Abstract

Non-alcoholic fatty liver disease (NAFLD) is the first cause of liver disease worldwide, leading to non-alcoholic steatohepatitis (NASH), cirrhosis and finally death. The available evidence suggests that oxidative stress plays a key role in the pathophysiology of NAFLD, participating in mitochondrial increased lipid peroxidation involved in mitochondrial dysfunction. Polyunsaturated fatty acids (PUFAs) are present in the cell and mitochondrial membrane, and can act through several molecular pathways such as the peroxisome proliferator-activated receptor-α (PPAR-α) activation and sterol regulatory element-binding protein 1c (SREBP-1c) regulation to finally promote an antioxidant status within cell physiology. Vitamin E has antioxidant and anti-inflammatory properties that have been proved to reduce liver steatosis and inflammation, acting through free radical trapping and preventing docosahexaenoic acid (DHA) molecules damage through a membrane stabilization action. These two molecules could thereby be a potential target for promising therapies within the multiple pathways of this disease.