• Preventive Nutrition and Food Science
• /
• v.2 no.2
• /
• pp.96-100
• /
• 1997

Carcinogenicity of di(2-ethylhexyl)phthalate(DEHP) to the mose forestomach and its inhibitor activity for the initiation of Benzo[a]pyrene(BP)-induced mouse forestomach neoplasia were studied on the mouse forestomach carcinogenesis regimen. One hundred female ICR mice(6~7 weeks of age) were hosed in a poly-carbonate cage (4 mice/cage) in a humidity- and temperature-controlled room subjected to a semipurified diet for a week. Mice were divided into 4 treatment groups (25 mice/treatment): Basal diet, DEHP, BP, and BP+DEHP. On Monday and wednesday, 0.1ML DEHP mixed with 0.1ml olive oil (for DEHP and DEHP+BP treatment groups) or 0.1ml saline+0.1ml olive oil (for basal diet group) was intubated, p.o., and on Friday, 2mg BP dissolved in 0.2ml olive oil (for BP and BP+DEHP treatment groups) was intubated, p.o. This cycle was repeated for 4 weeks. Beginning with the first intubation of BP an continuing thereafter, body weight and food intake were recorded once and twice weekly, respectively. All surviving mice were sacrificed 22 weeks after the first dose of BP intubation and countered forestomach tumor. No tumor was formed by DEHP treatment. 5.75 tumors per mouse was formed by BP treatment, whereas its number was reduced to 4.53 by BP+DEHP treatment. Similar results were seen in the tumor incidence. Body weight gain was not affected by DEHP treatment, when compared to that b basal diet treatment. The body weight was significantly reduced by BP treatment, but its reduction was recovered to the level of the basal diet group by BP+DEHP treatment. No significant difference was seen in food intake among all treatment groups. These results indicate that DEHP lacks carcinogenic activity to the mose forestomach and rather inhibits the initiation of BP-induced mose forestomach neoplasia.

• Applied Biological Chemistry
• /
• v.40 no.6
• /
• pp.490-494
• /
• 1997

Anticarcinogenic activity of astaxanthin-containing egg yolks (designate AEY) was investigated for benzo[a]pyrene (BP)-induced mouse forestomach tumorigenesis initiating regimen. Female ICR mouse (6-7 weeks of age) were housed in polycarbonated cages (5 mice/cage; 20 mice/treatment) in a humidity-and-temperature-controlled facility and permitted free access to water and food. One week later, four and 2 days prior to p.o. treatment with BP (2 mg/0.2 ml corn oil), mice were given 0.2 ml PBS containing 50 mg AEY, 100 mg AEY, 150 mg AEY, or 150 mg CEY. Control mice were only given 0.2 ml PBS. Three days later this sequence was repeated for a total of 4 times. Beginning with the first intubation and continuing thereafter, body weight and food intake were recorded once weekly. All surviving mice were sacrificed 24 weeks after the first dose of BP. Mice treated with AEY developed only about one third as many neoplasms/animal as mice in control or CEY-treated group (p<0.05). Reduction effect of tumor development by AEY was dependent upon doses applied. Tumor incidence was also reduced by AEY treatments, but significantly reduced only by 150 mg AEY treatment when compared to that by control or CEY. Food intake and body weight were not affected by AEY treatment. These results indicate that AEY inhibits tumorigenesis of mouse forestomach induced by BP.