Mass M J
Respiratory Carcinogenesis Group, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711.
Anticancer Res. 1990 Jan-Feb;10(1):241-5.
Five retinoids were evaluated for their ability to inhibit N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced transformation of primary rat tracheal epithelial (RTE) cells in culture. Two retinoidal benzoic acids (arotenoids), Ro 13-6298 and Ro 13-7410, suppressed the transformation frequency by 80-90% at 330 pM; 330 pM retinoic acid (RA) suppressed the transformation frequency by 50%. Retinol and retinyl acetate were tested at 33 nM and found to be much less effective than RA at this concentration. In studies with all retinoids, the amount of inhibition of spontaneously occurring transformed epithelial foci was greater than the amount of inhibition of foci that arose in response to carcinogen treatment. A biological difference between carcinogen-induced and spontaneously arising foci is suggested by this result.
评估了五种维甲酸抑制培养的原代大鼠气管上皮（RTE）细胞由N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱导转化的能力。两种维甲酸苯甲酸（类胡萝卜素），Ro 13-6298和Ro 13-7410，在330 pM时可将转化频率抑制80-90%；330 pM视黄酸（RA）可将转化频率抑制50%。视黄醇和醋酸视黄酯在33 nM下进行了测试，发现在该浓度下其效果远不如RA。在所有维甲酸的研究中，对自发出现的转化上皮灶的抑制量大于对致癌物处理后出现的灶的抑制量。该结果表明致癌物诱导的灶和自发出现的灶之间存在生物学差异。
