Increase in microvascular permeability induced by enzymatically generated free radicals

Maestro, Rolando F. Del; Björk, Jakob; Arfors, Karl-E.

doi:10.1016/0026-2862(81)90096-0

Cited by 173 publications

(37 citation statements)

References 26 publications

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“…Unlike studies using the whole vascular bed, our studies focused on the direct interaction of reactive species with endothelial cells, which were conducted in the absence of the effect of ROS-stimulated leukocyte on leakage formations. Furthermore, our results showed that perfusing vessels with XO alone did not have effect on microvessel L p , unlike the results from whole vascular bed (6,7). It appears that in the absence of blood, endothelial cells in the vessel walls do not have sufficient substrate to interact with XO to produce superoxide.…”

Section: Superoxide Induced Immediate and Transient Increases In Endocontrasting

confidence: 79%

“…Early studies by Del Maestro (6,7) demonstrated that superfusion of XO in the hamster check pouch transiently increased the number of leakage sites and leukocyte interactions with endothelium. Based on their observations that presuperfusion of either SOD or catalase resulted in decreased macromolecular extravasation, it was concluded that superoxide and H 2 O 2 presence is necessary for the transiently increased leakage.…”

Section: Superoxide Induced Immediate and Transient Increases In Endomentioning

confidence: 99%

See 1 more Smart Citation

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Zhou¹,

Wen²,

Dong³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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He P. Calcium influxdependent differential actions of superoxide and hydrogen peroxide on microvessel permeability. Am J Physiol Heart Circ Physiol 296: H1096 -H1107, 2009. First published February 6, 2009 doi:10.1152/ajpheart.01037.2008.-Our previous study demonstrated that reactive oxygen species (ROS) released from activated blood cells contribute significantly to the increased microvessel permeability during inflammation. This study aims to define the individual roles of hydrogen peroxide (H 2O2) and superoxide in ROSinduced increases in permeability and endothelial intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) in individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (L p). Endothelial [Ca 2ϩ ]i was measured in fura-2 AM-loaded microvessels. Perfusing microvessels with superoxide generated by hypoxanthine and xanthine oxidase (HX/XO) induced immediate and transient increases in L p. The mean peak value, which occurred within 5 min of HX/XO exposure, was 4.3 Ϯ 0.6 times that of the control. In contrast, the perfusion of H 2O2 (100 and 500 M) caused no immediate increases in L p. A significant Lp increase, 3.6 Ϯ 0.6 times the control value, occurred 30 min after the perfusion of H 2O2 at 500 M. The perfusion of H2O2 at 100 or 500 M for 1 h increased L p to 6.6 Ϯ 0.9 and 11.3 Ϯ 3.6 times the control value, respectively. The increased endothelial [Ca 2ϩ ]i in HX/XO or H 2O2 perfused vessels was correlated with the time course of the increases in L p. Inhibiting Ca 2ϩ influx by LaCl3 prevented the permeability increase induced by HX/XO or H 2O2. These results demonstrated differential actions of superoxide and H 2O2 on microvessel permeability and endothelial [Ca 2ϩ ]i. Superoxide-induced permeability increases were immediate and transient, whereas H 2O2-induced permeability increases were progressive, demonstrating concentration and time dependence. Ca 2ϩ influx plays an essential role in both superoxide and H 2O2-induced permeability increases. hydraulic conductivity; reactive oxygen species; endothelial calcium imaging REACTIVE OXYGEN species (ROS) contribute to various pathological conditions such as inflammation and ischemic reperfusion as well as atherosclerosis. A major source of ROS in the vascular system is from activated blood cells during respiratory burst. Our previous studies demonstrated that the ROS released from formyl Met-Leu-Phe-OH (fMLP)-stimulated neutrophils, either in suspension or from adherent leukocytes, cause immediate and transient increases in microvessel permeability (37,38). Prolonged permeability increases were observed with leukocyte/platelet aggregate adhesion to microvessel walls after initial endothelial cell activation by inflammatory mediators and endothelial gap formation (15). However, whether superoxide or hydrogen peroxide (H 2 O 2 ) converted from superoxide is the main species causing the increases in permeability under such experimental conditions remains unknown. Currently, most ROS-induced si...

