期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：1994
卷号：16
期号：2
页码：111-114
DOI：10.3164/jcbn.16.111
出版社：The Society for Free Radical Research Japan
摘要：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.
