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Fatty liver disease: spent antioxidant and liver cell death An imbalance between ROS and antioxidant molecules, induced by a high-fat diet, is a major contributor to non-alcoholic fatty liver disease in a mouse model. Dr. Zhenyuan Song from the University of Illinois at Chicago, USA, and colleagues showed that a 12-week high-fat diet consumption led to increased expression of the pro-inflammatory signaling molecule TNFα in the liver. It also resulted in conversion of the antioxidant molecule glutathione (GSH) into a “spent” form called glutathione disulfide (GSSG), a sign that the liver has dealt with a lot of cellular stress. Experiments in human liver cells showed that intracellualr GSSG accumulation sensitizes hepatocytes to cell death via a molecular cascade triggered by TNFα activity. These findings point to GSSG as a potential drug target for treating non-alcoholic fatty liver disease.