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Updated: Aug 30, 2026
Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
Published on: November 27, 2019
Mangafodipir prevents liver injury induced by acetaminophen in the mouse
Sassia Bedda1, Alexis Laurent, Filomena Conti
1Laboratoire d'Immunologie, UPRES 1833, Faculté Cochin, Pavillon Hardy, Université Paris V, AP-HP, 75679 Paris Cedex 14, France.
Background/Aims:
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.
Methods/Results:
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.
Conclusions:
Those data point out the potential interest of Mangafodipir in the treatment of toxic ALF in humans.
