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Oxidative stress-induced apoptosis in retinal photoreceptor cells is mediated by calpains and caspases and blocked by the oxygen radical scavenger CR-6

AuthorsSanvicens, Nuria ; Gómez-Vicente, Violeta ; Masip, Isabel ; Messeguer Peypoch, Ángel ; Cotter, Thomas G.
KeywordsReactive Oxygen Species
Retinal photoreceptor cells
Molecular mechanism
Sodium nitroprusside
Issue Date21-Jun-2004
PublisherAmerican Society for Biochemistry and Molecular Biology
CitationJournal of Biological Chemistry 279(38): 39268-39278 (2004)
AbstractA critical role for reactive oxygen species (ROS) in photoreceptor apoptosis has been established. However, the exact molecular mechanisms triggered by oxidative stress in photoreceptor cell death remain undefined. This study delineates the molecular events that occur after treatment of the photoreceptor cell line 661W with the nitric oxide donor sodium nitroprusside (SNP). Cytosolic calcium levels increased during photoreceptor apoptosis, leading to activation of the calcium-dependent proteases calpains. Furthermore, caspase activation also occurred following SNP insult. However, although treatment with the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone inhibited caspase activity per se in SNP-treated 661W cells, it did not prevent apoptosis. On the other hand, CR-6 (3,4-dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran) acted as a scavenger of ROS and reduced 661W photoreceptor apoptosis induced by SNP by preventing the activation of a pathway in which calpains have a key role. In summary, we report for the first time that both caspases and calpains are involved in 661W photoreceptor apoptosis and that calpain activation can be prevented by the ROS scavenger CR-6.
Description11 pages, 8 figures.-- PMID: 15210718 [PubMed].-- Printed version published Sep 17, 2004.
Publisher version (URL)http://dx.doi.org/10.1074/jbc.M402202200
Appears in Collections:(IQAC) Artículos
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