Inhibition and reversal by beta-retinoic acid of hyperplasia induced in cultured mouse prostate tissue by 3-methylcholanthrene or N-methyl-N'-nitro-N-nitrosoguanidine.
Inhibition and reversal by beta-retinoic acid of hyperplasia induced in cultured mouse prostate tissue by 3-methylcholanthrene or N-methyl-N'-nitro-N-nitrosoguanidine.
复制标题
β-视黄酸对 3-甲基胆蒽或 N-甲基-N-硝基-N-亚硝基胍在培养的小鼠前列腺组织中诱导的增生的抑制和逆转。
DOI：
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发表时间：
1976
期刊：
影响因子：
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通讯作者：
L. Wilkoff
中科院分区：
文献类型：
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作者：
D. Chopra;L. Wilkoff
研究了β -维甲酸（RA）对癌变诱导的小鼠前列腺增生的影响。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）诱导增生变化。用MCA或MNNG处理培养物可刺激细胞增殖并引起肺泡上皮增生。当RA与MCA或MNNG同时加入时，这种增生的发展受到抑制。然而，在未经处理的对照培养中，RA对细胞增殖没有显著影响。治疗8天后，从增生培养物中消除致癌物并没有逆转肺泡上皮的增生。当停用MCA或MNNG后再治疗RA培养物，增生在96小时内明显逆转。因此，RA积极抑制和逆转了MCA和MNNG这两种可能具有不同作用机制的致癌物的作用。
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.