CYTOKINES EXPRESSION AND LYE AND NO-LYE RELAXERS 115 ratios in the early and late phases of epidermal response. However, no-lye relaxer treatment results in higher ratio compared to lye at 24 h suggesting better control of the infl amma- tory response. DISCUSSION AND CONCLUSION Given the well-known biological activity of PGE2 and other prostaglandins, we hypoth- esize that the increased expression resulting from exposure to lye relaxer may in part explain the perceived difference in the level of discomfort associated with the use of the relaxer. In this work, we show that in the early phase (4 h) of epidermal response, lye relaxer induced over 1.5-fold higher level in PGE2 than no-lye relaxer (Figure 2). Our hypothesis as stated above is in agreement with other authors that showed dose-dependent induction and intensity of sensory discomfort by PGE2, which is a by-product of arachi- donic acid metabolism (14–17). These authors suggested that the level of discomfort and the time it takes to feel the sensation are time and dose dependent. It is therefore tempt- ing to speculate that perceived differences in discomfort levels between the two relaxers may be due in part to higher level of PGE2 induced by lye relaxer. This level probably exceeded the threshold needed to saturate and activate nociceptive receptors on peripheral nerves compared to no-lye relaxer induced level. To our knowledge, this is the fi rst time an expression of a specifi c mediator has been associated with discomfort induced by hair relaxers. Our data also showed that although both types of relaxers induce expression of selected cytokines associated with irritation, kinetics and the levels of released cytokines are different, which may infl uence the intensity of discomfort. IL-1α has consistently been shown by in vitro and in vivo studies to be the main cytokine produced by keratinocytes that initiates and propagates epidermal infl ammatory response to irritants (5–8,18). It is able to act in an autocrine and paracrine fashion to infl uence production of other infl ammatory cytokines from keratinocytes and other immune cells. We show in our study that both lye and no-lye relaxers induce expression of IL-1α how- ever, no-lye induces slightly higher level in the early phase of keratinocyte response along Figure 3. Post-relaxer induced expression of IL-1α by EpiSkin. IL-1α was extracted from tissue into the medium and determined by ELISA after treatment with relaxer as described. Each data point represents the mean of six tissues run in duplicate ± SE showing increased IL-1α expression by no-lye at 24 and 48 h (*p 0.05).

JOURNAL OF COSMETIC SCIENCE 116 with a signifi cant increase of the cytokine at 24 h (Figure 3). As may be expected, no-lye relaxer with a greater ability to induce the expression of IL-1α results in higher produc- tion of IL-1ra. Both relaxer types in fact show increased levels of IL-1ra however, no-lye relaxer elicits a statistically signifi cant higher level at all time intervals. With this result, we show IL-1ra/IL-1α ratio is higher with no-lye than lye relaxer at 24 h (Figure 4B), suggesting it is better able to control the infl ammatory process compared to the lye. However, this difference is absent at 4 and 48 h indicating that both relaxers elicit simi- lar control at those time points. This seems contrary to the fact that the no-lye is reported to be less irritating to the scalp in the early phase. Therefore, one may conclude that the irritation experienced by the users of lye relaxer, which occurs within 20 min of contact is not directly related to the level of IL-1α induced. Both lye and no-lye relaxers are high pH complex formulations so it is not known at this time if a specifi c ingredient or pH is responsible for the perceived phenomenon. A differ- ence in pH may be suspected to infl uence the level of sensory response as it is known that alkaline reagents at pH 12 or higher are corrosive to mammalian tissues. Regular strength lye relaxers have an alkalinity of 0.51 meq/g compared with 0.65 meq/g for regular strength no-lye relaxers. Since no-lye relaxers have higher alkalinity but are perceived to be less irritating, the differences in sensory perception are not likely related to differences Figure 4. Hair relaxers induce expression of IL-1ra. Exposure of EpiSkin™ to no-lye relaxer induced signifi - cantly higher level of IL-1ra compared to lye (A) at all time points. Each data point represents the mean of six tissues run in duplicate ± SE (*p 0.05). (B) IL-ra/IL-1 ratio was determined, which shows that no-lye is better able to control IL-1α–induced acute epidermal response.