• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.6
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• pp.867-873
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• 1995

This study was done ot investigate the effect of chronic alcohol feeding and acetylaminofluorene(2-AAF) treatment on hepatic mitochondrial ATPase activity andmembrane lipid composition. Male Sprague-Dawley rats, weighing 120~125g, were fed for 6 weeks on a liquid diet containing 35% of calories as ethanol. After 4 weeks of experiment diet feeding, 2-AAF(100mg/kg body weight) was injected twice a week intraperitoneally. Body weight and percent liver weight per body weight were significantly changed by ethanol feeding. Hepatic mitochondrial ATPase activity significantly decreased by ethanol feedings but not by 2-AAF treatment. In comparison to control, the ATPase activity of ethanol-AAF group decreased 29.3%. Since phospholipid(PL) content of mitochondria has an interaction effect between ethanol and 2-AAF treatment, 2-AAF treatment significantly increased phospholipid content in only ethanol fed group. Total cholesterol(C) level of mitochondria significantly increased by ethanol feeding. Consequently C/PL ratio of ethanol group was significantly higher than that of control group. The analysis of mitochondrial PL composition showed that cardiolipin(CL) significantly increased by 2-AFF treatment in control group. Phosphatidyl choline(PC) significantly increased by ethanol feeding, whereas PC significanlty decreased and phosphatidyl ethanolamine(PE) significantly increased by 2-AAF treatment. 2-AAF treatment also showed a significant increase in PE/PC ratio. Fatty acid patterns of mitochondria were also changed by either ethanol or 2-AAF although the severity of the changes was not great. These data suggest that the reduced mitochondrial ATPase activity in ethanol-AAF group may be a consequence of a changes in mitochondrial membrane lipid composition such as PE/PC ratio, C/PL ration and fatty acid patterns.

• Toxicological Research
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• v.24 no.2
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• pp.113-117
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• 2008

Chronic exposure to ethanol induces cumulative damage to the liver starting from fatty infiltration to cirrhosis depending on the dose and duration of exposure. The whole process leading to the development of alcoholic liver disease is very complex and the mechanisms involved are not fully understood. Among many experimental animal models, Lieber-DeCarli liquid diet provides moderate to severe pathophysiological outcome depending on the compositional changes. In the present study, we investigated the temporal changes in the early phase hepatic disease in rats fed with standard Lieber-DeCarli diet. Male Wistar rats were fed with Lieber-Decarli ethanol diet for 6 weeks and the liver samples were obtained after 2, 4 and 6 weeks. Mild fatty infiltration was observed in 2 weeks of feeding and it became evident in 4 and 6 week samples. The level of hepatic triglyceride showed a good agreement with the data obtained in the pathological analysis. Feeding mice with ethanol diet resulted in the maturation and translocation of SREBP-1 to nucleus in the liver. Western blot analysis of the pooled liver sample of control and ethanol fed animals showed a clear-cut time-dependent increase in the expression of nSREBP-1. These data provide important information for selecting proper time point in experimental intervention study in the field of drug development for alcoholic liver disease.

• Journal of Nutrition and Health
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• v.33 no.6
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• pp.613-618
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• 2000

This study was to investigate the effect of dietary protein and fiber on the antioxidant enzyme activities of brain in acute or chronic ethanol-treated rats. Male Sprague-Dawley rats were fed on diets containing two levels of protein(7%, 20%) with two levels of fiber (5%, 10%) Rats were administered 40%(v/v) ethanol(5g/kg body weight)orally 90min before decaptiation in acute ethanol-treated groups and 25%(v/v) ethanol(5g/kg body weight) once a day for 5 weeks in chronic ethanol treated-groups. The rats were sacrificed after 5 weeks of feeding periods. Superoxide dismutase and gluthathione S-transferase activities were lower in chronic ethanol-treated groups than acute ethanol-treated groups whereas catalase and glutathuone peroxidase activities were significantly increased by chronic ethanol treatment. Low protein supplement accelerated to change of their activities however dietary fiber levels did not affect antioxidant enzyme activities. Chronic ethanol treatment and/or low protein supplement results in increasing the brain lipid peroxide content but in lowering glutathione level. (Korean J Nutrition 33(6) ; 613~618, 2000)

• Natural Product Sciences
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• v.23 no.3
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• pp.222-226
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• 2017

Flavonoids including quercetin and rutin are a group of naturally occurring compounds widely distributed in plants, especially in buckwheat. Thus, cereal and the leaf of the plant have increasingly used as a source of nutritional and functional foods such as noodle, cake or soup in Korea, Japan and other countries. This study investigated comparative effects of dietary rutin rich in buckwheat and its aglycone, quercetin, on serum biomarkers and antioxidant parameters in rats treated with chronic ethanol. Rats were fed with the liquid diets prepared by the method of Lieber Decarli. Serum alanine transaminase (ALT) and aspartate transaminase (AST) activities increased significantly by alcohol feeding. Dietary flavonoids including rutin, quercetin and their mixtures (1/1, v/v) decreased significantly the activities of serum ALT whereas the feeding of quercetin decreased only the activity of serum AST. The concentration of serum malondialdehydes elevated by chronic alcohol feeding decreased markedly in all the experimental groups that were fed with the flavonoids; however, the combined administration of quercetin or rutin, but not that of rutin or quercetin alone decreased significantly the concentration of liver malondialdehydes to the normal range in rats fed without ethanol. Our results suggested that dietary combined mixture of rutin and quercetin might be effective in ameliorating adverse responses seen in rats exposed to ethanol chronically.

