4 JOURNAL OF COSMETIC SCIENCE under occlusive conditions for 30 min. Then 100 µl of the respective test product was applied to the same area. This two-step treatment was repeated twice daily for a total of five days. The rate of transepidermal water loss (TEWL) was measured immediately prior to each SOS challenge using the Tewameter (Courage & Khazaka, Cologne, Germany). Measurements were performed at 23°C and at a constant humidity. All data were normalized to t0 and integrated. STATISTICAL ANALYSIS Statistical analysis was performed using the two-tailed and unpaired Student's t-test. RES UL TS AND DISCUSSION Exposure of epidermal cells to anionic surfactants such as sodium dodecyl sulfate (SOS) involves a cytotoxic and inflammatory response. To characterize the impact of taurine on surfactant-induced keratinocyte insults, reconstructed epidermis was topically incubated with 0.18% SOS for 1 h, and cellular viability, membrane integrity, and release of proinflammatory cytokines were monitored after a 24-h post-incubation phase. Taurine was incorporated into an o/w-emulsion that was topically applied to the reconstructed epidermis for 24 h. A vehicle control as well as a positive control based on 0.1 % glucocorticoid was analyzed in parallel. As expected, the application of SOS induced a decrease in cellular viability (Figure 2A) and an increased secretion of lactate dehydro- genase (LOH) to the culture medium (Figure 2B). These data indicate cell membrane permeabilization by SOS. Moreover, the levels of the proinflammatory cytokines, IL- lalpha and PGE2, in the culture medium were increased by SOS (Figure 2C,O). Ap- plication of 0.1 % glucocorticoid improved both viability and integrity when compared to control tissues treated with water (Figure 2A,B). As expected, glucocorticoid treat- ment also decreased the SOS-induced release of IL-lalpha and PGE2 (Figure 2C,0). With the exception of PGE2 levels, the vehicle had only minor effects on SOS-induced irritation. In contrast, the vehicle containing 1 % taurine displayed similar effects on viability, membrane integrity, IL-lalpha-, and PEG2-levels compared to the positive control. In summary, taurine treatment of reconstructed epidermis stressed by SOS resulted in a comprehensive anti-inflammatory profile. It is unlikely, however, that taurine and glu- cocorticoids share the same mechanism of action. Glucocorticoids such as triamcinolone acetonide are potent inhibitors of cyclooxygenase, the first enzyme in the conversion of arachidonic acid to prostaglandins (23). In contrast, there is no evidence that taurine directly regulates the synthesis of arachidonic acid metabolites such as PGE2. Our data show that taurine renders epidermal keratinocytes more resistant to cell membrane permeabilization by SOS, and this might at least in part account for the decreased release of inflammatory mediators. According to the well-established cellular osmolyte strategy, taurine plays a key role in cell volume regulation and the maintenance of membrane potential (24). Moreover, osmolytes such as taurine have been shown to stabilize the native structure of proteins (9). It remains unknown, however, whether SOS treatment imparts osmotic changes to epidermal cells or whether taurine displays direct effects on the interaction of SOS with membrane lipids and/or proteins.

TAURINE AND PREVENTION OF DRY SKIN 5 A B 120 3�---------------� 100 � 80 i 60 40 20 0 C 600 =- 500 E J:400 1300 "! {200 iii J 100 □ untreated control ■ (i) 1h 0.18% SOS (ii) 24h Aqua demin. D � (i) 1 h 0.18% SDS (ii) 24h 0.1% Triamcinolone acetonide (i) 1 h 0.18% SOS (ii) 24h Vehicle ■ (i) 1h 0.18% SOS (ii) 24h Vehicle+ 1% Taurine Figure 2. Effect of taurine on SOS-induced irritation of reconstructed epidermis. An aqueous solution of 0.18% SDS was topically applied to reconstructed epidermis for 1 h. To evaluate the impact ofSDS, control tissues were left untreated. After rinsing, emulsions containing either no active ingredient (vehicle) or 0.1 % of a glucocorticoid (triamcinolone acetonide) or 1 % taurine were applied topically for 24 h. Control tissues were treated with SDS alone, with a further 24 h of incubation with demineralized water. Cellular viability was quantified using the MTT assay (panel A). Lactate dehydrogenase activity (panel B), ILl-alpha (panel C), and PEG2 (panel D) were quantified in the culture medium. Note that the vehicle containing 1 % taurine improved both cell viability and integrity and decreased levels of both IL-1 alpha and PGE2 when compared to the vehicle control. Data represent the mean +/- SEM (n=3). LDH, lactate dehydrogenase. Epidermal IL-lalpha is stimulated by various environmental factors related to epidermal inflammation and hyperproliferation, including UV irradiation and repeated barrier perturbation (16-18). 11-lalpha can induce other cytokines such as 11-6, 11-8, granu- locyte/macrophage colony-stimulating factor, and intercellular adhesion molecule-I ( 19), and is expressed in the whole epidermis when epidermal hyperplasia is induced by repeated barrier disruption (20). Because taurine inhibits the release of 11-lalpha and PGE2, it is likely that taurine inhibits epidermal hyperplasia and inflammation induced by repeated barrier disruption. To test the possible in vivo relevance of taurine effects on epidermal cells stressed by surfactants, skin barrier function was repetitively perturbed by application of 0. 75% SDS over a period of five days and barrier function was monitored by measuring trans- epidermal water loss (TEWL). Figure 3 shows that application of the vehicle containing 1 % taurine directly after rinsing the SDS solution significantly (p 0.05) improved barrier function when compared to the vehicle control. Application of the vehicle also decreased TEWL when compared to control sites treated with SDS alone, but this effect did not reach statistical significance (Figure 3). These data indicate that topical appli- cation of taurine improves barrier repair after perturbation with SDS. It remains un-