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KMID : 0359320010410040549
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Korean Journal of Veterinary Research
2001 Volume.41 No. 4 p.549 ~ p.555
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Pre-initiation treatment of indole-3-carbinol(I3C) inhibits 7,12-Dimethylbenz[α] anthracene(DMBA)-induced rat mammary carcinogenesis
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강진석/Kang, Jin Seok
안병우/남기택/최미나/김지영/김대중/장동덕/Ahn, Byeong Woo/Nam, Ki Taek/Choi, Mi Na/Kim, Ji Young/Kim, Dae Joong/Jang, Dong Deuk
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Abstract
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Indole-3-carbinol (I3C), one component of cruciferous vegetables (the Fammily of Cruciferae), has been shown to exert its chemopreventive effect in liver, colon and mammary tissue before or concurrent exposure of carcinogen, but there have been several evidences that consumption of I3C induced tumor promotion in some tissues. Our studies were investigated to examine the modifying effects of I3C in the 7,12-dimethylbenz[α]anthracene (DMBA) induced rat mammary gland tumor model. Fifty-two female Sprague-Dawley rats were randomly divided into five groups. Animals fo teh group 1 were given the diet containing 100ppm I3C and animals of the groups 2 and 4 were given the diet containing 300ppm I3C from 6 weeks of age. At 7 weeks of age, the animals of the groups 1, 2 and 3 were intubated with DMBA. All amimals were killed at 20 weeks after carcinogen treatment. There were significant increases of food consumption in I3C feeding groups compared with those of basal diet feeding groups. The incidences of the mammary tumors in the group 1, 2 and 3 were 75.0% (9/12), 56.3% (9/16) and 93.8% (15/16), respectively and the average number of tumors of group 1 (DMBA+I3C 100ppm: 2.08±0.61) and 2 (DMBA+I3C 300ppm: 1.19±0.32) were significantly lower than that of group 3 (DMBA alone: 4.63±0.72) at the value of P＜0.05 and P＜0.001, respectively. In the pathological examination of appearing tumors, most of them were adenocarcinoma. Many epithelial cells of tumors showed strong estrogen receptor (ER) α expression but there were slight difference of ER α expression among the type of tumors. We suggest that pre-initiation treatment of I3C has an inhibitory effects on mammary carcinogenesis induced by DMBA.
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KEYWORD
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