Evaluation of oxidative stress during apoptosis and necrosis caused by d-galactosamine in rat liver

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Eighteen and twenty-four hours after intraperitoneal administration of d-galactosamine (1 g/kg body weight) to rats, the activity of caspase-3-like protease in the liver increased significantly compared with that in the control group given saline. Histological examinations including the in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method found apoptotic hepatocytes 18 hr after the administration of d-galactosamine. Caspase-3 activity was barely detectable in the plasma of control rats, but increased significantly 24 hr after drug administration along with a dramatic increase in glutamate-oxaloacetate transaminase (GOT). These results indicated that d-galactosamine causes apoptosis in the liver by activating caspase-3, which is released to the plasma by secondary necrosis. The concentration of lipid hydroperoxides in the liver increased significantly 24 hr after d-galactosamine administration. In contrast, the concentration of vitamin C in the liver decreased significantly 18 and 24 hr after d-galactosamine administration. These results suggest that d-galactosamine induces severe oxidative stress in the liver, leading to extensive necrosis.

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