• Title/Summary/Keyword: experimental hepatocarcinogenesis

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Anti-carcinogenic Effects of Korean Mistletoe Extract and Lectin in Experimental Hepatocarcinogenesis (실험적 간암모델에서 한국산 겨우살이(Mistletoe)추출물 및 렉틴의 발암 억제효과 탐색)

  • 김미정;김정희
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.30 no.4
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    • pp.697-702
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    • 2001
  • This study was done to investigate effects of Korean mistletoe extract and lectin on serum GOT, GPT and $\alpha$-L-fucosidase activities and the preneoplastic lesion in chemically induced rat hepatocarcinogenesis. To attain the above objectives weanling Sprangue-Dawley male rats were fed modified AIN-76 diets containing 10% corn oil for 9 weeks. One week after feeding rats were intraperitonealy injected twice with a dose of diethylnitrosamine (DEN, 50 mg/kg body weight(BW)) and were provided 0.05% phenobarbita (PB) with drinking water from one week after DEN treatment until the end of experiment. For the same period as PB treatment, rats were injected mistletoe extract (10 $\mu\textrm{g}$/kg BW European mistletoe, 10 $\mu\textrm{g}$/kg BW and 100 $\mu\textrm{g}$/kg BW Korean mistletoe) and lectin(1 ng/kg BW, 10 ng/kg BW) twice a week. At the end of 9th week rats were sacrificed and the formation of hepatic glutthione S-transferase placental form positive (GST-P+) foci serum GOT, GPT and $\alpha$-L-fucosidase activities were determined. By treatment of mistletoe extract or lectin there were no significant effects on serum GOP, GPT and $\alpha$-L-fucosidase activities whereas those activities showed a tendency to increase by DEN treatment. The formation of GST-P+ foci was significantly decreased by mistletoe extract or lectin treatment especially in group of 100$\mu\textrm{g}$/kg BW Korean mistletoe. These results suggest that Korean mistletoe extract and lectin have a possibility to inhibit hepatocarcinogenesis of animals.

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High Vitamin E Supplement is Needed to Have an Anticarcinogenic Effect of Fish Oil (어유와 비타민 E 보강 수준이 쥐간의 전암성 병변에 미치는 영향)

  • 김숙희;강상경;김유미;최혜미
    • Journal of Nutrition and Health
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    • v.31 no.6
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    • pp.1014-1023
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    • 1998
  • The influences of fish oil and different levels of vitamin I supplement on hepatocellular chemical carcinogenesis have been studied. Male Sprague-Dawley rats received diethylnitrosamine (DEN)(200mg/kg body weight) and were subjected to two-thirds partial hepatectomy to induce murine chemical hepatocarcinogenic procedure. Placental glutathione S-transferase(GST-P) positive foci area, antioxidant enzymes(Cu/Zn-superoxide dismutase(SOD), catalase, glutathione reductase (GR), total- glutathione peroxidase (TGPx), glutathione S -transferase (GST)), glucose 6-phosphatase (G6Pase) activities, and lipid peroxidation of microsomes(thiobarbituric acid reactive substances (TBARS)) were measured. Experimental animals were fed 15% corn or fish oil with 0, 40, 1,000, 10,000IU vitamin E /kg diet for 8 weeks. Vitamin E supplements decreased the area of GST-P positive foci in both groups. The higher the vitamin E levels, the smaller the area of GST-P positive foci were noticed. Compared to 0 IU vitamin E, 40 IU in corn oil and 1,000 IU in fish oil groups were effective in decreasing G57-P positive foci area. Fish oil groups tended to have smaller area of GST-P positive foci. fish oil groups showed lower body weight, lower activities of Cu/Zn-SOD and TGPx, higher TBARS contents, higher activities of GST, catalase, G6Pase, GR and higher liver/body ratio than corn oil groups. As the level of vitamin I increased, GST-P positive foci count, catalase activities, and TBARS tended to decrease. G6Pase activities tended to increase in both groups. At higher vitamin E levels, GST activities tended to decrease in fish oil groups. These results suggest that vitamin I has suppressive offects on hepatocellular chemical carcinogenesis probably through antioxidant eH:cts decreasing TBARS contents, $H_2O$$_2$, and organic peroxides. fish oil tended to have greated suppressive offects than corn oil on hepatocellular carcinogenesis. (Korean J Nutrition 31(6) : 1014-1023, 1998)

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Suppression of Experimental Liver Tumors by Estradiol-3-Benzoate Treatment or Castration in Male Rats

