Chronic hepatitis C (CHC) infection is a liver disease caused by the hepatitis C virus (HCV). It is a major public health problem, affecting approximately 71 million people worldwide, and is one of the leading causes of cirrhosis, hepatocellular cancer and liver-related deaths. It is estimated that approximately 400 000 people died in 2015 from complications related to CHC. 1 Although the mechanism of how HCV induces liver damage is not fully understood to date, it has been suggested that oxidative stress plays a pivotal role in the pathogenesis of CHC. [2][3][4] Oxidative stress, caused by the deterioration of homeostasis between reactive oxygen species (ROS) and antioxidants, triggers liver damage by inducing DNA damage, lipid peroxidation and protein oxidation in the organism. The increased oxidative stress in HCV infection induces hepatic stellate cell activation, DNA damage and gene mutation, which progresses towards liver fibrosis/cirrhosis and hepatocellular carcinoma. 5 Thiols containing the sulfhydryl (SH) group are part of the antioxidant defence system as they are metal chelators, free radical scavengers and thiol/disulphide redox buffer components. The thiol groups of sulphur-containing compounds, the main targets of ROS, react with oxidant molecules to form disulphide bonds (S-S). This process