pathways upon reoxygenation. Here, we report that ataxia telangiectasia mutated-dependent phosphorylation and activation of Chk2 occur in the absence of DNA damage during hypoxia and are maintained during reoxygenation in response to DNA damage. Our studies involving oxidative damage show that Chk2 is required for G2 arrest. Following exposure to both hypoxia and reoxygenation, Chk2−/− cells exhibit an attenuated G2 arrest, increased apoptosis, reduced clonogenic survival, and deficient phosphorylation of downstream targets. These studies indicate that the combination of hypoxia and reoxygenation results in a G2 checkpoint response that is dependent on the tumor suppressor Chk2 and that this checkpoint response is essential for tumor cell adaptation to changes that result from the cycling nature of hypoxia and reoxygenation found in solid tumors.
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Yokoyama, S., R. J. Korthuis i J. N. Benoit. "Hypoxia-reoxygenation impairs endothelium-dependent relaxation in isolated rat aorta". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, nr 5 (1.05.1996): R1126—R1131. http://dx.doi.org/10.1152/ajpregu.1996.270.5.r1126.
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The effects of hypoxia followed by reoxygenation on endothelium-dependent relaxation in isolated rat aorta were investigated. Acetylcholine (ACh, 3 nM-10 microM) and calcium ionophore A-23187 (3 nM-300 nM)-induced endothelium-dependent vasorelaxation of isolated rate aortic vessel rings was impaired after 15 min of hypoxia followed by 30 min of reoxygenation. Impairment of ACh-induced relaxation was prevented by pretreatment with the combination of superoxide dismutase (200 U/ml) and catalase (1,000 U/ml). Hypoxia-reoxygenation did not affect sodium nitroprusside (0.1 nM-1 microM)-induced endothelium-independent relaxation nor the dissociation constant of ACh to endothelial M3 muscarinic receptors. Propidium iodide staining of the vascular endothelium revealed a significant increase in the number of dead endothelial cells on the aortic vessel rings following hypoxia-reoxygenation, but not on those pretreated with superoxide dismutase and catalase. These results suggest that hypoxia-reoxygenation impairs endothelium-dependent relaxation of rat aorta by a mechanism that involves oxidant-mediated endothelial cell death.
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Sun, Zhiting, Kangni Yang i Hongyun Zhao. "Mir-36a Inhibits Hypoxia Reoxygenation and Promotes Bone Marrow Mesenchymal Stem Cells to Promote Cardiomyocyte Repair". Journal of Biomaterials and Tissue Engineering 11, nr 12 (1.12.2021): 2491–96. http://dx.doi.org/10.1166/jbt.2021.2817.
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This study explores the mechanism of miR-36a in the hypoxia-reoxygenation process and its engagement in the repair of cardiomyocytes via modulating bone marrow mesenchymal stem cells (BMSCs). Thirty-two patients with myocardial injury were enrolled after hospitalization. Meanwhile, 32 normal patients were recruited as controls. The miR-36a levels were quantified via ELISA. BMSCs were isolated and cultured. The qRT-PCR was employed to determine the expression of genes involved in myocardial injury and hypoxia-reoxygenation, including KGF, SpB, SpA, CK18, SpC and Occludin. Specific mRNAs related to myocardial damage repair were also measured after miR-36a was knockdown and overexpressed during the process of repair induction. The expression of miR-36a in 32 patients with myocardial injury was elevated compared to that in controls. BMSCs can quantitatively retard the expression of hypoxia-reoxygenation-related genes. The knockdown of miR-36a can significantly enhance the expression of hypoxia-reoxygenation-related genes which were engaged in myocardial injury. miR-36a overexpression can significantly impede the expression of the hypoxia-reoxygenation-related genes which were involved in myocardial injury. miR-36a contributes to the repair of myocardial injury via functionally enhancing BMSCs’ function and interfering with the hypoxia-reoxygenation process.
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Yang, Long, Jianjiang Wu, Peng Xie, Jin Yu, Xin Li, Jiang Wang i Hong Zheng. "Sevoflurane postconditioning alleviates hypoxia-reoxygenation injury of cardiomyocytes by promoting mitochondrial autophagy through the HIF-1/BNIP3 signaling pathway". PeerJ 7 (24.06.2019): e7165. http://dx.doi.org/10.7717/peerj.7165.
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Background Sevoflurane postconditioning (SpostC) can alleviate hypoxia-reoxygenation injury of cardiomyocytes; however, the specific mechanism remains unclear. This study aimed to investigate whether SpostC promotes mitochondrial autophagy through the hypoxia-inducible factor-1 (HIF-1)/BCL2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) signaling pathway to attenuate hypoxia-reoxygenation injury in cardiomyocytes. Methods The H9C2 cardiomyocyte hypoxia/reoxygenation model was established and treated with 2.4% sevoflurane at the beginning of reoxygenation. Cell damage was determined by measuring cell viability, lactate dehydrogenase activity, and apoptosis. Mitochondrial ultrastructural and autophagosomes were observed by transmission electron microscope. Western blotting was used to examine the expression of HIF-1, BNIP3, and Beclin-1 proteins. The effects of BNIP3 on promoting autophagy were determined using interfering RNA technology to silence BNIP3. Results Hypoxia-reoxygenation injury led to accumulation of autophagosomes in cardiomyocytes, and cell viability was significantly reduced, which seriously damaged cells. Sevoflurane postconditioning could upregulate HIF-1α and BNIP3 protein expression, promote autophagosome clearance, and reduce cell damage. However, these protective effects were inhibited by 2-methoxyestradiol or sinBNIP3. Conclusion Sevoflurane postconditioning can alleviate hypoxia-reoxygenation injury in cardiomyocytes, and this effect may be achieved by promoting mitochondrial autophagy through the HIF-1/BNIP3 signaling pathway.
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Zhao, Guochang, Abu B. Al-Mehdi i Aron B. Fisher. "Anoxia-reoxygenation versus ischemia in isolated rat lungs". American Journal of Physiology-Lung Cellular and Molecular Physiology 273, nr 6 (1.12.1997): L1112—L1117. http://dx.doi.org/10.1152/ajplung.1997.273.6.l1112.
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Oxidant generation in anoxia-reoxygenation and ischemia-reperfusion was compared in isolated rat lungs. Anoxia-reoxygenation was produced by N2 ventilation followed by O2 ventilation. After anoxia, lung ATP content was decreased by 59%. Oxygenated ischemia was produced by discontinuing perfusion while ventilation with O2 was maintained. With anoxia-reoxygenation, oxidant generation, evaluated by oxidation of dichlorodihydrofluorescein (H2DCF) to fluorescent dichlorofluorescein, increased 3.6-fold, lung thiobarbituric acid reactive substances (TBARS) increased 342%, conjugated dienes increased 285%, and protein carbonyl content increased 46%. Pretreatment of lungs with 100 μM allopurinol inhibited the reoxygenation-mediated increase in lung fluorescence by 75% and TBARS by 69%. Oxygenated ischemia resulted in an approximately eightfold increase in lung H2DCF oxidation and a fourfold increase in TBARS, but allopurinol had no effect. On the other hand, 100 μM diphenyliodonium (DPI) inhibited the ischemia-mediated increase in lung fluorescence by 69% and lung TBARS by 70%, but it had no effect on the increase with anoxia-reoxygenation. Therefore, both ischemia-reperfusion and anoxia-reoxygenation result in oxidant generation by the lung, but a comparison of results with a xanthine oxidase inhibitor (allopurinol) and a flavoprotein inhibitor (DPI) indicate that the pathways for oxidant generation are distinctly different.