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Protective Effects of Ruitn and / or Hesperidin Against Doxorubicin-Induced Hepatotoxicity

1Biochemistry Department, Faculty of Science, Beni-Suef University

2Medical Physiology Department, National Research Center, Cairo, Egypt

3University of Connecticut Health Center, Farmington Avenue Farmington, Connecticut, USA

International Journal of Clinical Nutrition. 2014, Vol. 2 No. 1, 11-17
DOI: 10.12691/ijcn-2-1-2
Copyright © 2014 Science and Education Publishing

Cite this paper:
Walaa G. Hozayen, Howida S. Abou Seif, Susan Amin. Protective Effects of Ruitn and / or Hesperidin Against Doxorubicin-Induced Hepatotoxicity. International Journal of Clinical Nutrition. 2014; 2(1):11-17. doi: 10.12691/ijcn-2-1-2.

Correspondence to: Walaa  G. Hozayen, Biochemistry Department, Faculty of Science, Beni-Suef University. Email:


The present study was conducted to evaluate the protective role of rutin and hesperidin on experimental doxorubicin induced hepatotoxicity. Doxorubicin (DXR) administered rats (25 mg / kg; three times intraperitoneally / week for two weeks) were pretreated with rutin, hesperidin, or their mixture (50 mg / kg body weight) three times per week for three weeks. Results showed that DXR caused a marked rise in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT) activities alongside an increase in serum total bilirubin, α-fetoprotein (AFP) and sialic acid levels Concerning oxidative stress and antioxidant defense system, the depleted hepatic glutathione content of DXR-administered rats was increased above normal levels as a result of pretreatment with rutin, hesperidin and both rutin and hesperidin. However, while elevated lipid peroxidation was noticed in DXR treated rats, pretreatment with rutin, hesperidin or both produced a detectable decrease in the lipid peroxidation level. Taken these data together, it can be concluded that natural plant components such as Rutin and Hesperidin could protect the liver against DXR-induced liver toxicity.