KERATIN PEPTIDE HAND CREAM 107 (3) E. Berardesca and the EEMCO Group, EEMCO guidance for the assessment of stratum corneum hydration: Electrical methods, Skin Res. Tech., 3, 126-132 (1997). (4) L. Rodrigues and the EEMCO Group, EEMCO guidance to the in vivo assessment of tensile functional properties of the skin, Skin Pharmacol. Appl. Skin Physiol., 14, 52-67 (2001). (5) R. A. Tupker, C. Willis, E. Berardesca, C.H. Lee, M. Fartasch, T. Agner, and J. Serup, Guidelines on sodium lauryl sulphate (SLS) exposure tests: A report from the Standardization Group of the European Society of Contact Dermatitis, Contact Dermatitis, 3 7, 5 3-69 (1997). (6) L. Coderch, M. de Pera, J. Fonollosa, A. de la Maza, and J. L. Parra, Efficacy of stratum corneum lipid supplementation on human skin, Contact Dermatitis, 47, 139-146 (2002). (7) M. de Pera, L. Coderch, J. Fonollosa, A. de la Maza, and J. L. Parra, EtTect of internal wool lipid liposomes on skin repair, Skin Pharmacol. Appl. Skin Physiol., 13, 188-195 (2000).
J. Cosmet. Sci., 58, 109-133 (March/April 2007) The role of sodium dodecyl sulfate (SDS) micelles in inducing skin barrier perturbation in the presence of glycerol SASWATA GHOSH and DANIEL BLANKSCHTEIN, Department of Chemical Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139. Accepted for Publication November 29, 2006. Synopsis The stratum corneum (SC) serves as the skin barrier between the body and the environment. When the skin is contacted with an aqueous solution of the surfactant sodium dodecyl sulfate (SDS), a well-known model skin irritant, SDS penetrates into the skin and disrupts this barrier. It is well established, both in vitro and in vivo, that the SDS skin penetration is dose-dependent, and that it increases with an increase in the total SDS concentration above the critical micelle concentration (CMC) of SDS. However, when we added the humectant glycerol at a concentration of 10 wt% to the aqueous SDS contacting solution, we observed, through in vitro quantitative skin radioactivity assays using 14 C-radiolabeled SDS, that the dose dependence in SDS skin penetration is almost completely eliminated. To rationalize this important observation, which may also be related to the well-known beneficial effects of glycerol on skin barrier perturbation in vivo, we hypothesize that the addition of 10 wt% glycerol may hinder the ability of the SDS micelles to penetrate into the skin barrier through aqueous pores that exist in the SC. To test this hypothesis, we conducted mannitol skin permeability as well as average skin electrical resistivity measurements in vitro upon exposure of the skin to an aqueous SDS contacting solution and to an aqueous SDS + 10 wt% glycerol contacting solution in the context of a hindered-transport aqueous porous pathway model of the SC. Our in vitro studies demonstrated that the addition of 10 wt% glycerol: (i) reduces the average aqueous pore radius resulting from exposure of the skin to the aqueous SDS contacting solution from 33 ± 5 A to 20 ± 5 A, such that a SDS micelle of radius 18.5 ± 1 A (as determined using dynamic light-scattering measurements) experiences significant steric hindrance and cannot penetrate into the SC, and (ii) reduces the number density of aqueous pores in the SC by more than 50%, thereby further reducing the ability of the SDS micelles to penetrate into the SC and perturb the skin barrier. INTRODUCTION AND SIGNIFICANCE Human skin consists of three stratified layers, the stratum corneum, the viable epider­ mis, and the dermis (1). The stratum corneum (SC), which is the topmost layer of the skin, possesses an ordered brick-and-mortar structure, which consists of the flat corneo- Address all correspondence to Daniel Blankschtein. 109
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