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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 424692, 19 pages
Research Article

Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

1Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico (UNAM), University City, 04510 Mexico City, DF, Mexico
2Renal Pathophysiology Laboratory, Department of Nephrology, National Institute of Cardiology “Ignacio Chávez”, 14080 Mexico City, DF, Mexico
3Department of Cardiovascular Biomedicine, National Institute of Cardiology “Ignacio Chávez”, 14080 Mexico City, DF, Mexico
4Experimental Pathology Section, National Institute of Medical Sciences and Nutrition “Salvador Zubirán”, 14000 Mexico City, DF, Mexico
5Department of Preclinical Toxicology, National Polytechnic Institute, 14740 Mexico City, DF, Mexico

Received 18 March 2013; Revised 7 June 2013; Accepted 16 June 2013

Academic Editor: Shrikant Anant

Copyright © 2013 Wylly Ramsés García-Niño et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Curcumin is a polyphenol derived from turmeric with recognized antioxidant properties. Hexavalent chromium is an environmental toxic and carcinogen compound that induces oxidative stress. The objective of this study was to evaluate the potential protective effect of curcumin on the hepatic damage generated by potassium dichromate (K2Cr2O7) in rats. Animals were pretreated daily by 9-10 days with curcumin (400 mg/kg b.w.) before the injection of a single intraperitoneal of K2Cr2O7 (15 mg/kg b.w.). Groups of animals were sacrificed 24 and 48 h later. K2Cr2O7-induced damage to the liver was evident by histological alterations and increase in the liver weight and in the activity of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase in plasma. In addition, K2Cr2O7 induced oxidative damage in liver and isolated mitochondria, which was evident by the increase in the content of malondialdehyde and protein carbonyl and decrease in the glutathione content and in the activity of several antioxidant enzymes. Moreover, K2Cr2O7 induced decrease in mitochondrial oxygen consumption, in the activity of respiratory complex I, and permeability transition pore opening. All the above-mentioned alterations were prevented by curcumin pretreatment. The beneficial effects of curcumin against K2Cr2O7-induced liver oxidative damage were associated with prevention of mitochondrial dysfunction.