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Bibliografia__________________________________________________________________________

Hidaka S, Abe K. The effects of sodium lauryl sulphate and its oxidative breakdown products on calcium phosphate precipitation and transformation. Arch Oral Biol. 1992 Mar;37(3):159-65. doi: 10.1016/0003-9969(92)90085-m. 

Abstract. Most commercial dentifrices contain sodium lauryl sulphate, which oxidizes upon storage. The effects of aged sodium lauryl sulphate and its oxidative breakdown products on the conversion of amorphous calcium phosphate to hydroxyapatite were studied in vitro by a pH drop method. Hydroxyapatite was identified from its X-ray diffraction pattern. With storage time, the concentration of dodecanol [CH3(CH2)11OH], a breakdown product of sodium lauryl sulphate, increased. The storage dodecanol-containing sodium lauryl sulphate accelerated the conversion of amorphous calcium phosphate to hydroxyapatite. Dodecanol mixed with sodium lauryl sulphate accelerated the conversion when added both before and after initial formation of amorphous calcium phosphate. A stored commercial dentifrice also accelerated the conversion of amorphous calcium phosphate to hydroxyapatite. It was found that the concentration of dodecanol increased 2-fold over a 2-month period.

Mizutani T, Mori R, Hirayama M, Sagawa Y, Shimizu K, Okano Y, Masaki H. Sodium Lauryl Sulfate Stimulates the Generation of Reactive Oxygen Species through Interactions with Cell Membranes. J Oleo Sci. 2016 Dec 1;65(12):993-1001. doi: 10.5650/jos.ess16074. 

Abstract. Sodium lauryl sulfate (SLS), a representative anionic surfactant, is well-known to induce rough skin following single or multiple topical applications. The mechanism by which SLS induces rough skin is thought to result from the disruption of skin moisture function consisting of NMF and epidermal lipids. However, a recent study demonstrated that topically applied SLS easily penetrates into the living cell layers of the epidermis, which suggests that physiological alterations of keratinocytes might cause the SLS-induced rough skin. This study was conducted to clarify the effects of SLS on keratinocytes to demonstrate the contribution of SLS to the induction of rough skin. In addition, the potentials of other widely used anionic surfactants to induce rough skin were evaluated. HaCaT keratinocytes treated with SLS had increased levels of intracellular ROS and IL-1α secretion. Application of SLS on the surface of a reconstructed epidermal equivalent also showed the increased generation of ROS. Further, SLS-treated cells showed an increase of intracellular calpain activity associated with the increase of intracellular Ca2+ concentration. The increase of intracellular ROS was abolished by the addition of BAPTA-AM, a specific chelator of Ca2+. In addition, IL-1α also stimulated ROS generation by HaCaT keratinocytes. An ESR spin-labeling study demonstrated that SLS increased the fluidity of membranes of liposomes and cells. Together, those results indicate that SLS initially interacts with cell membranes, which results in the elevation of intracellular Ca2+ influx. Ca2+ stimulates the secretion of IL-1α due to the activation of calpain, and also increases ROS generation. IL-1α also stimulates ROS generation by HaCaT keratinocytes. We conclude from these results that the elevation of intracellular ROS levels is one of the causes of SLS-induced rough skin. Finally, among the other anionic surfactants tested, sodium lauryl phosphate has less potential to induce rough skin because of its lower generation of ROS.

Piret J, Désormeaux A, Cormier H, Lamontagne J, Gourde P, Juhász J, Bergeron MG. Sodium lauryl sulfate increases the efficacy of a topical formulation of foscarnet against herpes simplex virus type 1 cutaneous lesions in mice. Antimicrob Agents Chemother. 2000 Sep;44(9):2263-70. doi: 10.1128/AAC.44.9.2263-2270.2000. 

Abstract. The influence of sodium lauryl sulfate (SLS) on the efficacies of topical gel formulations of foscarnet against herpes simplex virus type 1 (HSV-1) cutaneous infection has been evaluated in mice. A single application of the gel formulation containing 3% foscarnet given 24 h postinfection exerted only a modest effect on the development of herpetic skin lesions. Of prime interest, the addition of 5% SLS to this gel formulation markedly reduced the mean lesion score. The improved efficacy of the foscarnet formulation containing SLS could be attributed to an increased penetration of the antiviral agent into the epidermis. In vitro, SLS decreased in a concentration-dependent manner the infectivities of herpesviruses for Vero cells. SLS also inhibited the HSV-1 strain F-induced cytopathic effect. Combinations of foscarnet and SLS resulted in subsynergistic to subantagonistic effects, depending on the concentration used. Foscarnet in phosphate-buffered saline decreased in a dose-dependent manner the viability of cultured human skin fibroblasts. This toxic effect was markedly decreased when foscarnet was incorporated into the polymer matrix. The presence of SLS in the gel formulations did not alter the viabilities of these cells. The use of gel formulations containing foscarnet and SLS could represent an attractive approach to the treatment of herpetic mucocutaneous lesions, especially those caused by acyclovir-resistant strains.