Warner R R, Boissy Y L, Lilly N A, Spears M J, McKillop K, Marshall J L, Stone K J
Miami Valley Laboratories, Procter & Gamble, Cincinnati 452539, USA.
J Invest Dermatol. 1999 Dec;113(6):960-6. doi: 10.1046/j.1523-1747.1999.00774.x.
Using electron microscopy, we investigated the effect of (i) a dilute surfactant and of water alone on the ultrastructure of stratum corneum lipids in pig skin exposed in vitro at 46 degrees C, and (ii) of water alone on human skin exposed in vivo at ambient temperature. For pig skin, the surfactant sodium dodecyl sulfate disrupts stratum corneum intercellular lamellar bilayers, leading to bilayer delamination and "roll-up" in a water milieu after 1 h, extensive bilayer disruption after 6 h, and nearly complete dissociation of corneocytes after 24 h. Corneodesmosomes show progressive degradation with exposure time. Water alone also disrupts the stratum corneum, but with a slower onset. Alterations in intercellular lamellar bilayers, but not intercellular lamellar bilayer roll-up, are detected after 2 h. Intercellular lamellar bilayer roll-up occurs after 6 h. Extensive dissociation of corneocytes occurs after 24 h of water exposure. Unlike sodium dodecyl sulfate, water exposure results in the formation of amorphous intercellular lipid. Corneodesmosome degradation parallels intercellular lamellar bilayer disruption; calcium appears to offer some protection. Similar disruption of intercellular lamellar bilayers occurs in human skin in vivo at ambient temperature. Our studies show that water can directly disrupt the barrier lipids and are consistent with surfactant-induced intercellular lamellar bilayer disruption being due at least in part to the deleterious action of water. Intercellular lamellar bilayer disruption by water would be expected to enhance permeability and susceptibility to irritants; accordingly, increased attention should be given to the potential dangers of prolonged water contact. For common in vitro procedures, such as skin permeation studies or isolation of stratum corneum sheets, exposure to water should also be minimized.
(i)一种稀释的表面活性剂以及仅用水,在体外46摄氏度下对猪皮肤角质层脂质超微结构的影响;(ii)仅用水,在环境温度下对人体皮肤角质层脂质超微结构的影响。对于猪皮肤,表面活性剂十二烷基硫酸钠会破坏角质层细胞间的层状双分子层,在水介质中1小时后导致双分子层分层和“卷起”,6小时后双分子层出现广泛破坏,24小时后角质形成细胞几乎完全解离。随着暴露时间的延长,角质桥粒逐渐降解。仅用水也会破坏角质层,但起效较慢。2小时后可检测到细胞间层状双分子层的改变,但未出现细胞间层状双分子层卷起现象。6小时后出现细胞间层状双分子层卷起。水暴露24小时后角质形成细胞出现广泛解离。与十二烷基硫酸钠不同,水暴露会导致无定形细胞间脂质的形成。角质桥粒的降解与细胞间层状双分子层的破坏平行;钙似乎提供了一些保护作用。在环境温度下,人体皮肤在体内也会出现类似的细胞间层状双分子层破坏。我们的研究表明,水可直接破坏屏障脂质,这与表面活性剂诱导的细胞间层状双分子层破坏至少部分归因于水的有害作用是一致的。预计水引起的细胞间层状双分子层破坏会增强皮肤的通透性和对刺激物的敏感性;因此,应更加关注长时间接触水的潜在危险。对于常见的体外实验步骤,如皮肤渗透研究或角质层片的分离,也应尽量减少皮肤与水的接触。