摘要
Oxidative stress is becoming recognized as a key factor in the progression of chronic liver disease(CLD) and hepatocarcinogenesis. The metabolically important liver is a major reservoir of mitochondria that serve as sources of reactive oxygen species, which are apparently responsible for the initiation of necroinflammation. As a result, CLD could be a major inducer of oxidative stress. Chronic hepatitis C is a powerful generator of oxidative stress, causing a high rate of hepatocarcinogenesis among patients with cirrhosis. Non-alcoholic steatohepatitis is also associated with oxidative stress although its hepatocarcinogenic potential is lower than that of chronic hepatitis C. Analyses of serum markers and histological findings have shown that hepatocellular carcinoma correlates with oxidative stress and experimental data indicate that oxidative stress increases the likelihood of developing hepatocarcinogenesis. However, the results of antioxidant therapy have not been favorable. Physiological oxidative stress is a necessary biological response, and thus adequate control of oxidative stress and a balance between oxidative and anti-oxidative responses is important. Several agents including metformin and L-carnitine can reportedly control mechanistic oxidative stress. This study reviews the importance of oxidative stress in hepatocarcinogenesis and of control strategies for the optimal survival of patients with CLD and hepatocellular carcinoma.
Oxidative stress is becoming recognized as a key factorin the progression of chronic liver disease （CLD） andhepatocarcinogenesis. The metabolically importantliver is a major reservoir of mitochondria that serve assources of reactive oxygen species, which are apparentlyresponsible for the initiation of necroinflammation. As aresult, CLD could be a major inducer of oxidative stress.Chronic hepatitis C is a powerful generator of oxidativestress, causing a high rate of hepatocarcinogenesisamong patients with cirrhosis. Non-alcoholic steatohepatitisis also associated with oxidative stress although itshepatocarcinogenic potential is lower than that of chronichepatitis C. Analyses of serum markers and histologicalfindings have shown that hepatocellular carcinomacorrelates with oxidative stress and experimental dataindicate that oxidative stress increases the likelihoodof developing hepatocarcinogenesis. However, theresults of antioxidant therapy have not been favorable.Physiological oxidative stress is a necessary biologicalresponse, and thus adequate control of oxidative stressand a balance between oxidative and anti-oxidativeresponses is important. Several agents including metforminand L-carnitine can reportedly control mechanisticoxidative stress. This study reviews the importance ofoxidative stress in hepatocarcinogenesis and of controlstrategies for the optimal survival of patients with CLDand hepatocellular carcinoma.
