Evaluation of oxidative stress during apoptosis and necrosis caused by carbon tetrachloride in rat liver

After 12, 18, and 24 h of oral administration of carbon tetrachloride (as a 1:1 mixture with mineral oil: 4 ml/kg body weight) to rats, the activity o f caspase-3-like protease in the liver increased significantly compared to that in the control group that was given mineral oil (4 ml/kg). In plasma, the activity of caspase-3 was barely detectable in the control rat, but inc reased significantly 24 h after drug administration along with a dramatic i ncrease in glutamate oxaloacetate transaminase. These results indicate that carbon tetrachloride causes apoptosis in the liver by activating caspase-3 , which is released to plasma by secondary necrosis. After 18 and 24 h of c arbon tetrachloride administration, the liver concentration of hydrophilic vitamin C was decreased significantly, while that of hydrophobic vitamin E was not affected. The plasma concentration of vitamins C and E was not infl uenced significantly. These results suggest that carbon tetrachloride induc es oxidative stress mainly in the aqueous phase of the liver cell. (C) 2001 Elsevier Science B.V. All rights reserved.