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A significant reduction of antioxidant defenses is usually associated with aging and leading to an increased susceptibility to oxidative stress.35 This reduction may explain, at least in part, the increased rate of fibrosis progression seen in chronic HCV patients.36 Viral hepatitis and oxidative stress Cellular damage in viral hepatitis is predominantly determined by an immunological response and a large amount of data demonstrate that the persistence of infection, the progression of liver damage and, eventually, carcinogenesis are all steps in which oxidative-stress mediated pathways are involved.4 Hepatitis C virus (HCV) infection is associated with elevated levels of circulating ROS in the serum of patients.37 This increase in ROS seems to be due at least in part, to a direct activation by the HCV NS3 protein of the NADPH oxidase in monocytes38 and by the core protein and NS5A on other cells, with mechanisms involving intracellular calcium mobilization.39,40 Since chronic HCV infection may be associated with the development of hepatocellular carcinoma (HCC) and alteration of cellular redox state is also associated with tumor transformation and progression, these links could explain some aspects of the pathogenesis of hepatocarcinogenesis in HCV infection

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Additionally, the bacterial colony-counting assay confirmed that the nanoassemblies do not affect bacterial viability throughout the repeated illumination cycles (Supplementary Fig

doi: 10.1152/ajplegacy.1961.200.1.34 141 BaiSCSampsonDAMorrisJGRogersQR

Plasma and RBCs were aliquoted into separate vials and stored at -20C