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dc.creatorLopez-Sanchez, L.M. (Laura M.)-
dc.creatorCorrales, F.J. (Fernando José)-
dc.creatorLopez-Pedrera, C. (Chary)-
dc.creatorAranda, E. (E)-
dc.creatorRodriguez-Ariza, A. (Antonio)-
dc.identifier.citationLopez-Sanchez LM, Corrales FJ, Lopez-Pedrera C, Aranda E, Rodriguez-Ariza A. Pharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cells. Anticancer Res 2010 Feb;30(2):415-421.es_ES
dc.description.abstractBACKGROUND/AIM: S-Nitrosoglutathione reductase (GSNOR) and thioredoxin enzyme systems participate in cellular defence against nitrosative stress. Pharmacological interventions against these enzyme systems might represent valuable strategies to impair S-nitrosothiol (SNO) homeostasis in tumour cells. MATERIALS AND METHODS: Human HepG2 cells were pre-treated with mithramycin A or auranofin and exposed to S-nitroso-L-cysteine. GSNOR mRNA levels were analyzed by quantitative real-time reverse transcriptase-polymerase chain reaction and S-nitrosated proteins were detected and purified using the biotin-switch approach. Proteins were identified using electrospray ionization tandem mass spectrometry. RESULTS: Mithramycin interfered with GSNOR induction resulting in an increased cellular sensitivity to protein S-nitrosation. Moreover, the thioredoxin reductase inhibitor auranofin also increased cellular susceptibility to S-nitrosoprotein formation. The impairment of these two cellular defense systems against nitrosative stress resulted in different sets of S-nitrosated proteins, as revealed by the proteomics approach. CONCLUSION: Our results suggest that pharmacological intervention with mithramycin or auranofin may constitute promising tools for altering SNO homeostasis in tumour cells.es_ES
dc.publisherInternational Institute of Anticancer Researches_ES
dc.subjectPlicamycin/analogs & derivativeses_ES
dc.subjectThioredoxin-Disulfide Reductase/antagonists & inhibitorses_ES
dc.subjectThioredoxin-Disulfide Reductase/metabolismes_ES
dc.titlePharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cellses_ES

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