Alleviation of doxorubicin-induced nephrotoxicity and hepatotoxicity by chrysin in Wistar rats. (June 2013)

• Record Type: Journal Article
• Authors: Rashid, Summya; Ali, Nemat; Nafees, Sana; Ahmad, Shiekh Tanveer; Arjumand, Wani; Hasan, Syed Kazim; Sultana, Sarwat
• Is Part Of: Toxicology mechanisms and methods. Volume 23:Number 5(2013)
• Page Start: 337
• Page End: 345
• Publication Date: 2013-06
• Subjects: Analytical toxicology -- Periodicals; Toxicology -- Periodicals; Toxicology -- Methodology -- Periodicals; 615.907
• DOI: 10.3109/15376516.2012.759306
• Languages: English
• ISSNs: 1537-6516

Abstract

<abstract> <title>Abstract</title> <p> <italic>Objective</italic>: Doxorubicin (DXR) is an anticancer drug used in the treatment of many human malignancies. However, its clinical use is limited because of several side effects like cardiotoxicity, nephrotoxicity and hepatotoxicity. In the present study, we investigated the protective efficacy of chrysin against DXR-induced oxidative stress, nephro- and hepatotoxicity in male Wistar rats using biochemical and histopathological approaches.</p> <p> <italic>Methodology</italic>: Wistar rats were subjected to concomitant pre- and post-phylactic oral treatment of chrysin (40 and 80 mg/kg b.wt.) against nephro- and hepatotoxicity induced by single i.p. injection of DXR (40 mg/kg b.wt). Nephrotoxicity and hepatotoxicity were assessed by measuring the level of serum creatinine, BUN, AST, ALT and LDH. The level of antioxidant armory of kidney and liver tissue was also measured.</p> <p> <italic>Key findings</italic>: Treatment with chrysin significantly decreased the levels of serum toxicity markers and additionally elevated antioxidant defense enzyme levels. Histopathological changes further confirmed the biochemical results showing that DXR caused significant structural damage to kidney and liver tissue architecture which were reversed with chrysin.</p> <p> <italic>Conclusion</italic>: The results suggest that chrysin attenuated nephro and hepatic damage induced by DXR.</p> </abstract>