Increased Nitroxidative Stress Promotes Mitochondrial Dysfunction in Alcoholic and Nonalcoholic Fatty Liver Disease

Figure 1

Synergistic interaction between gene and environment. Many toxic agents alone or in combination with other comorbidity factors including genetic elements synergistically interact and produce ROS/RNS, which decrease the levels of antioxidants and inhibit protective defensive enzymes, resulting in increased nitroxidative stress. Consequently, mitochondrial DNA, lipids, and proteins are oxidized and/or nitrated, leading to mitochondrial dysfunction, accompanied with fat accumulation, inflammation, ATP depletion, necrosis/apoptosis, and DNA damage. All these changes likely contribute to tissue injury, as observed in many disease states.