<原著>ラット肝障害における内因性活性酸素消去系変動の及ぼす影響
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The relationship between the impaired endogenous defense system against active oxygen species and liver injury was examined. Diethyldithiocarbamate (DDC), an inhibitor of Cu, Zn-superoxide dismutase (Cu, Zn-SOD), was administered to rats at a dose of 1,000 mg/kg. DDC caused liver injury. Hepatic Cu, Zn-SOD activity decreased marked to about 10% of the pretreatment level 1 h after DDC administration, and its low level continued for more than 12 h. Hepatic catalase activity decreased significantly after 12 h. Hepatic lipid peroxide (LPO) and serum transaminases were increased serially. A small dose of D-galactosamine (GalN : 200mg/kg) or carbon tetrachloride (CCl_4 : 0.1 ml/kg) was administered to rats pretreated with or without DDC. GalN caused a slight increase in serum transaminases, but hepatic LPO was not increased. Hepatic SOD and catalase activity were not changed. On the other hand, marked increases in hepatic LPO and serum transaminases were produced by DDC+GalN treatment. CCl_4 caused a slight increase in serum transaminases accompanied with increased hepatic LPO and decreased activities of antioxidant enzymes. DDC+CCl_4 treatment caused significant increases of hepatic LPO and serum transaminases. However, these increases indicated additive effects of DDC and CCl_4 in contrast with the synergistic increase produced by DDC+GalN treatment. Thus DDC pretreatment caused enhancement of liver damage by GalN. These findings suggest that decrease in endogenous Cu, Zn-SOD activity is an important factor in the promotion of liver injury.
- 1992-03-25