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N‐Acetyl cysteine (NAC) attenuates neuronal cell death in culture not solely by up regulating glutathione (GSH).
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Titel: |
N‐Acetyl cysteine (NAC) attenuates neuronal cell death in culture not solely by up regulating glutathione (GSH). |
In: | Acta Ophthalmologica, 87, 2009, s244, S. 0-0 |
veröffentlicht: |
Wiley
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Umfang: | 0-0 |
ISSN: |
1755-3768 1755-375X |
DOI: | 10.1111/j.1755-3768.2009.262.x |
Zusammenfassung: | <jats:title>Abstract</jats:title><jats:p> <jats:bold>Purpose</jats:bold> To show that NAC attenuates GB (glutamate/buthionine sulfoximine)‐induced death to retinal ganglion cells (RGC‐5 cells) in culture by a mechanism that does not solely involve GSH.</jats:p><jats:p> <jats:bold>Methods</jats:bold> Transformed retinal ganglion (RGC‐5) cells grown in culture were exposed to an insult of GB for defined periods. NAC at different concentrations or vehicle was added to the cultures over 24 hours. Reactive oxygen species (ROS) generation was measured using a dye 20,70‐dihydroethidium. Cell death was measured by use of an MTT and resazurin‐assays and evidence for apoptosis was obtained with an APOPercentage™ procedure. Glutathione (GSH), catalase (CAT), gluthathione‐S‐transferase (GST) and superoxide dismutase (SOD) were also determined using a different fluorescent procedure.</jats:p><jats:p> <jats:bold>Results</jats:bold> NAC dose‐dependently attenuated GB‐induced generation of ROS and death by a form of apoptosis to RGC‐5 cells in culture. NAC also independently stimulated the production of not only GSH but also GST, CAT and SOD. Moreover, NAC attenuated GB‐induced loss of intracellular GSH, CAT and GST.</jats:p><jats:p> <jats:bold>Conclusion</jats:bold> NAC significantly blunts oxidative‐induced death to RGC‐5 cells induced by GB. Evidence is also provided to show that NAC increases intracellular GSH, GST, CAT and SOD levels. The neuroprotective action of NAC is therefore complex and is not solely caused by an action on GSH.</jats:p> |
Format: | E-Article |
Quelle: | Wiley (CrossRef) |
Sprache: | Englisch |