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Sunscreen cosmetic protects human fibroblast cultures against UVA-induced autophagy

Sunscreen cosmetic protects human fibroblast cultures against UVA-induced autophagy
Posted by: Samara Eberlin in 08 de Outubro de 2014

23th EADV Congress (European Academy of Dermatology and Venereology); Amsterdam, October, 8-12, 2014.
Clerici SP, Eberlin S, Polettini AJ, Pereira AFC,,Dolis E; Cascais LC, Lage R, Torloni LBO; Costa A.

Autophagy is an evolutionarily conserved process in eukariotic cell for degradation and recycling of long-lived proteins and cytoplasmic organelles. Autophagy has a survival and cytoprotective function and can be activated by various stress stimuli including nutrient starvation and DNA damage triggered by chemical substances, reactive oxygen species and ionizing radiation. The ultraviolet (UV) radiation induces DNA damage, autophagy and apoptosis in prolonged exposure. A physiological event like aging or deleterious events like UV radiation induces oxidation and aggregate formation of oxidized proteins. Lipofucsin is one of them and is considered a biological marker of senescence. In this study, we evaluated the protective effect of a sunscreen cosmetic product (SC) against UVA-induced autophagy with sudan black B (SBB) specific stain of lipofucsin using an in vitro model of human fibroblasts. UVA-induced autophagy can be measured by the presence of visible perinuclear and cytoplasmic aggregates of lipofucsin in HFF-1 cells staining with SBB as dark blueblack granules, when compared to control group. Concomitant Incubation of HFF-1 with SC promoted a clear reduction in lipofucsin accumulation, acquiring the same characteristics of the control group. Considering the reduced lipofucsin formation in fibroblasts cultures treated with SC, we suggest a possible effect of this product on the optimization of protein recycling process culminating in a reduction in the accumulation of oxidized proteins. Studies are in progress in our laboratory in order to investigate additional mechanisms underlying autophagy process, as well as, synthesis of proteasome and MAP1LC3.