Thymoquinone supplementation reverses acetaminophen-induced oxidative stress,nitric oxide production and energy decline in mice liver |
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| Authors: | Mahmoud N Nagi Hussain A Almakki Mohamed M Sayed-Ahmed Abdullah M Al-Bekairi |
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| Institution: | 1. Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran;2. Department of Physiology and Pharmacology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran;3. Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran;4. Student Research Committee, Esfarayen Faculty of Medical Sciences, Esfarayen, Iran;5. Zahedan University of Medical Sciences, Zahedan, Iran;6. Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran;7. Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran;1. Department of Pharmacology, Faculty of Medicine, Assiut University, Assiut, Egypt;2. Department of Anesthesia, South Egypt Cancer Institute, Assiut University, Assiut, Egypt;3. Department of Forensic Medicine and Toxicology, Faculty of Medicine, Assiut University, Assiut, Egypt;1. V.V. Voevodsky Institute of Chemical Kinetics and Combustion, 3 Institutskaya str., 630090 Novosibirsk, Russian Federation;2. Novosibirsk State University, 2 Pirogova St., 630090 Novosibirsk, Russian Federation;3. Department of Environmental Science, Hubei Biomass-Resource Chemistry and Environmental Biotechnology Key Laboratory, Wuhan University, Wuhan 430079, PR China;4. International Tomography Center, 3a Institutskaya str., 630090 Novosibirsk, Russian Federation;1. Dept. of Chemistry, University of Torino, Via P. Giuria 7, 10125 Turin, Italy;2. Dept. of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093-0358, United States;3. Dept. of Drug Science and Technology, University of Torino, Via P. Giuria 9, 10125 Turin, Italy;4. INSTM and NIS Centre, University of Torino, Via Quarello 15A, 10135 Turin, Italy |
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| Abstract: | This study was undertaken to evaluate the protective effect of thymoquinone (TQ) 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. |
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