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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Hepatología bioquímica > DA - CIMA - Terapia génica y Hepatología - Hepatología bioquímica - Artículos de revista >

Pharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cells
Autor(es) : Lopez-Sanchez, L.M. (Laura M.)
Corrales, F.J. (Fernando José)
Lopez-Pedrera, C. (Chary)
Aranda, E. (E)
Rodriguez-Ariza, A. (Antonio)
Palabras clave : Auranofin/pharmacology
Plicamycin/analogs & derivatives
Proteins/metabolism
S-Nitrosoglutathione/metabolism
Thioredoxin-Disulfide Reductase/antagonists & inhibitors
Thioredoxin-Disulfide Reductase/metabolism
Fecha incorporación: 2010
Editorial : International Institute of Anticancer Research
Versión del editor: http://ar.iiarjournals.org/content/30/2/415
ISSN: 1791-7530
Cita: 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.
Resumen
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.
Enlace permanente: http://hdl.handle.net/10171/21474
Aparece en las colecciones: DA - CIMA - Unidad de Proteómica, Genómica y Bioinformática - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Hepatología bioquímica - Artículos de revista

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