Evans C H, Greiner J W
Cancer Lett. 1981 Mar;12(1-2):23-7. doi: 10.1016/0304-3835(81)90033-1.
Cortisol and dexamethasone, at 10(-9)--10(-11) M, inhibit benzo[a]pyrene and ultraviolet irradiation-induced morphological transformation of hamster embryo fibroblasts without inhibiting cell proliferation in a cell culture model of carcinogenesis. Inhibition varies directly with steroid concentration and is complete at equimolar doses for these glucocorticosteroids possessing a 30-fold difference in anti-inflammatory activity. Corticosteroids are known to affect enzymes metabolizing carcinogenic polycyclic aromatic hydrocarbons (PCH) and to inhibit complete PCH and phorbol ester promotion of PCH tumorigenesis. The pleotropic anti-carcinogenic action of corticosteroids is further demonstrated by the prevention of transformation induced by ultraviolet irradiation, a carcinogen not requiring metabolic activation.
在致癌作用的细胞培养模型中,皮质醇和地塞米松浓度为10⁻⁹至10⁻¹¹M时,可抑制苯并[a]芘和紫外线照射诱导的仓鼠胚胎成纤维细胞形态转化,而不抑制细胞增殖。抑制作用与类固醇浓度直接相关,对于这些抗炎活性相差30倍的糖皮质激素,在等摩尔剂量时抑制作用完全。已知皮质类固醇会影响代谢致癌多环芳烃(PCH)的酶,并抑制PCH的完全代谢以及佛波酯对PCH肿瘤发生的促进作用。紫外线照射是一种无需代谢激活的致癌物,皮质类固醇对其诱导的转化具有预防作用,进一步证明了皮质类固醇的多效抗癌作用。