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Relative and Combined Effects of Chronic Alcohol Consumption and HCV Infection on Serum Zinc, Copper, and Selenium
Authors:Emilio González-Reimers  M Candelaria Martín-González  M Remedios Alemán-Valls  María José de la Vega-Prieto  Luis Galindo-Martín  Pedro Abreu-González  Francisco Santolaria-Fernández
Institution:1. Servicio de Medicina Interna, Hospital Universitario, Universidad de La Laguna, Ofra s/n., Tenerife, Canary Islands, Spain
2. Servicio de Laboratorio, Hospital Universitario, Universidad de La Laguna, Tenerife, Canary Islands, Spain
3. Dpto. de Química Analítica, Facultad de Química, Universidad de La Laguna, Tenerife, Canary Islands, Spain
4. Dpto de Fisiología, Facultad de Medicina, Universidad de La Laguna, Tenerife, Canary Islands, Spain
Abstract:In alcoholic hepatitis, Kupffer cells are activated by intestinal gram-bacteria, leading to cytokine production and free radicals release, which, enhancing cytokine secretion, create a positive feedback loop which contributes to liver inflammation. Free radicals also damage the liver in chronic hepatitis C virus (HCV) infection, a condition frequently associated to alcohol consumption. In both situations, activity of antioxidant enzymes and of its cofactors zinc (Zn), selenium (Se), and copper (Cu) is important. This study was performed to assess the relative and combined effects of chronic alcoholism and HCV infection on serum Se, Zn, and Cu, and its relation with serum malondialdehyde (MDA) and tumor necrosis factor-α, interferon-γ, and interleukins (IL) 4, 6, and 8, in 19 HCV? alcoholic patients, 12 HCV+ alcoholic patients, nine HCV+ non-alcoholic patients, and 20 controls. Serum Zn and Se were lower in both HCV+ and HCV? alcoholic patients, whereas serum Cu was lower in HCV+ individuals. Serum Zn and Se were related to liver function derangement. MDA levels were higher in alcoholics, but no relation was observed between trace elements and MDA or cytokines, so that our results do not support a relevant role of the analyzed trace elements in the pathogenesis of chronic liver disease.
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