• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.2
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• pp.278-286
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• 2003

Alcohol is well known agent which can damage the human tissues such as liver via stimulating lipid peroxidation. On the other hand, carotenoids in addition to vitamins A, C and I play important roles in protecting these oxidative damages as well as preventing the production of free radicals. This study was carried out to investigate the effect of dietary vitamin A on lipid peroxidation and antioxidants status in ethanol-treated rats. In the experiment, male Sprague-Dawley rats weighing 160~180 g were given a liquid diet containing 36% of total calories as ethanol for 7 weeks. The pair-fed control rats received an isocaloric amount of diet containing sucrose instead of ethanol on the following day Additionally, the liquid diet contained adequate amount of $\beta$-carotene, retinyl acetate or 13-sis-reinoic acid except vitamin A-deficient diet. The results obtained are as follows. The levels of plasma and hepatic lipid peroxide were increased after chronic ethanol feeding in rats. Retinyl acetate supplementation significantly reduced lipid peroxidation induced by ethanol feeding Glucose 6-phosphatase activity was significantly reduced in rats fed vitamin A-deficient diet with ethanol and alkaline phosphatase activity was significantly induced in rats fed 13-cis-reinoic acid diet with ethanol. Catalase and alcohol dehydrogenase activities did not show a consistent tendency in experiment groups. The hepatic antioxidant enzyme activities did not significantly changed by chronic ethanol feeding groups. The striking decrease in conversion of $\beta$-carotene to retinol was observed in rats fed a $\beta$-carotene diet with ethanol feeding The level of retinol and retinoic acid in plasma and liver was decreased after chronic ethanol administration Based on this result, these data suggest that ethanol feeding enhances oxidative stress especially in those fed a vitamin A-deficient diet, and vitamin A supplementation, especially, retinyl acetate intake can prevent enhanced lipid peroxidation and related damage to some extent.

• Journal of Nutrition and Health
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• v.39 no.6
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• pp.513-519
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• 2006

The effects of fractions of ethanol extract of Benincasa hispida (wax gourd) on lipid levels and lipid peroxidation in streptozotocin (STZ) induced diabetic rats were examined. Sprague-Dawley rats were induced diabetes mellitus by STZ injection (45 mg/kg) into the tail vein and were divided into 5 groups: normal, STZ-control, three experimental diabetic groups [chloroform $(CHCl_3)$ fraction group, butanol (BuOH) fraction group, and water fraction group]. Fractions of ethanol extract of Benincasa hispida were administered orally into the diabetic rats for 14 days. The liver glycogen levels of $CHCl_3$ fraction group and the muscle glycogen levels of BuOH and water fraction groups were significantly higher than that of STZ-control group. Pancreas protein levels of BuOH and water fraction groups were significantly higher than that of STZ-control group. The liver cholesterol level of BuOH and water fraction groups were significantly lower when compared with the STZ-control group. The level of liver triglyceride in BuOH and water fraction groups were significantly higher than that of STZ-control group. Malondialdehyde (MDA) levels in liver of normal and diabetic groups were not significantly different. In the pancreas, the MDA levels of BuOH and water fraction group were significantly lower than that of STZ-control group. The results suggested that the supplementation of the BuOH and water fractions of Benincasa hispida extract could be beneficial for the diabetic complications and damages from the lipid peroxidation.