Abstract
Oxidative stress is being recognized as a key factor in the progression of chronic liver disease (CLD), especially non-alcoholic fatty liver disease (NAFLD). Many NAFLD treatment guidelines recommend the use of antioxidants, especially vitamin E. Many prospective studies have described the beneficial effects of such agents for the clinical course of NAFLD. However, as these studies are usually short-term evaluations, lasting only a few years, whether or not antioxidants continue to exert favorable long-term effects, including in cases of concomitant hepatocellular carcinoma, remains unclear. Antioxidants are generally believed to be beneficial for human health and are often commercially available as health-food products. Patients with lifestyle-related diseases often use such products to try to be healthier without practicing lifestyle intervention. However, under some experimental NAFLD conditions, antioxidants have been shown to encourage the progression of hepatocellular carcinoma, as oxidative stress is toxic for cancer cells, just as for normal cells. In this review, we will highlight the paradoxical effects of antioxidants against NAFLD and related hepatocellular carcinoma.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease associated with obesity and metabolic syndrome [1,2]
We previously reported that L-carnitine controls the mitochondrial function in hepatic non-cancerous tissue from a mouse Non-alcoholic steatohepatitis (NASH) model by upregulating the Lactobacillales population related to the secondary bile acid production in the gut microbiota [76]
We examined the effect of L-carnitine administration after hepatocarcinogenesis in NASH-related cholangiocarcinoma-like tumors [88]
Summary
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease associated with obesity and metabolic syndrome [1,2]. Non-alcoholic steatohepatitis (NASH) is a severe form of NAFLD that causes cirrhosis and hepatocellular carcinoma (HCC) because of persistent inflammation associated with hepatic steatosis [4,5]. The mechanism underlying the development of NASH from simple steatosis, namely non-alcoholic fatty liver (NAFL), has been considered as either a two-hit theory or a multiple hit-process [6,7,8]. The two-hit theory comprises a first hit of hepatic steatosis and second hit of several cellular stress responses, such as oxidative stress or endoplasmic reticulum (ER). Reactive oxygen species (ROS) are generated during free fatty acid metabolism in microsomes, peroxisomes, and mitochondria, and comprise an established source of oxidative stress [9]. We reviewed the relationship between antioxidant nutrients and NASH progression including the carcinogenic risk
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