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UV-induced free radical formation in skin refers to the generation of reactive oxygen species (ROS) and other radical species following exposure to ultraviolet radiation [1]. This process is primarily driven by UVA-mediated photosensitization and UVB-induced photochemical reactions, leading to oxidative damage of cellular components such as DNA, proteins, and lipids [1]. The accumulation of these radicals triggers inflammatory pathways, including the activation of NF-kappaB, and degrades the extracellular matrix through the induction of matrix metalloproteinases (MMPs) [2]. These molecular events are central to the pathogenesis of photoaging, characterized by wrinkles and loss of skin elasticity, as well as photocarcinogenesis [2]. While not a single molecular target like a receptor or enzyme, this physiological process is the primary focus of photoprotective strategies in dermatology. Therapeutic interventions involve the use of topical antioxidants, such as Vitamin C and Vitamin E, which neutralize radicals, and UV filters that prevent radical formation by absorbing or reflecting radiation [3]. Managing this process is essential for reducing the long-term risk of skin cancers, including melanoma and squamous cell carcinoma [2]. Sources: [1] https://pubmed.ncbi.nlm.nih.gov/23903066/ [2] https://www.ncbi.nlm.nih.gov/books/NBK482277/ [3] https://pubchem.ncbi.nlm.nih.gov/compound/Ascorbic-acid
Antioxidants neutralize free radicals by donating electrons to stabilize them, while sunscreens prevent their formation by absorbing or reflecting UV radiation before it can interact with skin sensitizers.
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