The Dermatology Unit, Kaplan Medical Center, Rehovot 76100, Israel.
Clin Dermatol. 2012 May-Jun;30(3):297-300. doi: 10.1016/j.clindermatol.2011.08.021.
The past decade has witnessed an explosion of new impartial information about the complex interaction of the skin with topically applied substances, including soaps and detergents. Despite of all these new data, our knowledge on the exact pathomechanism and molecular events leading to detergent-induced barrier dysfunction remains incomplete and the answers continue to elude us. The longtime prevailing opinion which contends that the damaging effect of soaps and detergents is related to their property to extract and remove useful intercellular lipids has mostly been abandoned. Although this effect might be involved in the damaging effect, it is definitely not the sole mechanism, nor, indeed, is it even the main one. Skin proteins damage, the interaction with keratins and their denaturation, swelling of cell membranes and collagen fibers, cytotoxicity expressed with cellular lysis are other important mechanisms. One proposed mechanism is that an initial stratum corneum hyper-hydration results from a continuous disruption of the secondary and tertiary structures of keratin protein by surfactants, exposing new water-binding sites, thereby increasing the hydration of the membrane. Following evaporation of excess water, the denatured keratin possesses a decreased water-binding capacity and decreased ability to function as a barrier. Recent studies have also emphasized the effects of detergents on lipid synthesis, on lipid-metabolizing enzymes and on keratinocyte differentiation.
过去十年见证了新的、公正的关于皮肤与局部应用物质（包括肥皂和洗涤剂）复杂相互作用的信息的爆发。尽管有了所有这些新的数据，我们对于导致洗涤剂引起的屏障功能障碍的确切病理机制和分子事件的了解仍然不完整，答案仍然难以捉摸。长期以来，一种观点认为肥皂和洗涤剂的破坏性影响与其提取和去除有用细胞间脂质的特性有关，但这种观点已基本被摒弃。虽然这种作用可能与破坏作用有关，但它绝对不是唯一的机制，甚至不是主要的机制。皮肤蛋白损伤、与角蛋白的相互作用及其变性、细胞膜和胶原纤维肿胀、细胞溶解表达的细胞毒性是其他重要的机制。一种提出的机制是，表面活性剂连续破坏角蛋白蛋白的二级和三级结构，导致初始角质层过度水合，从而暴露出新的水结合位点，从而增加膜的水合作用。多余水分蒸发后，变性角蛋白的水结合能力降低，作为屏障的功能降低。最近的研究还强调了洗涤剂对脂质合成、脂质代谢酶和角质形成细胞分化的影响。
