• The Journal of Korean Medicine
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• v.26 no.1 s.61
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• pp.76-84
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• 2005

Objective: The purpose of this study was to examine the protective efficacy of GHT on alcoholic liver injury. Methods: We measured the rate of alcohol oxidation, serum level of liver enzyme, lipid peroxidation level in liver tissue, and inflammatory related cytokine expressions in the liver. Results : GHT showed liver protective effects, lowered the levels of AST and LDH in serum and inhibited lipid peroxidation in liver tissue, and enhanced alcohol oxidation. GHT treatment up-regulated IL-10 in the liver, whereas it down­regulated $TNF-\alpha,\;TGF-\beta$, and Fas ligand. Conclusion : From these results, GHT is presumed to work in the liver in protective roles not through the pathway of alcohol metabolism but mainly by anti-inflammation activity in our model.

• Journal of Nutrition and Health
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• v.36 no.3
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• pp.255-261
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• 2003

Food irradiation has been steadily increasing in many countries in line with increasing international trade and concerns about naturally occurring harmful contaminants in food. Although irradiation provides an excellent safeguard for the consumer by destroying almost 100% of harmful bacteria, it is necessary to ensure the safety of irradiated foods. This study was performed to investigate the effect of an irradiated diet on lipid peroxidation in the plasma, liver, small intestinal mucosa, and lymphocyte DNA damage in mice. Eight-week old ICR mice were assigned to two groups to receive either non-irradiated or irradiated (10 kGy) diets containing 20.38% fish powder and 6.06% sesame seeds for 4 weeks. The resulting changes in the degrees of lipid peroxidation were evaluated based on the level of plasma and liver thiobarbituric acid reactive substance (TBARS), transmission electron micrograph of jejunal mucosa, and free radical-induced oxidative DNA damage in lymphocytes, as measured by alkaline comet assay (single cell gel electrophoresis). The peroxide values of the gamma irradiated diet were measured every week, and the sample for comet assay was taken at the end of the four week experimental period. There was no significant difference in food efficiency ratio between the two groups. The peroxide values of the diet were immediately increased to 35.5% after gamma irradiation and kept on increasing during storage. After 4 weeks, no differences in tissue or plasma TBARS value were observed between the two groups, but epithelial cells of jejumum showed osmiophillic laminated membranous structures, considered as myelin figures,. The oxidative DNA damage expressed as tail moment (TM) increased 30% in the blood lymphocytes of the mice fed the irradiated diet. In conclusion, the comet assay sensitively detected differences in lymphocyte DNA damage after feeding with the irradiated diet for 4 weeks. However, in order to ensure the safety of irradiated foods, it would be more useful to conduct a long-term feeding regimen using an irradiated diet and examine the level of lipid peroxidation and the state of oxidative stress in a greater range of organs.

• Journal of Nutrition and Health
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• v.24 no.1
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• pp.12-19
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• 1991

The chronic effects of long-term ozone exposure and dietary factors on the lipid peroxidation were investigated in mouse lung and liver tissues. Eighteen groups of mice were exposed to ozone(0.25 or 0.50 ppm) or ambient air over an 18-month period. Within each esposure regimen. animals were fed diets containing different levels of antioxidants and unsaturated fat. Ozone exposure did not have an effect on the production of thiobarbituric acid-reactive substances in lung and liver or free malondialdehyde in the liver at all levels of dietary vitamin E. An inverse relationship between the level of vitamin I supplementation and the concentration of lipid peroxidation products was observed. Results indicate the possible adaptation of animals to long-term continuous ozone exposure by unknown mechanism and the effectiveness of dietary vitamin I at sufficient level(30ppm) to protect against tissue lipid peroxidation regardless of the degree of unsaturation of the dietary fat.

