Abstract
The chemoprotection extended by eugenol against carbon tetrachloride (CCl 4) intoxication was established by studies on drug-metabolizing phase I and phase II enzymes. An overall decrease in drug-metabolizing enzymes, namely NADPH-cytochrome c reductase, NADH-cytochrome reductase, coumarin hydroxylase, 7-ethoxy coumarin- O-deethylase, UDP-glucuronyltransferase and glutathione- S-transferase, was observed with CCl 4 intoxication, with a subsequent decrease in cytochrome P450 and cytochrome b 5 content. CCl 4 caused a significant decrease in microsomal phospholipids and the marker enzymes glucose-6-phosphatase and 5′-nucleotidase, and an increase in thiobarbituric acid reactive substances (TBARS). Simultaneous administration of eugenol with CCl 4 inhibited the accumulation of TBARS and the decrease in the microsomal phospholipids and marker enzymes. Further, the chemical onslaught imposed by CCl 4 on the drug-metabolizing system was removed successfully by eugenol. Eugenol appears to act as an in vivo antioxidant and as a better inducer of phase II enzymes than phase I enzymes. It is therefore suggested that eugenol could be an interesting basic structure for drug design.
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