INHIBITED LIPID-PEROXIDATION IN GRISEOFULVIN-INDUCED EXPERIMENTAL PROTOPORPHYRIA

The pathogenesis of the liver damage in human erythropoietic protoporp hyria is poorly understood. It has been suggested that an increased li pid 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 co ntent in the liver. Male Balb C mice had free access to standard powde r diet containing 1% griseofulvin for 1 week. Excessive amounts of hep atic protoporphyrin were established. The lipid peroxide level (expres sed in terms of malondialdehyde) in total liver homogenate was decreas ed more than twice compared with that of control animals. The total co ntent of liver iron was also significantly reduced. These results sugg est that most probably lipid peroxidation does not Flay an essential r ole in the liver damage in hepatic protoporphyria.