Ley R D, Applegate L A, Padilla R S, Stuart T D
Photochem Photobiol. 1989 Jul;50(1):1-5. doi: 10.1111/j.1751-1097.1989.tb04123.x.
Several lines of evidence support the hypothesis that ultraviolet radiation (UVR) is involved in the etiology of cutaneous melanoma in humans. However, progress in understanding the mechanisms involved in induction of melanotic tumors by UVR has been hindered by lack of a suitable animal model. During the course of multiple exposures (3 times/wk for 70 wk) of the South American opossum, Monodelphis domestica, to UVR, we first observed the appearance of areas of dermal melanocytic hyperplasia (MH) on the exposed skin. Post-UVR exposure to photoreactivating light (320-500 nm) suppressed the occurrence of MH. We also observed at 100 weeks from first exposure that 10 of 46 surviving animals had developed melanotic tumors which arose, presumably, from areas of MH. Tumors on three of the 10 animals have been classified as malignant melanomas based on metastasis to lymph nodes. We conclude from these results that UVR can act as a complete carcinogen for melanoma induction and, based on the photoreactivation of MH induction, that DNA damage is involved in melanoma formation.
有几条证据支持紫外线辐射(UVR)参与人类皮肤黑色素瘤病因的假说。然而,由于缺乏合适的动物模型,在理解UVR诱导黑素瘤的机制方面进展受阻。在南美负鼠(Monodelphis domestica)多次暴露于UVR(每周3次,共70周)的过程中,我们首先在暴露的皮肤上观察到真皮黑素细胞增生(MH)区域的出现。UVR暴露后再暴露于光复活光(320 - 500nm)可抑制MH的发生。我们还在首次暴露100周时观察到,46只存活动物中有10只发生了黑素瘤,推测这些肿瘤起源于MH区域。根据转移至淋巴结的情况,这10只动物中有3只的肿瘤被归类为恶性黑色素瘤。从这些结果我们得出结论,UVR可作为诱导黑色素瘤的完全致癌物,并且基于MH诱导的光复活,DNA损伤参与了黑色素瘤的形成。