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      Curcumin protects sodium nitrite-induced hepatotoxicity in Wistar rats

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          Abstract

          In this study, the protective effect of curcumin on sodium nitrite (NaNO 2) induced hepatotoxicity was assessed in male Wistar rats. Wistar rats were administered orally daily with 20 mg/kg of curcumin for 28 days and NaNO 2 was administered as a single dose of 60 mg/kg on day 28. Lipid profile, liver function biomarkers and C-reactive protein were assessed in the serum; lipid peroxidation, non-enzymatic and enzymatic antioxidants were assessed in the liver. Alanine amino transferases (94.67 U/L), aspartate amino transferases (194.33 U/L), alkaline phosphatases, C-reactive proteins (19.56 ng/L) and lipid peroxidation (8.03 × 10 −6 μmol/mg protein) were significantly elevated (P < 0.05), while a significant decrease in lipid profiles (total cholesterol, HDL,LDL, and triglycerides): (0.61,0.37, 0.4 and 0.47 mg/dl respectively), reduced glutathione level (4.16 μmol/mg protein), and decreased catalase, superoxide dismutase and glutathione peroxidase activities with severe histological alterations were observed in the livers of rats exposed to NaNO 2. Pre-treatment with curcumin significantly (P < 0.05) prevented these alterations by adjusting the lipid profile, liver function markers, and C-reactive proteins and abrogating the elevated markers of oxidative stress as supported by the liver histology. This suggests that dietary consumption of curcumin is beneficial against NaNO 2 induced oxidative stress of the liver via its antioxidant potential.

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          Selenium: biochemical role as a component of glutathione peroxidase.

          When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.
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                Author and article information

                Contributors
                Journal
                Toxicol Rep
                Toxicol Rep
                Toxicology Reports
                Elsevier
                2214-7500
                21 September 2019
                2019
                21 September 2019
                : 6
                : 1006-1011
                Affiliations
                [a ]Cancer Reasearch and Molecular Toxicology Laboratories, Department of Biochemistry, Faculty of Basic and Applied Sciences, Osun State University, Osogbo, Nigeria
                [b ]Cancer Research and Molecular Biology Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria
                [c ]Aquatic Ecology Laboratory, Department of Evolution, Ecology and Organismal Biology, The Ohio State University, Columbus, OH 43212, USA
                [d ]Department of Biology, Jackson State University, Jackson, MS 39217, USA
                Author notes
                [* ]Corresponding author. adewaleomowumi13@ 123456gmail.com
                Article
                S2214-7500(19)30198-2
                10.1016/j.toxrep.2019.09.003
                6816134
                31673502
                5fa2e249-1b7e-4ff8-8525-63016ca98994
                © 2019 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 8 April 2019
                : 3 September 2019
                : 16 September 2019
                Categories
                Article

                sodium nitrite,hepatotoxicity,curcumin,hepatoprotection,oxidative stress,wistar rats

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