Giannelli F, Botcherby P K, Marimo B, Magnus I A
Lancet. 1983 Jan 15;1(8316):88-91. doi: 10.1016/s0140-6736(83)91740-3.
Fibroblasts cultured from six patients with actinic reticuloid (AR) showed striking cytopathic changes and inhibition of RNA synthesis after exposure to near-ultraviolet radiation that had no effect on normal and other photosensitive cell strains, such as those of xeroderma pigmentosum and Bloom syndrome. An abnormal pattern of DNA fragmentation was observed after doses insufficient to cause cytopathic effects. These results suggest a cellular defect in the prevention or repair of some damage caused by free radicals and other photoproducts. In order to explain the pathogenesis of AR, it is proposed that a deficiency in the cellular mechanisms dealing with oxygen radicals leads to the establishment of a vicious circle favouring the persistence of a lymphohistiocytic infiltrate and hence the chronic clinical course characteristic of the disease.
从六名光化性类网状细胞增生症（AR）患者身上培养的成纤维细胞，在暴露于近紫外线辐射后，呈现出显著的细胞病变变化以及RNA合成受抑制的现象，而这种辐射对正常细胞以及其他光敏细胞株，如着色性干皮病和布卢姆综合征的细胞株，并无影响。在剂量不足以引起细胞病变效应的情况下，观察到了DNA片段化的异常模式。这些结果表明，在预防或修复由自由基和其他光产物造成的某些损伤方面存在细胞缺陷。为了解释AR的发病机制，有人提出，处理氧自由基的细胞机制存在缺陷，导致形成一个恶性循环，有利于淋巴细胞组织细胞浸润的持续存在，从而导致该疾病特有的慢性临床病程。
