Pravatà G, Noto G, Aricò M
Istituto di Dermatologia Sperimentale, University of Palermo, Policlinico P. Giaccone, Italy.
J Dermatol Sci. 1994 Feb;7(1):14-23. doi: 10.1016/0923-1811(94)90017-5.
We have studied the distribution of SH groups and SS linkages in solar elastosis, in comparison with that in aged and juvenile sun-unexposed skin, using N-(7-dimethylamino-4-methyl-3-coumarinyl) maleimide (DACM) stain. In heavy solar elastosis we found increased fluorescence for SS bonds in the upper and middle reticular dermis in the elastotic masses; these were separated from the epidermis by a network of actinically-damaged, SS-positive elastic fibers, showing irregularly and variously interwoven oxytalan and elaunic fibers. These latter, unlike the elastotic masses, revealed also SH groups. In moderate and weak elastosis, where the thick irregular masses were absent, the fluorescence for SH and SS linkages was present in equal proportions in the altered elastic fibers; collagen bundles revealed only fluorescence for SS bonds. Aged and juvenile sun-unexposed skin showed the same proportions of SH and SS linkages in the changed elastic fibers. Collagen bundles of aged and juvenile skin showed fluorescence for SS bonds; SH groups were present on a few collagen fibers only in aged skin. Our results are consistent with opinion supporting an elastic origin of elastotic degeneration, which could be the consequence of a defect, due to chronic solar exposure, in one of the steps--degradation or synthesis--of metabolic turnover of elastic fibers, resulting in abnormal and excessive polypeptide chains extremely rich in disulfide bonds.
我们使用N-(7-二甲基氨基-4-甲基-3-香豆素基)马来酰亚胺（DACM）染色法，研究了日光性弹力组织变性中SH基团和SS键的分布情况，并与未暴露于阳光下的老年和青少年皮肤进行了比较。在重度日光性弹力组织变性中，我们发现弹力组织块中上网状真皮和中网状真皮中SS键的荧光增强；这些与表皮之间被光损伤的、SS阳性的弹性纤维网络隔开，显示出不规则且交织的氧化弹性纤维和弹力纤维。与弹力组织块不同的是，后者也显示有SH基团。在中度和轻度弹力组织变性中，不存在粗大的不规则组织块，改变的弹性纤维中SH和SS键的荧光比例相等；胶原束仅显示SS键的荧光。未暴露于阳光下的老年和青少年皮肤在改变的弹性纤维中SH和SS键的比例相同。老年和青少年皮肤的胶原束显示有SS键的荧光；仅在老年皮肤的少数胶原纤维上存在SH基团。我们的结果与支持弹力组织变性源于弹性纤维的观点一致，这可能是由于长期阳光照射导致弹性纤维代谢周转的降解或合成步骤之一出现缺陷，从而产生异常且富含二硫键的过量多肽链的结果。
