Evaluation of oxidative stress during apoptosis and necrosis caused by D-galactosamine in rat liver |
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Authors: | Sun Fang Hamagawa Eri Tsutsui Chihiro Sakaguchi Naomi Kakuta Yuri Tokumaru Sadako Kojo Shosuke |
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Institution: | Department of Food Science and Nutrition, Nara Women's University, Nara 630-8506, Japan. |
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Abstract: | Eighteen and twenty-four hours after intraperitoneal administration of D-galactosamine (1g/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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Keywords: | Ac-DEVD-MCA acetyl-Asp-Glu-Val-Asp-α-(4-methylcoumaryl-7-amide) AMC aminomethylcoumarin GOT glutamate-oxaloacetate transaminase TBARS thiobarbituric acid-reactive substances TUNEL in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling |
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