scholarly journals Development of an in vitro model of excess intracellular reactive oxygen species

AGE ◽  
2005 ◽  
Vol 27 (2) ◽  
pp. 97-105 ◽  
Author(s):  
K. A. Greer ◽  
M. Pine ◽  
D. L. Busbee
Keyword(s):  
Reactive Oxygen Species ◽  
In Vitro Model ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Vitro Model

scholarly journals Effects of uremic solutes on reactive oxygen species in vitro model systems as a possibility of support the renal function management

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Renata P Assis ◽  
Juliana FA Castro ◽  
Vânia O Gutierres ◽  
Carlos A Arcaro ◽  
Renata S Brotto ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Renal Function ◽  
In Vitro Model ◽  
Reactive Oxygen ◽  
Model Systems ◽  
Oxygen Species ◽  
Uremic Solutes ◽  
Function Management ◽  
Vitro Model

Sevoflurane Protects Rat Mixed Cerebrocortical Neuronal–Glial Cell Cultures against Transient Oxygen–Glucose Deprivation

2006 ◽  
Vol 105 (5) ◽  
pp. 990-998 ◽  
Author(s):  
Paula T. Canas ◽  
Lionel J. Velly ◽  
Christelle N. Labrande ◽  
Benjamin A. Guillet ◽  
Valérie Sautou-Miranda ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
In Vitro Model ◽  
Glutamate Uptake ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Oxygen Species ◽  
Lactate Dehydrogenase Release ◽  
Vitro Model ◽  
Glial Cell Cultures

Background The purpose of this study was to clarify the role of glutamate and reactive oxygen species in sevoflurane-mediated neuroprotection on an in vitro model of ischemia-reoxygenation. Methods Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane, were exposed to 90 min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber followed by reoxygenation. Cell death was quantified by lactate dehydrogenase release into the media and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium by mitochondrial succinate dehydrogenase. Extracellular concentrations of glutamate and glutamate uptake were assessed at the end of the ischemic injury by high-performance liquid chromatography and incorporation of L-[H]glutamate into cells, respectively. Free radical generation in cells was assessed 6 h after OGD during the reoxygenation period using 2',7'-dichlorofluorescin diacetate, which reacts with intracellular radicals to be converted to its fluorescent product, 2',7'-dichlorofluorescin, in cell cytosol. Results Twenty-four hours after OGD, sevoflurane, in a concentration-dependent manner, significantly reduced lactate dehydrogenase release and increased cell viability. At the end of OGD, sevoflurane was able to reduce the OGD-induced decrease in glutamate uptake. This effect was impaired in the presence of threo-3-methyl glutamate, a specific inhibitor of the glial transporter GLT1. Sevoflurane counteracted the increase in extracellular level of glutamate during OGD and the generation of reactive oxygen species during reoxygenation. Conclusion Sevoflurane had a neuroprotective effect in this in vitro model of ischemia-reoxygenation. This beneficial effect may be explained, at least in part, by sevoflurane-induced antiexcitotoxic properties during OGD, probably depending on GLT1, and by sevoflurane-induced decrease of reactive oxygen species generation during reoxygenation.

Surgery-Derived Reactive Oxygen Species Produced by Polymorphonuclear Leukocytes Promote Tumor Recurrence: Studies in an In Vitro Model

2007 ◽  
Vol 140 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Wilhelmina M.U. van Grevenstein ◽  
Arend G.J. Aalbers ◽  
Sander ten Raa ◽  
Wim Sluiter ◽  
Leo J. Hofland ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Tumor Recurrence ◽  
In Vitro Model ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Vitro Model
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