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Effects of β‐carotene on antioxidant status in rats with chronic alcohol consumption
Authors:Wan‐Teng Lin  Chi‐Chang Huang  Tien‐Jen Lin  Jiun‐Rong Chen  Ming‐Jer Shieh  Hsiang‐Chi Peng  Suh‐Ching Yang  Chih‐Yang Huang
Institution:1. Department of Hospitality Management, College of Agriculture, Tunghai University, Taichung;2. Wan‐Teng Lin and Chi‐Chang Huang contributed equally to this work.;3. Agricultural Biotechnology Research Center, Academia Sinica, Taipei;4. Division of Neurosurgery, Department of Surgery, Municipal Wan Fang Hospital;5. Graduate Institute of Injury Prevention, Taipei Medical University, Taipei;6. School of Nutrition and Health Sciences, Taipei Medical University, Taipei;7. Graduate Institute of Basic Medical Science, Graduate Institute of Chinese Medical Science;8. China Medical University, Taichung;9. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan, ROC
Abstract:This study examined the effects of β‐carotene on antioxidant status in rats with chronic alcohol consumption. At the beginning of experiment (week 0), according to both the plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, rats (n = 24) were divided into 3 groups and fed with a standard diet (group C), a diet containing ethanol (group E), or a diet containing ethanol and β‐carotene (group E+B). After 10 weeks, plasma AST and ALT, fat accumulation in the liver, antioxidant enzyme activities in erythrocytes and the liver, malondialdehyde (MDA), and α‐tocopherol and retinol in plasma and hepatic samples were analyzed. The chronic alcohol diet significantly increased AST and ALT levels in plasma, and these changes were prevented by supplementing the diet with β‐carotene. Glutathione (GSH) in erythrocytes and in the liver was significantly elevated in rats fed with a diet containing β‐carotene. The results indicate that β‐carotene supplementation can prevent ethanol‐induced liver damage and increase GSH concentrations in erythrocytes and the liver. Copyright © 2009 John Wiley & Sons, Ltd.
Keywords:alcoholic liver disease  antioxidant capacity  β  ‐carotene  lipid peroxidation  oxidative stress
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