Chitosan and blueberry treatment induces arginase activity and inhibits nitric oxide production during acetaminophen‑induced hepatotoxicity
Eda Ozcelik1★, Sema Uslu2, Dilek Burukoglu3, Ahmet Musmul4★ Corresponding author
- 1Department of Nutrition and Dietetics, Healthy Sciences, Artvin Coruh University, Artvin, Departments of, Turkey.
- 2Biochemistry, Turkey.
- 3Histology and Embryology and, Turkey.
- 4Biostatistics, Eskisehir Osmangazi University, School of Medicine, Eskisehir, Turkey.
CORRESPONDENCE
Eda Ozcelik
Department of Nutrition and Dietetics, Healthy Sciences, Artvin Coruh University, Artvin, Departments of, Turkey.
Received: 02-07-2013; Revised: 17-08-2013.
Volume 10, Issue 38s · pp. 217–224 · PUBLISHED 28 May 2014 · DOI: 10.4103/0973-1296.133234
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ABSTRACT
Background: Liver diseases have become a major problem of the worldwide. More than 50% of all cases of liver failure can be attributed to drugs. Among these, acetaminophen is the most common cause. Objective: The aim of this study was to investigate the the hepatoprotective effects of blueberry and chitosan on tissue arginase activity, ornithine and nitric oxide levels during the acetaminophen‑induced hepatotoxicity. Materials and Methods: Acetaminophen (250 mg/kg body weight per day), blueberry (60 mg/kg body weight per day) and, chitosan (200 mg/kg body weight per day) were administered to the rats by oral gavage during the experimental period. Results: Blueberry and chitosan significantly decreased liver arginase activity and ornithine levelsand and increased nitric oxide levels. Glutathione levels were remarkably increased by chitosan and blueberry treatments. Conclusion: The results of the present study indicate that blueberry and chitosan effectively protected against the acetaminophen‑induced hepatotoxicity. The hepatoprotective effect afforded by blueberry and chitosan can be attributed to its antioxidant and anti‑inflammatory activities.
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Ozcelik, E., Uslu, S., Burukoglu, D., & Musmul, A. (2014). Chitosan and blueberry treatment induces arginase activity and inhibits nitric oxide production during acetaminophen‑induced hepatotoxicity. Pharmacognosy Magazine, 10(38s), 217–224. https://doi.org/10.4103/0973-1296.133234
