Section : Notes de congrès/conférences

Molecules AGAINST Tanning in the cosmetic world

  • In early 20th century Europe, it was considered a mark of « low-class », as it was assimilated with outdoor professional activities.
  • It is quite fashionable to tan in Western societies (Europe and North America), but is definitely not fashionable in Asia.
  • Tanning is a process induced by ultraviolet light and is a protective mechanism to shield the nucleus from its damaging effects.
  • It does this by creating an « umbrella » of melanin over the nucleus.
  • Skin repigmentation has been shown to be inducible in vitro by arginase 1 (ARG1), an enzyme which catalyzes the conversion of L-arginine to L-ornithine and urea. (The effect of arginase was shown in 1951: http://www.nature.com/jid/journal/v17/n1/full/jid195159a.html)
  • Ultraviolet-light irradiation (UV) induces overexpression of proteins such as ARG1 (methodology: proteomic analysis)
  • BEC is an inhibitor of ARG1 as shown in this study (3 cultures: BEC 3.3mM, 10mM, control)
  • Addition of BEC to cell cultures of keratinocytes (tapped stripped stratum corneum) induces:
    • increased nitrogen oxide (NO) levels  (in a statistically significant way from day 4 onwards): this implies increased NO production
    • reduced levels of urea. (in a statistically significant way and dose-dependent manner at concentrations of 10mM and over): this implies reduced urea production
  • These results were correlated with increased iNOS (inducible nitric oxide substrate), phosphorylated-p53, p53 and the Precursor of alpha melanocyte-stimulating hormone (POMC) (methodology: Western Blot and compared with non treated cultures)
  • In artificial cell cultures (Melanoderm, MatTek), the pigmentation area was increased in models treated with BEC

The authors conclude that ARG1-induced pigmentation is through activation of the p53 signaling pathway.

Comment: Although done in vitro: this study shows two things. The first one is that Ultraviolet irradiation activates p53 expression, which is the last gatekeeper against cell degenerescence. The second one, is that its effects on pigmentation could be reversed by ARG1 (study done by Fancl)

Contributors

Dr Christophe Hsu – dermatologist. Geneva, Switzerland

Source of information: P13-20. Arase N, Inhibition of melanogenesis by HLA class II molecules (Fancl study). JSID Annual Meeting (Japanese Society of Investigative Dermatology, 日本研究皮膚科学会) 2014 – Osaka, Japan