Chopra D P, Wilkoff L J
J Natl Cancer Inst. 1976 Mar;56(3):583-9. doi: 10.1093/jnci/56.3.583.
The effect of beta-retinoic acid (RA) on carcinogen-induced hyperplasia was studied in organ cultures of mouse prostate gland. 3-Methylcholanthrene (MCA), requiring metabolic activation, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), not requiring activation, were used to induce hyperplastic changes. Treatment of cultures with MCA or MNNG stimulated cell proliferation and caused the alveolar epithelium to become hyperplastic. The development of this hyperplasia was inhibited when RA was added simultaneously with MCA or MNNG. However, RA had no significant effect on cell proliferation in untreated control cultures. Elimination of carcinogen from the hyperplastic cultures after 8 days of treatment did not reverse hyperplasia of the alveolar epithelium. When the withdrawal of MCA or MNNG was followed by treatment of the cultures with RA, hyperplasia was markedly reversed within 96 hours. Thus RA actively inhibited and reversed the effect of MCA and MNNG, two carcinogens that may have different mechanisms of action.
在小鼠前列腺器官培养物中研究了β-视黄酸（RA）对致癌物诱导的增生的影响。使用需要代谢激活的3-甲基胆蒽（MCA）或不需要激活的N-甲基-N'-硝基-N-亚硝基胍（MNNG）来诱导增生性变化。用MCA或MNNG处理培养物可刺激细胞增殖并导致肺泡上皮增生。当RA与MCA或MNNG同时添加时，这种增生的发展受到抑制。然而，RA对未处理的对照培养物中的细胞增殖没有显著影响。处理8天后从增生性培养物中去除致癌物并没有逆转肺泡上皮的增生。当停用MCA或MNNG后用RA处理培养物时，增生在96小时内明显逆转。因此，RA可有效抑制并逆转MCA和MNNG这两种可能具有不同作用机制的致癌物的作用。
