Evaluation of sunscreens efficacy in cytoprotection against UV radiation in human dermal fibroblast
Author: Samara Eberlin
Published at: September 21, 2015
23rd IFSCC (International Federation of Societies of Cosmetic Chemists) Conference, Zurich, 21-23 September, 2015.
Pereira AFC, Torloni LBO, Lage R, Cascais LC, Andrade CC, Yamashita JT, Moreira F, Clerici SP, Eberlin S, Pinheiro ALTA, Pinheiro AS.
The generation and activation of reactive oxygen species and other reactive agents can cause damage to cellular DNA, and the immediate repair capacity of such damage is an important cellular mechanism that protects cells and maintains genetic stability, preventing early oncogenesis. Mammalian cells have a defense mechanism designed to maintain genomic integrity and prevent the establishment of permanent damage resulting from genotoxic stress. In this context, the GADD45a protein (growth arrest DNA damage 45 alpha) plays a key role as a cellular stress sensor through interaction with other proteins. In response to stress, GADD45a can promote the control of cell cycle regulation, DNA repair, epigenetic changes, apoptosis, survival, and senescence. The purpose of this study was to evaluate the in vitro effectiveness of 18 sunscreen formulations in protecting against photodamage caused by ultraviolet radiation (UV) in cultured human fibroblasts. Our results showed that UV radiation produced a significant reduction of approximately 60% in the production of GADD45a when compared to the non-irradiated control baseline (P<0.001). One possible explanation for this effect is the increased consumption and degradation of this protein as a result of genotoxic stress, which could result in a transient reduction in the levels of GADD45a in fibroblast cultures. As mentioned, the absence of this protein can lead to genomic instability and deficiencies in the repair of DNA damage. On the other hand, concomitant incubation of cell cultures with photoprotective formulations prevented the marked reduction of this protein caused by UV radiation, promoting up to 100% protection against the decrease in GADD45a. Extrinsic aging is attributed to changes in the skin due to lifestyle, being influenced mainly by ultraviolet radiation (UV), but also by pollution resulting from smoking, chemicals, heat, and other environmental insults. One of the main targets of UV radiation is DNA. The nitrogenous bases may undergo structural changes resulting in pyrimidine dimers that can destabilize the DNA molecule. Under normal exposure conditions, the body has enzyme systems that repair these changes in thymines, but with cumulative and prolonged exposures, this system can fail, and UV radiation can trigger mutations in the DNA structure that lead to the activation of proto-oncogenes. The results presented in this work allow us to infer that cosmetic sunscreens have an important effect in the process of DNA damage repair generated as a result of genotoxic stress from UV radiation by reducing GADD45a consumption and degradation.