抄録
The pathogenesis of the liver damage in human erythropoietic protoporphyria is poorly understood. It has been suggested that an increased lipid peroxidation could be responsible for the hepatocellular injury in this condition. A model of mouse griseofulvin-induced protoporphyria was used for measurement of lipid peroxide formation and total iron content in the liver. Male Balb C mice had free access to standard powder diet containing 1% griseofulvin for 1 week. Excessive amounts of hepatic protoporphyria were established. The lipid peroxide level (expressed in terms of malondialdehyde) in total liver homogenate was decreased more than twice compared with that of control animals. The total content of liver iron was also significantly reduced. These results suggest that most probably lipid peroxidation does not play an essential role in the liver damage in hepatic protoporphyria.
