| 相互作用 | It was ... shown to enhance leukemogenic effects of x-irradiation.The antipellagratic vitamin, nicotinamide, significantly suppressed urethane induced malformations, when it was given intraperitoneally to pregnant JCL:ICR mice immediately after a single subcutaneous injection of urethane (1.0 mg/g) on the 9th day of gestation. The level of inhibition increased with the doses of nicotinamide: 33.0, 55.8, and 70.0% at doses of 0.2, 0.3, and 0.5 mg/g, respectively. Polydactyly and tail anomalies were markedly suppressed by the post treatment with nicotinamide, while cleft palates were less effectively suppressed. Nicotinamide was still effective, when it was given during the period of 24-48 hr after urethane treatment. The level of inhibition was 39.4 and 61.1% at 0.5 and 1.0% of nicotinamide in the diet, respectively. Higher doses of nicotinamide (3 and 5% in diet) also inhibited urethane induced malformations, but not so effectively as lower doses. The inhibiting effects of nicotinamide on the spontaneous incidence of cleft lips and palates in CL/Fr mice were significant at a low dose (0.5% in diet), but not at a higher dose (1.0%).The progression of papillomas to squamous cell carcinomas (malignant conversion) was studied in the skin of Sencar and Charles River CD-1 mice, using a three stage treatment protocol. After initiation with 7,12-dimethylbenz(a)anthracene (stage 1) and limited promotion by 12-O-tetradecanoylphorbol-13-acetate (stage II), papilloma bearing mice were treated (stage III) with either tumor initiators, such as urethane, N-methyl-N'-nitro-N-nitrosoguanidine or 4-nitroquinoline-n-oxidethe promoter 12-O-tetradecanoylphorbol-13-acetate, or solvent (acetone). Treatment with tumor initiators in stage III increased both the rate of appearance and the final yield of carcinomas. Similar results were obtained in both Sencar and CD-1 mice. A papilloma stage appears to be necessary for carcinoma development since elimination of 12-O-tetradecanoylphorbol-13-acetate treatment in stage II greatly reduced the incidence of both papillomas and carcinomas in both stocks of mice. The carcinomas that develop using the three stage regimen vary in metastatic potential. In CD-1 mice, the frequency of metastases to lymph nodes were similar in groups treated in stage III with N-methyl-N'-nitro-N-nitrosoguanidine, urethane, 4-nitroquinoline-n-oxide, 12-O-tetradecanoylphorbol-13-guanidine or acetone, but treatment with urethane substantially increased metastases to the lung.N-homocysteine thiolactonyl retinamide was synthesized from trans-retinoic acid and the free base of homocysteine thiolactone. In doses of 90-1800 mg/kg given ip in mixed lipid vehicle over nine weeks, the compound decreased to 60% of controls the number of lung tumors which was induced in A/J mice by 20 mg of ethyl carbamate. The highest dose also decreased the mean volume of lung tumors to 505 of controls, resulting in a total tumor volume of 30% of controls. Retinoic acid itself of 450 mg/kg was toxic, and no chemopreventive activity was observed. The free base and the lipophilic perchlorate salt of homocysteine thiolactone both increased the number of lung tumors to 114-117% of controls, indicating a co-carcinogenic effect. In C57BL/6N mice with transplanted MUO4 rhabdomyosarcoma, N-homocysteine thiolactonyl retinamide in a dose of 1000 mg/kg given over 11-21 days decreased the weight of the tumors to 30-70% of controls. Therefore, N-homocysteine thiolactonyl retinamide has chemopreventive activity against chemical carcinogenesis and antineoplastic activity against a transplanted neoplasm.For more Interactions (Complete) data for ETHYL CARBAMATE (23 total), please visit the HSDB record page. |
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