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|dc.creator||Lopez-Sanchez, L.M. (Laura M.)||-|
|dc.creator||Corrales, F.J. (Fernando José)||-|
|dc.creator||Lopez-Pedrera, C. (Chary)||-|
|dc.creator||Aranda, E. (E)||-|
|dc.creator||Rodriguez-Ariza, A. (Antonio)||-|
|dc.identifier.citation||Lopez-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.abstract||BACKGROUND/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.publisher||International Institute of Anticancer Research||es_ES|
|dc.subject||Plicamycin/analogs & derivatives||es_ES|
|dc.subject||Thioredoxin-Disulfide Reductase/antagonists & inhibitors||es_ES|
|dc.title||Pharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cells||es_ES|
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