Chronic liver diseases are commonly characterized by continuous inflammation and oxidative stress in the hepatic parenchyma.
CS may impact incidence, severity and clinical course of chronic liver diseases 1.
Indeed, in adult smokers with chronic liver diseases such as primary biliary cirrhosis and chronic hepatitis C, an increased severity of hepatic fibrosis has been well established 2-4. Moreover, CS was identified as an independent risk factor for the onset of non-alcoholic fatty liver disease (NAFLD) 5 and was associated with advanced liver fibrosis in a large multi-center cohort of NAFLD patients 6.
CS can induce hepatotoxicity through different mechanisms. The vast quantities of carbon- and oxygen-centered free radicals contained in CS directly initiated and propagated the process of lipid peroxidation in hepatic and extra-hepatic tissues 7,8. Alternatively, via an indirect mechanism, CS induced abnormally high hemoglobin levels in the blood 9, subsequently resulting in hepatic iron overload and, finally, causing increased ROS generation in the liver 10.
Moreover, as the liver is the major site of synthesis and absorption of plasma lipids and lipoproteins, it has been suggested that CS-related liver dysfunction may contribute to the atherogenic plasma lipid profiles observed in cigarette smokers 11-14.