A Sirvent (1), C Lhéritier (1), A Moga (2), F Girard (1)
1. Laboratoire Dermscan: 114 Bd du 11 novembre 1918, 69100 Villeurbanne, FRANCE
2. Synelvia SAS, Prologue Biotech: 516 rue Pierre et Marie Curie, 31670 Labège Cedex, FRANCE

Introduction

If sunscreens protect against UV radiations, several studies point now the deleterious impact of infra-red (IR) and the fact that an IR protection should also be added to the products [1-3]. Indeed, IR is involved in cutaneous ageing and probably in carcinogenesis [4]; it is mainly responsible for the increase in skin temperature and leads to free radicals and matrix metalloproteinase-1 (MMP-1) production deep in the dermis [5-7].

An efficient protection against IR should be obtained via the presence of optical absorbers in the IR range, reflection of photons and scattering and/or free radical scavengers [8].
The aim of this study was to propose simple methodologies in order to evaluate the IR protection enabled by cosmetic products.

Materials and Methods

These two tests were open and intra-individual studies. They took place at Laboratoire Dermscan (France) and were conducted in accordance with the applicable regulations.

1. BLOCKING EVALUATION OF TWO SUNSCREEN PRODUCTS

Synelvia_BLOCKING EVALUATION OF TWO SUNSCREEN PRODUCTS
Synelvia_BLOCKING EVALUATION OF TWO SUNSCREEN PRODUCTS2

2. EVALUATION OF THE CELLULAR PROTECTION AGAINST IR OF A SUNS- CREEN PRODUCT

Synelvia_EVALUATION OF THE CELLULAR PROTECTION AGAINST IR OF A SUNS- CREEN PRODUCT
Synelvia_EVALUATION OF THE CELLULAR PROTECTION AGAINST IR OF A SUNS- CREEN PRODUCT2

Results and Discussion

1. BLOCKING EVALUATION OF TWO SUNSCREEN PRODUCTS

Effects of IR radiations on cutaneous parameters

Immediately after the end of IR radiation, significant increases in RBC concentration (+73.4%), redness (+77.6%) and temperature (8.7%) were recorded (p<0.05; student t test). During time, a mottled redness appeared on the zones under IR radiation (zones C and D). This sign evidences the deep penetration into dermis (and even the subcutis) of IR, heat generation and vasodilatation of vessels from the deep vascular plexus. This effect lasted up to 60 min.

Influence of phototype

Darker skin phototypes (IV) reacted greater than lighter ones (II) and recovered more slowly. They absorbed more heat, leading to higher vasodilation and redness.

Effect of sunscreens X or Y

• Just after application and without any IR radiation, sunscreens did not modify any of the 3 cutaneous parameters.
• Sunscreen X had no blocking effect against IR: measures on the D zone were very similar to the unprotected C zone (data not shown).
• Sunscreen Y decreased both vasodilatation and redness at the skin surface, immediately after the end of the IR radiation. The blocking effect of sunscreen Y
was still observed one hour after the end of IR radiation: all 3 parameters on D zone were reduced compared to the C zone. As an example, the variations in time obtained for RBC concentration is presented below.

Synelvia_BLOCKING EVALUATION OF TWO SUNSCREEN PRODUCTS

2. EVALUATION OF THE CELLULAR PROTECTION AGAINST IR OF A SUNSCREEN PRODUCT

In the second part of this study, we decided to test the cellular protection effect of sunscreen Y and to recrut only phototype IV in order to maximize the heat reaction.

Synelvia_EVALUATION OF THE CELLULAR PROTECTION AGAINST IR OF A SUNSCREEN PRODUCT3

Conclusion

• The 1st approach takes advantage of the blocking power of sunscreens. All the chosen parameters (cutaneous temperature, color and microcirculation) were increased after IR radiation. Darker skin types reacted more importantly than lighter ones: they absorbed more heat and vasodilation was more important. This approach allowed to discriminate two sunscreens: sunscreen X had no effect on skin heating under IR whereas sunscreen Y reduced the 3 parameters.
• The 2nd approach studied some cellular makers of stress: oxidation and detoxification. We were able to demonstrate that a sunscreen product that limit skin heating also limit the cellular aggression (reduced generation of MDA as well as reduced needs in SOD and CAT).
These two approaches can be used in the future in order to test the IR protection of a cosmetic product.

Bibliography

1. Schroeder P, Calles C, Benesova T, et al. Photoprotection beyond ultraviolet radiation – Effective sun protection has to include protection against infrared A radiation-in- duced skin damage. Skin Pharmacol Physiol. 2010; 23: 15-17.
2. Krutmann J, Morita A, Chung JH. Sun exposure: what molecular photodermatology tells us about its good and bad sides. J Invest Dermatol. 2012; 132: 976-84.
3. Dupont E, Gomez J, Bilodeau D. Beyond UV radiation: a skin under challenge. Int. J. Cosm. Sci. 2013; 35:224-232.
4. Kim MS, Kim YK, Cho KH, Chung JH. Regulation of type I procollagen and MMP-1 expression after single or repeated exposure to infrared radiation in human skin. 2006; 128: 2491-2497.

5. Cho S, Lee MJ, Kim MS et al. Infrared plus visible light and heat from natural sunlight participate in the expression of MMPs and type I procollagen as well as infiltration of in- flammatory cell in human skin in vivo. J Dermatol Sci. 2008; 50: 123-133.
6. Schroeder P, Lademann J, Darvin ME, et al. Infrared radiation-induced matrix metalloproteinase in human skin: implications for protection. J Invest Dermatol. 2008; 128: 2491-2497.
7. Darvin ME, Haag SF, Lademann J et al. Formation of free radicals in human skin during irradiation with infrared light. J Invest Dermatol. 2010; 130: 629-631.
8. Meinke M, Haag SF, Schanzer S et al. Radical protection by sunscreens in the infrared spectral range. Photochem Photobiol. 2011; 87:452-456.