  • Byeongwoo Ahn;Jin Seok Kang;Jeong-Hwan Che;Kookkyung Lee;Ki Taek Nam;Mina Choi;Seyl Kim;Na Jin Jung;Beom Seok Han
    • Proceedings of the Korean Society of Veterinary Pathology Conference
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    • 2002.11a
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    • pp.149-149
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    • 2002
  • Epidemiologically the incidence of liver cancer is markedly sex-differentiated, with a much higher frequency in men than in women. In experimental animals, it is also higher in male than in female irrespective of carcinogen-induced or spontaneous tumors. Therefore, we tried to investigate the modulating effects of sex hormones in experimental hepatocarcinogenesis. For induction of liver tumors, mini-osmotic pump containing diethylnitrosamine at a dose level of 47.5mg was implanted into the peritoneal cavity of the rat at 6 weeks old. To remove the effects of male sex hormones, the animals of group 2 were castrated one week prior to DEN treatment. To see the effects of estrogen, pellet containing 1g or 10g of estradiol-3-benzoate was infused subcutaneously to the animals of group 3 and 4 one week prior to DEN treatment. The pellets were exchanged every 4 weeks until sacrifice. All animals were sacrificed at 26 weeks after DEN treatment. The tumor incidences in group 1 (DEN alone), group 2 (DEN +castration), group 3(DEN +EB 1g) and group 4 (DEN +EB 10g) were 100% (15/15), 93.3% (14/15), 85.7% (12/14) and 66.7% (10/15), respectively, showing that the value of group 4 is significantly different from that of group 1. Tumor multiplicity data of group 1, 2, 3 and 4 were 5.470.73, 2.800.51, 2.070.41 and 1.670.46, respectively, showing castration or EB treatment reduced number of liver tumors significantly (P<0.001). With immunohistochemistry and Western blotting of ER the expressions were detected in normal adjacent liver cells but decreased or lost in tumor cells. From these results we conclude that female sex hormone, especially estrogen, may act as a liver tumor suppressor, and it seemed that the down regulation of ER may be associated with liver tumor development.

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Effects of Green Tea Infusion on the Preneoplastic Lesions and Peroxidation in Rat Hepatocarcinogenesis

  • Kim, Hee-Seon;Kim, Hyung-Sook;Park, Haymie
    • Korean Journal of Community Nutrition
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    • v.2 no.5
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    • pp.735-744
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    • 1997
  • The effect of green tea drinking on the hepatocellular chemical cacinogenesis have been studied. Placental glutathione S-transferase(GST-P) positive foci area in a liver tissue, contents of thiobarbituric acid reactive substances(TBARS), total cytochrome P450 and glucose 6-phospphatase(G6P) activity in hepatic microsomes were investigated. Weaning Sprague-Dawley male rats were fed AIN-76A diet with deionized water or green tea infusion, Rats of CTR and CTR+ groups were provided deionized water while GTI and GTI+ groups were provided green tea instead of deionized water for the entire experimental period of 13weeks. Rats of GTP and GTP + groups had deionized water for the first 6 weeks and switched to green tea for the last 7weeks of the experimental period. CTR+, GTI +, and GTP + groups were carcinogen treated groups, Diethylnitrosamine(DEN) was injected as a single dose of 200mg/kg body weight intraperitoneally after 4 weeks of feeding. 2-Acetyla-minofluorene(AAF) was used as a carcinogen proliferater and suppled in the diets of carcinogen treated rats as 0.02% content for the last 6weeks starting from 2weeks after DEN injection. Rats were sacrificed after 13week weeks of feeding. The area and number of GST-P positive foci detected in carcinogen treated rats were decreased by green tea ingestion but when timing and duration of green tea ingestion was delayed after promotion period as in GTP + group, GST-P positive foci were not decreased as much as in GTI+ group. TBARS contents of carcinogen treated rats decreased by 13weeks of green tea ingestion but GTP groups did not show statiscally significant differences. G6P activities tended to decrease by carcinogen treatment but changes were not statiscally significant by green tea ingestion. Total cytochrome P450 contents were increased by carcinogen treatment. Thirteen weeks of green tea ingestion (GTI) also increased to total cytochrome P450 contents while 7weeks of green tea ingestion(GTP) did show any effects. These results suggest that green tea has suppressive effects on hepatocellular chemical carcinogenesis probably through the activities of antioxidant compounds. (Korean J Community utrition 2(5) : 735∼744, 1997)

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