New strategies to slow down the photoaging of human skin

Abstract

This paper is concerned with the photoaging of human skin and strategies to slow down this process. These strategies have emerged from our experience with free radical mediated diseases like discoid lupus erythematosus and eczema solare, where sufferers are extremely sensitive to sunlight. The photoaging process of the skin in the presence of natural sunlight or artificial UV-sources happens continuously and leads in time to dryness, deep wrinkles, sagging, loss of elasticity, mottled pigmentation, and skin telangiectasia. Typical biomarkers include: a strong generation of free radicals, lipid peroxidation, collagenase activation, glycation/oxidation of proteins (AGE products), activation of p53 transcription factors, low DNA repair capacity, and cumulative DNA mutations. Clinically, the adverse effects of natural sunlight and other UV-sources on normal human skin may vary from sunburn with erythema, edema, and DNA damage (12-24 hrs. after UV-exposure) to polymorphic light reaction (eczema solare), solar actinic elastosis, and actinic hyperkeratosis (a common precancerous condition), up to different skin cancer forms like basal cell carcinoma (BCC), squamous cell carcinoma (SCC) or malignant melanoma (MM). The study of the lipid, protein, and DNA oxidative damage triggered by free radical attack and subsequent sunlight exposure has enabled us to develop appropriate strategies to slow down or block these reactions, and has also made it possible for us to design innovative skin care formulations. Studies have shown that the use of the described hypoallergenic topical products resulted in a significant improvement of the skin structure and appearance within 30 days, as documented with the standardized Surface Evaluation of Living Skin (SELS) methodology.