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https://hdl.handle.net/10316/4797
Título: | Cytosolic and mitochondrial ROS in staurosporine-induced retinal cell apoptosis | Autor: | Gil, Joana Almeida, Sandra Oliveira, Catarina R. Rego, A. Cristina |
Palavras-chave: | Apoptosis; Antioxidants; Calcium; Caspase-3; Mitochondria; Reactive oxygen species; Retinal cells; Staurosporine; Free radicals | Data: | 2003 | Citação: | Free Radical Biology and Medicine. 35:11 (2003) 1500-1514 | Resumo: | In this study, we investigated the involvement of reactive oxygen species (ROS) and calcium in staurosporine (STS)-induced apoptosis in cultured retinal neurons, under conditions of maintained membrane integrity. The antioxidants idebenone (IDB), glutathione-ethylester (GSH/EE), trolox, and Mn(III)tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP) significantly reduced STS-induced caspase-3-like activity and intracellular ROS generation. Endogenous sources of ROS production were investigated by testing the effect of the following inhibitors: 7-nitroindazole (7-NI), a specific inhibitor of the neuronal isoform of nitric oxide synthase (nNOS); arachidonyl trifluoromethyl ketone (AACOCF3), a phospholipase A2 (PLA2) inhibitor; allopurinol, a xanthine oxidase inhibitor; and the mitochondrial inhibitors rotenone and oligomycin. All these compounds decreased caspase-3-like activity and ROS generation, showing that both mitochondrial and cytosolic sources of ROS are implicated in this mechanism. STS induced a significant increase in intracellular calcium concentration ([Ca2+]i), which was partially prevented in the presence of IDB and GSH/EE, indicating its dependence on ROS generation. These two antioxidants and the inhibitors allopurinol and 7-NI also reduced the number of TdT-mediated dUTP nick-end labeling-positive cells. Thus, endogenous ROS generation and the rise in intracellular calcium are important inter-players in STS-triggered apoptosis. Furthermore, the antioxidants may help to prolong retinal cell survival upon apoptotic cell death. | URI: | https://hdl.handle.net/10316/4797 | DOI: | 10.1016/j.freeradbiomed.2003.08.022 | Direitos: | openAccess |
Aparece nas coleções: | FMUC Medicina - Artigos em Revistas Internacionais |
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filee631db6392ac4c68a1af41f6eab39b3e.pdf | 396.6 kB | Adobe PDF | Ver/Abrir |
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