Bürki K, Bresnick E
J Natl Cancer Inst. 1975 Jul;55(1):174-6.
The effects of topical administration of 3-methylcholanthrene (MCA) or its metabolites on BALB/cKi mice were reported on inflammatory skin reactions, the alterations in epidermal thickness, the number of nucleated cells, pyknotic nuclei and/or nuclear fragments, and mitotic figures in the interfollicular epidermis (IFE). In the two-stage carcinogenesis system, MCA, the powerful complete carcinogen, induced an ordered sequence of cell changes strikingly similar to those caused by tumor-promoting agents such as the phorbol esters. These changes were absent after application of the "K-region" oxide of MCA. Other MCA metabolites also failed to induce notable inflammation, epidermal hyperplasia, and/or hypertrophy. Several MCA derivatives, however, caused a thinning of IFE paralleled by an increase in the relative number of pyknotic nuclei and a decrease in the total number of epithelial cells. The inhibitor of polycyclic hydrocarbon metabolism alpha-naphthoflavone did not prevent MCA-mediated skin reactions but, under suitable conditions, apparently potentiated the hyperplastic effects of MCA. The findings indicate that important events in the promotion phase of MCA-mediated skin carcinogenesis might be associated with the parent compound rather than with one of its metabolites.
报道了局部施用3-甲基胆蒽(MCA)或其代谢产物对BALB/cKi小鼠炎性皮肤反应、表皮厚度改变、有核细胞数量、固缩核和/或核碎片以及毛囊间表皮(IFE)有丝分裂象的影响。在两阶段致癌系统中,强大的完全致癌物MCA诱导了一系列细胞变化,这些变化与肿瘤促进剂如佛波酯所引起的变化惊人地相似。施用MCA的“K区域”氧化物后,这些变化不存在。其他MCA代谢产物也未能诱导明显的炎症、表皮增生和/或肥大。然而,几种MCA衍生物导致IFE变薄,同时固缩核相对数量增加,上皮细胞总数减少。多环烃代谢抑制剂α-萘黄酮并不能阻止MCA介导的皮肤反应,但在合适的条件下,显然会增强MCA的增生作用。这些发现表明,MCA介导的皮肤致癌促进阶段的重要事件可能与母体化合物有关,而不是与其代谢产物之一有关。