Effect of Variable Glutathione Peroxidase Activity on H2O2-Related Cytotoxicity in Cultured Aortic Endothelial Cells

C, Ody; Junod, A.

doi:10.3181/00379727-180-42150

Cited by 20 publications

(16 citation statements)

References 23 publications

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“…In vitro, oxidative stress can be produced either by direct application 4 of H 2 O 2 or by continuous H 2 O 2 generation in enzymatic systems. 5 An interaction between H 2 O 2 and the endothelium may modulate the cellular redox balance. H 2 O 2 may also trigger multiple functions, such as the release of lactate dehydrogenase 6 and tissue factor.…”

Section: Methods and Results-kmentioning

confidence: 99%

Hydrogen Peroxide, Potassium Currents, and Membrane Potential in Human Endothelial Cells

et al. 1999

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Background-Hydrogen peroxide (H 2 O 2 ) and reactive oxygen species are implicated in inflammation, ischemiareperfusion injury, and atherosclerosis. The role of ion channels has not been previously explored. Methods and Results-K ϩ currents and membrane potential were recorded in endothelial cells by voltage-and current-clamp techniques. H 2 O 2 elicited both hyperpolarization and depolarization of the membrane potential in a concentration-dependent manner. Low H 2 O 2 concentrations (0.01 to 0.25 mol/L) inhibited the inward-rectifying K

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Section: Methods and Results-kmentioning

confidence: 99%

Hydrogen Peroxide, Potassium Currents, and Membrane Potential in Human Endothelial Cells

et al. 1999

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“…Other studies also used this concentration of SeMet. [23][24][25] In a previous study, we have tested other antioxidants including curcumin 26 and ginsenosides, 8 which also significantly blocked RTV-induced endothelial dysfunction in the porcine coronary arteries. These data are well correlated with O 2 2 production in these vessels, indicating that oxidative stress may be the major mechanism in HIV PI-induced vascular injury.…”

mentioning

confidence: 98%

Effects of 5 HIV Protease Inhibitors on Vasomotor Function and Superoxide Anion Production in Porcine Coronary Arteries

Chai

Yang

Yan

et al. 2005

JAIDS Journal of Acquired Immune Deficiency Syndromes

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HIV protease inhibitors (PIs) have been implicated to cause cardiovascular complications. Previous studies demonstrated that the PI ritonavir (RTV) caused endothelial dysfunction in porcine arteries. This study investigated and compared the effects of 5 commonly used PIs on vasomotor function, endothelial nitric oxide synthase (eNOS) expression, and oxidative stress in porcine coronary arteries. Vessel rings were incubated with 15 microM of RTV, amprenavir (APV), saquinavir (SQV), indinavir (IDV), or nelfinavir (NFV) for 24 hours. Vasomotor function was studied using a myograph system. The contractility of the rings was significantly reduced for RTV and SQV. In response to bradykinin at 10(-5) M, the endothelium-dependent relaxation was significantly reduced for RTV, APV, and SQV. The eNOS mRNA levels were significantly reduced for RTV, APV, and SQV. Furthermore, the superoxide anion (O(2)(-)) levels of the vessels were significantly increased for RTV and APV. It was found that nitric oxide production was decreased, whereas the level of nitrotyrosine proteins was increased in RTV-treated vessels. Furthermore, antioxidant seleno-L-methionine (SeMet) reversed RTV-induced O(2)(-) production and vasomotor dysfunction. Thus, the HIV PIs RTV, APV, and SQV at 15 microM have more potent in vitro effects on vasomotor dysfunction, eNOS downregulation, and O(2)(-) production than IDV and NFV. The antioxidant SeMet can block these adverse effects of RTV. The results suggest that antioxidant therapy may have applications for controlling PI-associated cardiovascular complications.

