The effect of citrus flavonoids on the redox state of alimentary-induced fatty liver in rats

• Published in: Natural product research Vol. 21; no. 3; pp. 274 - 281
• Main Authors: Rapavi, E., Kocsis, I., Fehér, E., Szentmihályi, K., Lugasi, A., Székely, E., Blázovics, A.
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis Group 01.03.2007
• Subjects: Alanine Transaminase - blood; Alkaline Phosphatase - metabolism; Animals; Aspartate Aminotransferases - blood; Cholesterol - metabolism; Cholesterol, HDL - metabolism; Citrus - chemistry; Diet; Dietary Fats; Diosmin; Fatty liver; Fatty Liver - chemically induced; Fatty Liver - metabolism; Fatty Liver - pathology; Flavonoids - pharmacology; Hepatocytes - pathology; Hesperidin; Homeostasis - drug effects; L-Lactate Dehydrogenase - metabolism; Liver Function Tests; Male; Oxidation-Reduction; Oxidative Stress - drug effects; Rats; Rats, Wistar; Redox homeostasis; Triglycerides - metabolism
• ISSN: 1478-6419; 1478-6427
• DOI: 10.1080/14786410500518545

Both chronic venous insufficiency (CVI) and fatty liver may develop at the same time. Hesperidin and diosmin are used for the treatment CVI. There is no information, however, on the effect of these flavonoids in the redox state of fatty liver. In this study, male Wistar albino rats were fed a lipid-rich diet with or without 450 mg diosmin-50 mg hesperidin-containing drug (60 mg kg −1 body weight/day, per os) for 9 days to determine the impact of treatment on antioxidant defence system of the fatty liver. We detected free SH-group concentration (SHC), hydrogen-donating ability (HDA), and natural scavenger capacity were decreased and hepatic malonaldehyde content and dien conjugate (DC) content in rats with fatty liver were increased compared to the control. After treatment in fatty liver, these parameters (except DC) significantly improved and approached the control value. Our results indicate that diosmin-hesperidin-containing drug may be a useful agent in improving the antioxidant defensive system in alimentary-induced fatty liver disease.