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African Journal of Biotechnology

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Oxidative stress pattern in hepatitis C patients co-infected with schistosomiasis

Kholoud S Ramadan, Olfat A Khalil, Amal H Hamza, Safinaz E El-Toukhy

Abstract


This study was designed to investigate the role of hepatitis C virus (HCV)-induced oxidative stress in the pathogenesis of the disease with the measurement of tumor necrosis factor (TNF-∝) and super oxide dismutase (SOD). Eighty patients from Hepatology Unit, Faculty of Medicine, Ain Shams University, were investigated. Thirty patients with bilharzial HCV and 30 patients with non-bilharzial HCV as compared to 20 healthy controls of the same age and sex ratio were investigated. The concentrations of liver enzymes [glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), alkaline phosphatase (ALP)], bilirubin (Bil), albumin (Alb) and total protein (TP) as well as TNF-α and Mn-SOD were determined. The mean level of the different liver function tests in the three groups in the study showed that the levels of GOT, GPT and ALP were significantly higher in the HCV groups as compared to the control group (p < 0.05). While serum bilirubin, albumin and total protein were non-significantly decreased in the HCV groups as compared to the control group (p > 0.05). Furthermore, the mean level of TNF-α was significantly higher in the HCV groups as compared to the control group (p < 0.001) and SOD was significantly decreased in the HCV groups as compared to the control group (p < 0.001). There is a cause-effect relationship between increased levels of TNF-α and decreased levels of SOD, relative to progression of chronic HCV, especially with bilharzias co-infection. Supporting the view that oxidative damage plays a role in chronic HCV infection, also TNF-α establishes a positive auto regulatory loop that can amplify the inflammatory response and lead to chronic inflammation. More evidence indicates that HCV block apoptosis and prolong survival of the host cell in order to gain time for replication and increase viral progeny production.

Key words: Hepatitis C virus, tumor necrosis factor-alpha, superoxide dismutase, oxidative stress, schistosomiasis.




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