Superoxide production by human umbilical vein endothelial cells in an anoxia-reoxygenation model

Schinetti, M. L.; Sbarbati, R; Scarlattini, M.

doi:10.1093/cvr/23.1.76

Cited by 58 publications

(24 citation statements)

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“…Previous in vitro studies have described that endothelial cells release 02-in res onse to various stimuli brecher, 1988; Schinetti et al, 1989;Holland et al, 1990). However, continuous 02-dismutation should also result in a production of H202.…”

Section: Resultsmentioning

confidence: 98%

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Bovine aortic endothelial cells release hydrogen peroxide

Sundqvist

1991

Journal Cellular Physiology

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Endothelial cells grown on microcarriers are able to release H2O2 to the extracellular environment without any added stimulus. The extracellularly released H2O2 can be detected by luminol-amplified chemiluminescence (CL) if horseradish peroxidase is added. The CL response can be reduced by catalase and blocked by superoxide dismutase, indicating that O2- could be a precursor for H2O2. The CL kinetics, i.e., a long lag time followed by a rapid shift to a new level, indicate activation of an O2(-)-producing enzyme. The cells are also able to protect themselves from H2O2 stimulation by both catalase and the glutatione system. Bradykinin stimulates the H2O2 release, but if the effect is directly stimulatory or if it acts by reduction of the protective system is at present unclear. The extracellularly released H2O2 could be a cause of injury to the endothelial cells or to the subendothelial matrix.

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Section: Resultsmentioning

confidence: 98%

“…This production by endothelial cells has also been demonstrated in anoxia-reoxygenation models (Schinetti et al, 1989;Ratych et al, 1987). The mechanism proposed is that, during ischemia, xantine dehydrogenase is converted to xantine oxidase, which generates superoxide oxide as reduction product.…”

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confidence: 73%

Bovine aortic endothelial cells release hydrogen peroxide

Sundqvist

1991

Journal Cellular Physiology

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“…Injury to cultured endothelial cells, cardiac myocytes, hepatocytes, and other cell types occurs after anoxia-reoxygenation in vitro, even in the absence of neutrophils. Endothelial cells themselves subjected to anoxia-reoxygenation release superoxide anions (O 2 Ϫ ) into the extracellular medium, as demonstrated by SOD-inhibitable, extracellular cytochrome c reduction and other assays (108). The quantity of O 2 Ϫ produced by reoxygenated cells depends on the duration of both anoxia and reoxygenation (99).…”

Section: Ros Mediate Reoxygenation Injurymentioning

confidence: 99%

Reactive species mechanisms of cellular hypoxia-reoxygenation injury

Jackson

2002

American Journal of Physiology-Cell Physiology

942

673

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Li, Chuanyu, and Robert M. Jackson. Reactive species mechanisms of cellular hypoxia-reoxygenation injury. Am J Physiol Cell Physiol 282: C227-C241, 2002; 10.1152/ajpcell.00112.2001.-Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, renal, and other ischemic syndromes. Cellular hypoxia and reoxygenation are two essential elements of ischemia-reperfusion injury. Activated neutrophils contribute to vascular reperfusion injury, yet posthypoxic cellular injury occurs in the absence of inflammatory cells through mechanisms involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine oxidase (XO) produces ROS in some reoxygenated cells, but other intracellular sources of ROS are abundant, and XO is not required for reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce excess superoxide (O 2 Ϫ ) and release H2O2, a diffusible long-lived oxidant that can activate signaling pathways or react vicinally with proteins and lipid membranes. This review focuses on the specific roles of ROS and RNS in the cellular response to hypoxia and subsequent cytolytic injury during reoxygenation.anoxia; ischemia; reperfusion BACKGROUND

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“…39 The activation of diacylglycerol-liberating enzyme, phospholipase C, in cerebrospinal fluid after SAH has been reported. 43 The vascular endothelium is able to produce significant amounts of superoxide radical 44,45 and hydrogen peroxide. 46 The vascular endothelium and perivascular clots together were the sites of the free radical generation, which is further supported by evidence of the ability of tirilazad to decrease in PCOOH.…”

Section: Discussionmentioning

confidence: 99%

Effects of Tirilazad Mesylate on Vasospasm and Phospholipid Hydroperoxides in a Primate Model of Subarachnoid Hemorrhage

Suzuki

Kanamaru

Kuroki

et al. 1999

Stroke

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Background and Purpose-Tirilazad mesylate has been used in the attempt to prevent cerebral vasospasm after subarachnoid hemorrhage (SAH), although the actual targets of this agent in vivo have thus far been controversial. Chemiluminescence/high-performance liquid chromatography provided a new method for direct measurements of phosphatidylcholine hydroperoxide (PCOOH) and phosphatidylethanolamine hydroperoxide (PEOOH) in vivo and showed that phosphatidylcholine is the lipid class most susceptible to lipid peroxidation. In the present study we measured those levels in a primate model of SAH for determination of the effects of tirilazad on vasospasm. Methods-Fourteen Macaca monkeys of both sexes were randomly assigned into 2 groups: a tirilazad group receiving a dosage of 0.3 mg/kg and a placebo group receiving only the vehicle in which tirilazad was delivered. After the induction of experimental SAH around the right middle cerebral artery on day 0, tirilazad or vehicle was administered intravenously every 8 hours for 6 days. On day 7, the animals were killed after angiography and regional cerebral blood flow measurements were performed. The levels of PCOOH and PEOOH were measured in the clots, bilateral parietal cortices, right frontal cortex contact with clots, cerebellar hemispheres, bilateral middle cerebral arteries, and basilar arteries. Results-In the placebo group, a significant vasospasm occurred in the cerebral arteries on both sides, but most prominently on the right side. The degree of vasospasm in the cerebral arteries was significantly attenuated in the tirilazad group (PϽ0.005). There were no significant differences in regional cerebral blood flow, PCOOH, and PEOOH levels in the clots, cerebral cortices, and cerebellar hemispheres between the 2 groups. In contrast, the levels of PCOOH in the cerebral arteries were significantly higher in the placebo group than in the tirilazad group (PϽ0.025). It was remarkable that the tirilazad treatments eliminated PCOOH in any vascular territory after SAH. Conclusions-PCOOH in the artery wall may be an important indicator for vasospasm, and the inhibition of PCOOH may explain the efficacy of tirilazad on vasospasm. (Stroke. 1999;30:450-456.)

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Superoxide production by human umbilical vein endothelial cells in an anoxia-reoxygenation model

Cited by 58 publications

References 0 publications

Bovine aortic endothelial cells release hydrogen peroxide

Bovine aortic endothelial cells release hydrogen peroxide

Reactive species mechanisms of cellular hypoxia-reoxygenation injury

Effects of Tirilazad Mesylate on Vasospasm and Phospholipid Hydroperoxides in a Primate Model of Subarachnoid Hemorrhage

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