• Journal of Nutrition and Health
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• v.34 no.3
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• pp.253-264
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• 2001

This study was carried out to examine a part of the mechanism for the etiology of diabetic complications. Thirty normal and forty streptozotocin(STZ)-induced diabetic rats were used as the animal models. The animals were sacrificed at the time points of 3 days, 1,2,4 and 6 weeks after STZ-injection and a time course changes in the concentrations of thiobarbituric acid-reactive substances(TBARS) in blood, urine, and tissues, along with the levels of conjugated dienes in tissues were measured as indices of in vivo lipid peroxidation. The activities of antioxidant enzymes, catalase, superoxide dismutase, glutathione peroxidase and the levels of blood retinol and alpha-tocopherol were also measured. The diabetic rats maintained a slightly higher plasma TBARS level throughout the experiment. The urinary TBARS level was significantly higher in diabetic group and gradually increased with time. Concentrations of TBARS in liver, heart, and kidney tissues from diabetic animals were higher than those from the normal group. An increase of conjugated dienes was also observed in the all tissues examined. The kidney tissue of diabetic animals revealed more significant lipid peroxidation state than any other organ tissues. The activities of hepatic antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase were higher in diabetic animals compared to the control ones and increased with the duration of diabetes mellitus. The plasma levels of vitamin A and E were loser in diabetic animals than in normal controls throughout the experimental period. The level of vitamin E in diabetic animals was significantly decreased with the duration of the disease. The results of this study suggest that an effective regimen to suppress the adverse changes in lipid peroxidation and antioxidant defense system is required from the early stage of the disease to prevent the development of diabetic complications. (Korean J Nutrition 34(3) : 253∼264, 2001)

• Korean Journal of Veterinary Research
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• v.39 no.4
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• pp.679-688
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• 1999

The combined effects of iron and selenium status on glutathione peroxidase (GSHPx) activity, cytochrome P-450 activity, and lipid peroxidation in the liver and intestinal mucosa of rats were investigated. In experiment one, four experimental groups (+Se+Fe, -Se+Fe, +Se++Fe, -Se++Fe) were manipulated for 3 weeks with intramuscular administration of irondextran (++Fe) and/or normal diet (+Fe) and deionized water (-Se) and/or selenium-supplemented deionized water (+Se). In experiment two, 2% dietary carbonyl iron (instead of the parenteral administration) was fed for 3 weeks to rats. Body weight of rats was significantly decreased in both parenterally and orally iron-overloaded groups (p<0.01), regardless of Se supplement. Serum iron was significantly increased in parenterally iron-overloaded groups but it was marginally increased in orally iron-overloaded groups. There was no significant difference in hemoglobin content among experimental groups in either experiment one or two. Total iron in the small intestine, intestinal mucosa, and livers was significantly high in both parenterally and orally iron-overloaded rats, regardless of selenium status. In the liver and intestine, GSHPx activity was significantly higher in all selenium-supplemented groups, compared to Se-deficient groups (p<0.01) and lipid peroxidation was significantly enhanced in both parenterally and orally iron-overloaded groups, compared to iron-adequate groups. There was no significant difference in cytochrome P-450 activity in the livers between groups in both experiment one and two. These results indicated that GSHPx activity in liver and intestinal mucosa was depended on selenium status, regardless of iron status, and iron-overload enhances lipid peroxidation in liver and intestinal mucosa by increasing the tissue iron content.

• The Korea Journal of Herbology
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• v.22 no.2
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• pp.169-174
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• 2007

Objectives : This study was designed to investigate protective effects of Sayeoksanhap-Pyeongweisan-Gamiban(SPG) on hematological changes in rats damaged by CCl4 Methods : We investigated the effects of SPG on hematological changes in terms of AST/ALT levels, Total cholesterol, HDL-cholesterol and triglyceride in serum and lipid peroxidation in rat liver. Results : Administration of SPG decreased AST level in serum effectively. In addition, lipid peroxidation in liver tissue, which was elevated by injection of CCl4, was decreased by administration of SPG. In contrast, ALT level, Total cholesterol, HDL-cholesterol and triglyceride in serum were not affected by administration of SPG. Conclusion : These results suggest that oral administration of SPG was useful to protect liver against CCl4 by its antioxidant action in liver tissues.

• Journal of Nutrition and Health
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• v.30 no.6
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• pp.639-647
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• 1997

The effect of excess L-ascorbic acid(AsA) in blood, liver lipid levels and peroxidation status were investigate . Ten Sprague-Dawley male rats weighing 150-200g were fed 300mg AsA/100g body weight/day, mixed into ground chow diet, for 4 weeks. And another set of then rats were fed only chow diet as the control. Average body weight gain was slightly lowered by AsA feeding without food intake change. The AsA group showed higher AsA levels in plasma and liver than the control group. In addition, the AsA group showed a higher plasma TBARS value. Liver TBARS seemed to be elevated in the AsA, but not significantly. The hemolysis of red cells tended to increase with excess AsA, accompanied by a raised GSH-Px activity and lowered total GSH levels. Plasma HDL-Chol level was increased while the levels of total Chol, LDL-plus VLDL-Chol , and triglyceride were unchanged . Atherogenic index decreased. Hepatic TG levels were also decreased, but the total amount of Chol increased slightly . Platelet TXA$_2$ production was inhibited by excess AsA feeding. Above results indicafe that oral feeding of excess AsA may be beneficial in reducing the risk of atherosclerosis ; however such practice may be detrimental for tissue lipid peroxidation and weight gain.