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Section: Superoxide Induced Immediate and Transient Increases In Endocontrasting

confidence: 79%

Section: Superoxide Induced Immediate and Transient Increases In Endomentioning

confidence: 99%

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Zhou¹,

Wen²,

Dong³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…4) It has been suggested that production of oxygen free radicals plays a crucial role in the development of ethanol-induced gastric lesions. [5][6][7][8] The present study investigated the in vivo protective effect of astaxanthin isolated from the Xanthophyllomyces dendrorhous mutant against ethanol-induced gastric mucosal injury in rats. Peroxidation of lipids and changes in the activities of healing-related enzymes such as superoxide dismutase, catalase, and glutathione peroxidase were also monitored.…”

Section: Discussionmentioning

confidence: 99%

“…4) It has been suggested that ethanol-induced gastric damage is mediated by the generation of free radicals. [5][6][7][8] Recently, astaxanthin (3,3 0 -dihydroxy-, 0 -carotene-4,4 0 -dione) has been documented to provide important metabolic functions in animals, including conversion to vitamin A, 9) enhancement of immune response, 10,11) and protection against diseases such as cancer by scavenging oxygen radicals. [12][13][14][15][16] The antioxidant activity of astaxanthin has been reported to be approximately 10 times stronger than that of other carotenoids tested, including zeaxanthin, lutein, canthaxanthin, and -carotene, and 100 times greater than that of -tocopherol.…”

Section: Suppressive Effect Of Astaxanthin Isolated From the Xanthophmentioning

confidence: 99%

Suppressive Effect of Astaxanthin Isolated from theXanthophyllomyces dendrorhousMutant on Ethanol-Induced Gastric Mucosal Injury in Rats

Kim¹,

Choi²,

Choi³

et al. 2005

Bioscience, Biotechnology, and Biochemistry

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“…Recently, it has been shown that the hypoxanthine/xanthine oxidase system generates free radicals (7), and that this system potently induces inflammatory changes both in the hamster cheek pouch (22) and the rat lung (16). Further, it has, by now, been well established that hypoxanthine accumulates in tissues (33), plasma (30,32,34,35), and other body fluids (12,23,25) during hypoxia.…”

Section: Abbreviationmentioning

confidence: 99%

Hypoxanthine and Oxygen Induced Lung Injury: A Possible Basic Mechanism of Tissue Damage?

et al. 1984

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Summaryoxygen exposure with simultaneous intravenous hypoxanthine infusion. Lung injury was induced in young rats by a continuous infusion of hypoxanthine intravenously and breathing 100% oxygen for 48 h (group 1). Control animals were rats infused glucose and MATERIALS AND METHODSbreathing 100% oxygen (group 2), rats infused hypoxanthine in room air (group 3), and untreated rats (group 4). In group 1 rats interstitial and alveolar edema was found with a tendency toward marked margination of polymorphonuclear neutrophils in small vessels (P < 0.025 compared with group 2). The main elastase inhibitor alphal-antitrypsin (a-1-PI) was significantly elevated in group 1; 2-, 3-and 5-fold, respectively, when compared with groups 2, 3, and 4. The surfactant phopholipids from alveolar lavage were normal in all groups. The protein-rich fraction of the lavage fluid from group I rats inactivated, however, the surface properties of lung surfactant. Minimum surface tension in group 1 rats was 14.5 dyn/cm compared with 7.0 dyn/cm in group 2, 2.9 dyn/cm in group 3 and 3.5 dyn/cm in group 4 (P < 0.05, group 1 and 2 versus 4). We conclude that the combination of hypoxanthine and high levels of oxygen causes lung injury, possibly via free oxygen radicals. We discuss the possibility that these findings demonstrate a basic pathogenetic mechanism for the hypoxic-hyperoxic insult and can contribute to the understanding of pathogenesis of a variety of diseases both in pediatrics and adult medicine. AbbreviationFree oxygen radicals have been shown to destroy cell membranes by lipid peroxidation (3, 8, 1 1, 2 1). It has been suggested that such radicals play an important role in the pathogenesis of the acute and chronic lung damage among patients treated with oxygen. Many authors have, however, suggested that oxygen must be combined with other more or less unknown factors, before injury occurs ( 14,27).Recently, it has been shown that the hypoxanthine/xanthine oxidase system generates free radicals (7), and that this system potently induces inflammatory changes both in the hamster cheek pouch (22) and the rat lung (16). Further, it has, by now, been well established that hypoxanthine accumulates in tissues (33), plasma (30,32,34,35), and other body fluids (12,23,25) during hypoxia. When high concentrations of oxygen are administered to the hypoxic patient, large amounts of free radicals may be produced by the hypoxanthine/xanthine oxidase system. We, therefore, have raised the question whether the combination of hypoxanthine and oxygen is more damaging than high oxygen alone to the lung. In the present study we evaluated this by investigating experimentally the effect on the rat lung to 100% Young female rats of the Wistar strain, weighing 170-230 g, were used. Four groups were investigated. Group 1, rats infused continuously with 5 mM hypoxanthine dissolved in 5% glucose and exposed to 98-100% oxygen (n = 10). Group 2, rats infused continuously with 5% glucose and exposed to 98-100% oxygen (n = 9). Group 3, rats infused continuously wit...

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Increase in microvascular permeability induced by enzymatically generated free radicals

Cited by 173 publications

References 26 publications

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Suppressive Effect of Astaxanthin Isolated from theXanthophyllomyces dendrorhousMutant on Ethanol-Induced Gastric Mucosal Injury in Rats

Hypoxanthine and Oxygen Induced Lung Injury: A Possible Basic Mechanism of Tissue Damage?

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