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“…A 60 min exposure, however, did not affect the relaxation induced by substance P, demonstrating that time is required to cause functional damage to the endothelium by the purine and XOD system, as reported in cultured endothelial cells. [32][33][34] Catalase completely prevented the inhibition of substance P-induced relaxation due to NO, whereas superoxide and mannitol were without effect, demonstrating that hydrogen peroxide was mostly responsible for the endothelial dysfunction, despite the existence of similar amounts of superoxide, hydrogen peroxide and presumably hydroxyl radicals. Although superoxide is well known to react with NO and inactivates the relaxing ability of NO, this is unlikely to have occurred in the present experiments, since the substance P test was done after wash out of the purine and XOD system.…”

Section: Fig 5 Inhibitory Effects Of Various Ros Scavengers On Dysfmentioning

confidence: 99%

Sustained Contraction and Endothelial Dysfunction Induced by Reactive Oxygen Species in Porcine Coronary Artery

Ishihara

Sekine

Hatano

et al. 2008

Biological & Pharmaceutical Bulletin

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Reactive oxygen species (ROS), including superoxide anions, hydrogen peroxide and hydroxyl radicals, can be produced in vivo by mechanisms related to mitochondrial respiration, xanthine oxidase (XOD), nitric oxide synthase (NOS), NADPH oxidase, and arachidonic acid metabolism.1,2) Disruption to one or more of these mechanisms is thought to be responsible for the pathogenesis of various diseases. [3][4][5][6] Of these mechanisms, XOD may be involved in the generation of ROS in the endothelium during ischemia and/or reperfusion. 7,8) Roy and McCord demonstrated that xanthine dehydrogenase is proteolytically converted to XOD in tissues within seconds or minutes of an ischemic episode, depending on the tissue involved. 9) Although both enzymes are involved in the catabolism of purine compounds, the latter transfers electrons to molecular oxygen to yield the ROS, superoxide anions and hydrogen peroxide. 10,11) Thus, the deleterious effects of reoxygenation or reperfusion in ischemic tissues can therefore be explained on the basis of the ROS produced by the xanthine-XOD (XϩXOD) system. For a better understanding of the pathogenesis of tissue damage by ROS, it is important to clarify which species of oxygen intermediates are involved in these events, and whether or not there are differences in sensitivity to ROS among various tissues.The direct effects of ROS on cultured vascular endothelial cells or isolated, perfused tissues have been extensively investigated, either by using ROS directly, or using a ROS-generating system, such as the XϩXOD system. [12][13][14][15][16][17] In these studies, ROS scavengers are used to clarify the species of ROS involved in these effects. Among the various biological effects attributed to ROS, vascular endothelial dysfunction has consistently been noted, irrespective of the preparations used. 2,18) In addition, ROS generated by the XϩXOD system caused contraction of rat pulmonary artery 19) and canine basilar artery, 20) whereas it relaxed canine coronary artery, 21) implying the existence of species or tissue differences in response to ROS. Furthermore, the responses of arteries to ROS are well-known to be influenced by the presence of endothelium. 12,13,16) Thus, the responses of the vasculature, including the endothelium, to ROS are complex, and the sensitivity to ROS probably varies depending on the tissue involved. Disruption to the functional integrity of blood vessels will inevitably alter the function of the organ supplied by these vessels. Thus, in the present study, we directed our attention to the effects of ROS on porcine coronary artery, in terms of muscular and endothelial functions, and attempted to determine characteristics of the responses of each vascular element, and to clarify the specific ROS involved. MATERIALS AND METHODS Preparation of Coronary Arterial RingsPorcine hearts, immersed in ice-cooled saline, were transported to the laboratory from an abattoir, usually within 1 h of death. The left anterior descending coronary artery was isolated 2-3 cm from its orig...

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Effect of Variable Glutathione Peroxidase Activity on H2O2-Related Cytotoxicity in Cultured Aortic Endothelial Cells

Cited by 20 publications

References 23 publications

Hydrogen Peroxide, Potassium Currents, and Membrane Potential in Human Endothelial Cells

Hydrogen Peroxide, Potassium Currents, and Membrane Potential in Human Endothelial Cells

Effects of 5 HIV Protease Inhibitors on Vasomotor Function and Superoxide Anion Production in Porcine Coronary Arteries

Sustained Contraction and Endothelial Dysfunction Induced by Reactive Oxygen Species in Porcine Coronary Artery

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