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

Superoxide dismutase in patients with chronic hepatitis C virus infection
Autor(es) : Larrea, E. (Esther)
Beloqui, O. (Óscar)
Muñoz-Navas, M. (Miguel)
Civeira, M.P. (María Pilar)
Prieto, J. (Jesús)
Palabras clave : Superoxide-dismutase
PCR
Oxidative stress
TNFalfa
Hepatitis C virus genotypes
Viral load
Free radicals
Fecha incorporación: 1998
Editorial : Elsevier
Versión del editor: http://www.sciencedirect.com/science/article/pii/S0891584997004371
ISSN: 1873-4596
Cita: Larrea E, Beloqui O, Munoz-Navas MA, Civeira MP, Prieto J. Superoxide dismutase in patients with chronic hepatitis C virus infection. Free Radic Biol Med 1998 May;24(7-8):1235-1241.
Resumen
It has been reported that hepatitis C virus (HCV) may cause oxidative stress in infected cells. Patients with chronic hepatitis C exhibit an increased production of tumor necrosis factor-alpha (TNF alpha), a cytokine that can produce oxidative stress by stimulating the generation of reactive oxygen species (ROS). Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme. To investigate cell defense against oxidative stress in HCV infection, we analyzed Mn-SOD mRNA in liver and in peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis C. Mn-SOD expression in PBMC was significantly increased in patients with HCV infection. Patients with sustained virological and biochemical response after therapy showed significantly lower Mn-SOD than patients with positive viremia. By contrast, Mn-SOD expression was not enhanced in the liver of patients with chronic hepatitis C. The values of Mn-SOD mRNA did not correlate with TNF alpha mRNA expression, viral load, or liver disease activity. Our results indicate that in HCV infection an induction of Mn-SOD was present in PBMC but absent in the liver, suggesting that this organ could be less protected against oxidative damage. Oxidative stress could participate in the pathogenesis of HCV infection.
Enlace permanente: http://hdl.handle.net/10171/23269
Aparece en las colecciones: DA - CUN - Medicina interna - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Inmunología clínica - Artículos de revista

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Fichero:  FreeRadBiolMed1998_24_7.pdf
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