Abstract
Thymoquinone (TQ), the main constituents of the volatile oil from Nigella sativa seeds is reported to protect laboratory animals against chemical carcinogenesis and toxicity through mechanisms) that is not fully understood. Among possible mechanism(s), protection could be mediated via induction of detoxifying enzymes, including quinone reductase and glutathione transferase. This study was undertaken to investigate whether oral administration of TQ increases the activities of quinone reductase and glutathione transferase in mice liver. Overdose of TQ, when administered intraperitoneally, caused a marked depletion of hepatic glutathione in both a time- and dose- dependent manner, a characteristic of a group of compounds known as Michael reaction acceptors which are known to act as inducers of enzymes that protect against chemical carcinogenesis and toxicity. TQ was given (1, 2 and 4 mg/kg/day p.o.) for five days to test the chemical inducibility of quinone reductase and glutathione transferase in mice liver. TQ administration produced significant increase in the activities of quinone reductase (147, 196 and 197% of control, respectively) and glutathione transferase (125, 152 and 154% of control, respectively). In conclusion, oral administration of TQ is effective in increasing the activities of quinone reductase and glutathione transferase and makes TQ a promising prophylactic agent against chemical carcinogenesis and toxicity. Copyright (c) 2009 John Wiley & Sons, Ltd.