• 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.

• The Korean Journal of Food And Nutrition
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• v.12 no.1
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• pp.33-38
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• 1999

This study was conducted to investigate the synergic effect of dietary selenium and methionine levels on hepatic lipid metabolism in ethanol treated rats. Sprague-Dawley male rats were fed diets containing three levels of methionine(0,3 and 9g/kg diet) with or without selenium(0.45mg/kg diet). Ethanol was administered with 25%(v/v) ethanol orally at the same time once a day in ethanol group and isocalori sucrose was administered to the control group. The rate were sacrificed after 5 and 10 weeks of feeding period. Glutathione content was decreased by ethanol treatment and significantly increased in proportion to level of dietary methionine and was higher in selenium deficiency group than that of selenium admin-istration group. Lipid peroxide content was significantly increased in deficiency of both methionine and selenium(LMet-Se+EtOH) group. Total lipid triglyceride and cholesteol contents in liver were increas-ed and phospholipid content was decreased in ethanol treated group and ethanol treatment accelerated those increment and decrement in methionine deficiency(LMt) group and excessive methionine admin-istration(HMet)group.

• Korean Journal of Plant Resources
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• v.11 no.2
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• pp.173-178
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• 1998

The feeding effects of Herba hottuynia extracts on the lipids profiles and the content of TAB-reactive substances were evaluated in rats fed a high cholesterol diet. Hot water or ethanol extracts of the dried leave were evaporated and lyophilized . The experimental animals wer edevided to four groups and fed the following diets for 4 weeks : BAsal (cholesterol-free diet), CHOL(cholesterol-enriched diet),CW (cholesterol plus water extract) and CE(cholesterol plus ethanol extract). Dietary cholesterol increased significantly the activities of serum GOT and GPT, but the extracts feeding (0.5% of diet) did not influence the activities induced by dietary cholesterol. Although dietary cholesterol increased significantly the concentrationof serum andliver cholesterol, it tended to decrease the concentation of serum triglycerides. CHolesterol feeding had a lowering effect on the lipid peroxidation value of serum, but not inliver.Furthermore, the extracts feeding, especially water extract, decreased markedly the liver peroxidation value. The results suggest that Houttyunia cordata extracts have an in vivo antioxidant effect, judged from the TBA value in the liver rats fed a high cholesterol diet.

• Nutrition Research and Practice
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• v.2 no.4
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• pp.195-199
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• 2008

Alcoholism has been associated with folate deficiency in humans and laboratory animals. Previous study showed that ethanol feeding reduces the dehydrogenase and hydrolase activity of 10-formyltetrahydrofolate dehydrogenase (FDH) in rat liver. Hepatic ethanol metabolism generates acetaldehyde and acetate. The mechanisms by which ethanol and its metabolites produce toxicity within the liver cells are unknown. We purified FDH from rat liver and investigated the effect of ethanol, acetaldehyde and acetate on the enzyme in vitro. Hepatic FDH activity was not reduced by ethanol or acetate directly. However, acetaldehyde was observed to reduce the dehydrogenase activity of FDH in a dose- and time-dependent manner with an apparent $IC_{50}$ of 4 mM, while the hydrolase activity of FDH was not affected by acetaldehyde in vitro. These results suggest that the inhibition of hepatic FDH dehydrogenase activity induced by acetadehyde may play a role in ethanol toxicity.

• Journal of Food Hygiene and Safety
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• v.17 no.3
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• pp.124-128
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• 2002

The effect of different ethanol feeding protocols on the oxidative stress in liver and blain of rats was studied. The rats were fed 5%-ethanol solution in drinking water (5%-EtOH group) or 2.5g ethanol/kg body wt. once daily intragastrically (2.5g-EtOH group). The levels of thiobarbituric acid reactive substances (TRARS) and vitamin EI in the liver, cerebrum and cerebellum were measured. In the liver of 5%-EtOH group, the level of TBARS was not changed, whereas vitamin I was significantly increased compared to control group. In the liver of 2.5g-EtOH group, the level of TBARS was significantly increased compared to control group and the vitamin E concentration was not affected. The levels of TBARS were increased and the vitamin E concentrations were decreased significantly both in the cerebrum and cerebellum in 5%-EtOH group as well as in 2.5g-EtOH group. These results show that lipid peroxidation and vitamin E concentration in liver were varied according to the conditions of ethanol treatment, however, the vitamin E contents in cerebrum and cerebellum were affected by both ethanol intoxications used in this study.

• Journal of Ginseng Research
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• v.9 no.1
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• pp.72-85
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• 1985

Attempts were made to see if feeding of ginseng ethanol extract could affect proper- ties of rat brain lactate dehydrogenase such as specific activity, heat stability, Km for substrate, inactivation by 3-bromopyruvate and trypsin, and immune response. The following results were obtained. Specific activity of LDH was observed to reach maximum in 5 month after birth and then decrease steadily. However, that of LDH from rat fed with ginseng ethanol extract was found in rat fed with ginseng ethanol extract. 3-bromopyruvate was shown to inactivate LDH-5 from old rat fed. Inactivation of LDH-5 by trypsin was remarkable in old rat fed. Km value for pyruvate in old rat fed was remarkably decreased. Cumulative results suggest that ginseng ethanol extract could affect conformational change of LDH responsible for altered properties through unknown mechanism.