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Alcohol and Alcoholism Advance Access originally published online on January 23, 2008
Alcohol and Alcoholism 2008 43(2):137-142; doi:10.1093/alcalc/agm171
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Copyright © The Author 2008. Published by Oxford University Press on behalf of the Medical Council on Alcohol.

Cytokines and lipid peroxidation in alcoholics with chronic hepatitis C virus infection

Ana Castellano-Higuera1, Emilio González-Reimers1,*, M. Remedios Alemán-Valls1, Pedro Abreu-González2, Francisco Santolaria-Fernández1, María José De La Vega-Prieto3, Juan Luis Gómez-Sirvent1 and Ricardo Pelazas-González1

1 Servicios de Medicina Interna, Hospital Universitario, Universidad de La Laguna. Tenerife, Canary Islands, Spain
2 Departamento de Fisiología, Hospital Universitario, Universidad de La Laguna. Tenerife, Canary Islands, Spain
3 Servicio de Laboratorio, Hospital Universitario, Universidad de La Laguna. Tenerife, Canary Islands, Spain

* Author to whom correspondence should be addresses: Tel: +34 –922 678600; E-mail: egonrey{at}ull.es

Received 9 September 2007; in revised form 19 October 2007; in revised form 5 November 2007; accepted 16 November 2007


   Abstract

A major cause of liver cirrhosis and hepatocarcinoma is chronic infection by hepatitis C virus. Ethanol consumption is the most significant environmental factor that exacerbates the progression of chronic hepatitis C to liver cirrhosis and hepatocarcinoma, perhaps due to increased cytokine secretion together with increased lipid peroxidation. In this study, we compare the intensity of lipid peroxidation (estimated as malondialdehyde (MDA) serum levels), the antioxidant status, (measured as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in red blood cells), and levels of cytokines derived from Th1 cells (such as interferon gamma (IFNG)), Th2 cells (such as interleukin (IL)-4), Th3 cells (such as transforming growth factor beta (TGF-β)), and IL-6, IL-8, and tumor necrosis factor (TNF)-{alpha} in patients affected by chronic hepatitis C virus infection, 26 drinkers of alcohol and 40 nondrinkers of alcohol. Patients showed significantly higher TNF-{alpha} (Z = 4.92, P < 0.001), IL-8 (Z = 4.95, P < 0.001), IFNG (Z = 2.81, P = 0.005), TGF-β (t = 2.12, P = 0.037), MDA (Z = 5, P < 0.001), but lower IL-6 (Z = 3.61, P < 0.001) and GPX (F = 4.30, P < 0.05) than controls, whereas no differences were observed regarding IL-4 (Z = 0.35, P = 0.72), GPX and SOD activities. Alcoholics showed significantly higher TNF-{alpha}, but lower IL-4, MDA, and GPX, than nonalcoholics. TNF-{alpha} was significantly related to albumin and prothrombin activity, whereas TGF-β was significantly related to MDA levels. Thus, cytokine secretion is altered in HCV infection. This alteration mainly consists of a stimulation of Th1 cytokines and an inhibition—or at least, no stimulation—of Th2 cytokines; these changes are especially marked among alcoholics with HCV infection, and are accompanied by raised TGF-β.


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