• YAKHAK HOEJI
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• v.37 no.3
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• pp.270-277
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• 1993

It is well known that lipidperoxide, formed in vivo, induced the denaturation of enzyme and destruction of cell membrane to acute injury of tissue. Aralia elata have physiological activates, the improvement of lipid metabolism, antidiabetic activity etc., which was thought to have the relationship to lipid peroxidation. The anti-lipidperoxidative effect of Aralia elata have not yet established. In this study, we examined the anti-lipidperoxidative effects of Aralia elata (Butanol fraction) on CCI$_{4}$ induced lipidperoxidation in rats, and elucidated the anti-lipidperoxidative mechanism. In rat liver homogenate intoxicated with CCI$_{4}$ (0.5 ml/100g), BuOH fraction of Aralia elata (80 mg/Kg/day) exhibited 85.41% anti-lipidperoxidative effect but in serum 69.63% inhibitory effects, respectively. In mitochondrial and microsomal fraction showed inhibition of 55.85% and 69.30%, respectively. In order to elucidate the mechanism of anti-lipidperoxidation effects of Aralia elata, enzymatic (NADPH dependent) and non-enzymatic (Ascorbic acid catalyzed) reaction, in vitro, were performed. In enzymatic reation, Aralia elata exhibited 59.43% anti-lipidperoxidation effects, but in non-enzymatic reaction exhibited 43.27% inhibition. Therefore, it is noteworthy that antioxidative power of them may mainly results from the inhibition by enzymatic reaction.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.4
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• pp.537-541
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• 1995

This study was designed to investigate the effects of methionine(Met) on the activities of heart lipid peroxidation related enzymes in ethanol administrated rats. Male Sprague-Dawley rats were fed on diets containing one of the three levels of Met(0%, 0.3%, 0.9% of kg diet) and ethanol(2.5g/kg of body weight) was administrated as 25v/v% ethanol to ethanol treated groups orally. The rats were sacrificed after 5 and 10 weeks of feeding. Xanthine oxidase(XO) and catalase activities increased with ethanol administration and those activities were higher n Met excessive and deficiency group than those of Met normal group at 5 and 10 weeks dieting. Superoxide dismutase(SOD) activity in heart decreased significantly in Met deficiency and Met excessive group as compared to that of control. Glutathione peroxidase(GSH-Px) activity in heart significantly decreased in Met deficiency group as compared to that of Met excessive and normal group. Glutathione S-transferase(GST) activity of heart tissue significantly increased by ethanol administration. Glutathione(GSH) content in heart decreased with ethanol administration and shwoed no significant differences with Met levels. Ethanol administration increased the content of lipid peroxide(LPO).

• Journal of Nutrition and Health
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• v.29 no.7
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• pp.721-728
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• 1996

The level of oxidative tissue damage caused by free radicals generated from ethanol oxidation was determined in the myocardium of chronic ethanol fed-rats and the protective action of various radical scavenging enzymes was monitored, also. Adult male Sprague-Dawley rats were given ethanol in an amount of 36% of total calories via Lieber-DeCarli liquid diet for 6 weeks. Control group was pair-fed with the diet containing isocaloric amount of dextrin-maltose instead of ethanol. Chronic ethanol administration resulted in the increased amount of myocardial thiobarbituric acid reactive substance(TBARS), th parameter of lipid peroxidation, under our experimental condition. Chronic ethanol ingestion did not cause any change in activities of either glutathione peroxidase or glutathione reductase and glucose-6-phosphate dehydrogenase were decreased after ethanol treatment. Therefore, chronic ethanol administration seemed to cause considerble changes in cellular defense function against oxidative tissue damage in rat myocardium through glutathione utilizing system and radical generation system. However the ultimate net result of chronic ethanol inestion on the myocardium of rat was the oxidative tissue damage revealed by increased TBARS content.