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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: Acetaminophen, Animals, Antibodies, Monoclonal, Antioxidants, Carcinoma, Hepatocellular, Caspase 3, Caspase Inhibitors, Cell Line, Tumor, Cytochromes c, Edetic Acid, Enzymes, Female, Glutathione, Humans, Liver, Liver Failure, Acute, Liver Neoplasms, Mice, Mice, Inbred BALB C, Oxidoreductases, Pyridoxal Phosphate, Reactive Oxygen Species, Superoxides, Survival Analysis, fas Receptor.
user
Does mangafodipir prevent liver injury induced by acetaminophen in the mouse? Context: Acute liver failure (ALF), characterized by massive hepatocyte necrosis, is often caused by drug poisoning, particularly with acetaminophen (APAP). Hepatocyte necrosis is consecutive to glutathione depletion by NAPQI, a metabolite of APAP, and to mitochondrial damages caused by reactive oxygen species (ROS) overproduction. Considering the structure of Mangafodipir, a contrast agent currently used in magnetic resonance imaging of the liver, we hypothesized that this molecule could exert an antioxidant activity and be possibly used as a treatment of APAP-induced ALF. Mangafodipir is endowed with superoxide dismutase, catalase, and glutathione reductase activities. It can inhibit ROS production by hepatocytes in culture, and protect those cells from oxidative stresses induced by exposure to xanthine oxidase, H(2)O(2), or UV light. Moreover, preventive or curative administration of Mangafodipir to mice with APAP-induced ALF significantly increases survival rates, and abrogates aspartate aminotransferase elevation and histological damage.
assistant
Those data point out the potential interest of Mangafodipir in the treatment of toxic ALF in humans. Final Decision: yes