Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 48, Issue 8-9, Pages 2361-2365Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2010.05.072
Keywords
Acetaminophen; Thymoquinone; Hepatotoxicity; Glutathione; Lipid peroxides; Nitric oxide
Categories
Funding
- King AbdulAziz City for Science and Technology [AT-14-067]
- College of Pharmacy Research Center and College of Graduate Studies, King Saud University
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This study was undertaken to evaluate the protective effect of thymoquinone (TO) against acetaminophen-induced hepatotoxicity. Mice were given TQ orally at three different doses (0.5, 1 and 2 mg/kg/day) for 5 days before a single hepatotoxic dose of acetaminophen (500 mg/kg i.p.). TQ supplementation dramatically reduced acetaminophen-induced hepatotoxicity, in a dose-dependent manner, as evidenced by decreased serum alanine aminotransferase (ALT) activities. Acetaminophen (500 mg/kg i.p.) resulted in a significant increase in serum ALT and total nitrate/nitrite, hepatic lipid peroxides and a significant decrease in hepatic reduced glutathione (GSH) and ATP in a time-dependent manner. Interestingly, supplementation of TQ (2 mg/kg/day) for 5 days before acetaminophen administration resulted in reversal of acetaminophen-induced increase in ALT, total nitrate/nitrite, lipid peroxide and a decrease in GSH and ATP. Moreover, TQ did not affect acetaminophen-induced early decrease in hepatic GSH indicating lack of the effect on the metabolic activation of acetaminophen. In conclusion, TQ is effective in protecting mice against acetaminophen-induced hepatotoxicity possibly via increased resistance to oxidative and nitrosative stress as well as its ability to improve the mitochondrial energy production. (C) 2010 Elsevier Ltd. All rights reserved.
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