The inflammatory liver diseases with a metabolic origin, such as alcoholic
liver disease (ALD) and nowadays, non-alcoholic fatty liver disease (NAFLD)
associated to the growing epidemic of metabolic syndrome, are two important health
care problems and common causes of cirrhosis and its complications in developed
countries and worldwide. The physiopathology of these conditions, importantly
involves oxidative stress. In ALD, alcohol metabolism comes from oxidative and nonoxidative
pathways. The oxidative pathway involves two major enzymes, alcohol
dehydrogenase (ADH), which oxidizes alcohol to acetaldehyde, and acetaldehyde
dehydrogenase (ALDH) that transforms acetaldehyde to acetate. Acetaldehyde is a
cardinal toxin involved in alcohol-related liver injury. Reduced nicotinamide
dinucleotide (NADH) generated by these enzymatic reactions also contributes to harm.
The oxidation of alcohol also occurs via cytochrome P450 to cause liver damage by
producing reactive oxygen species (ROS) that are guilty of activating redox-sensitive
transcription factors, such as nuclear factor-kappaB (NF-kB), triggering and
perpetuating a pro-inflammatory status. Similarly, oxidative stress, in addition to insulin
resistance, is considered as a main factor contributing to liver injury in patients with non
alcoholic steatohepatitis (NASH). Recently, oxidative stress constitutes a novel and
attractive target for therapy, in ALD, NAFLD and NASH.
Keywords: Alcoholic liver disease, antioxidants, inflammation, liver injury, non
alcoholic fatty liver disease, non alcoholic steatohepatitis, oxidative stress,
therapy.
