INTRODUCTION
Despite numerous public warnings about protecting the skin against sun's UV exposure and extensive research into topical protective formulations, the incidence of melanoma and non-melanoma skin cancers continues to rise.1 However, UV exposure to skin can also lead to signs of aging, such as wrinkling and pigmentary disorders, including hyperpigmentation and photocarcinogenesis.2,3 For decades, researchers have been working on topical skincare products that contain DNA repair enzymes, and collagen or collagen-protecting components to protect skin against UV-induced damage and reduce signs of skin aging and carcinogenesis.4-6 As DNA repair machinery works to remove UV-induced DNA damage, mutations can be introduced into DNA. If these mutations occur in tumor-suppressive genes such as p53 or others, skin carcinogenesis can occur.7 Active DNA repair enzymes themselves have been formulated to initiate the DNA repair process more quickly and effectively than the natural repair proteins.8 There remains a need to explore alternative methods that can potentially mitigate the effects of sun exposure. This involves considering innovative solutions that offer protection against the harmful effects of sunlight, thereby broadening the approach to sun-related issues more comprehensively.
UV-exposed cells generate mutagenic photoproducts, primarily from absorbing radiation in the UVB range (280-320 nm). These include cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) photoproducts within the DNA of cells in the epidermal skin layers. CPDs, being slower to repair compared to (6-4) photoproducts, emerge as the key contributors to mutations in mammals.9 Current photoprotective agents work by absorbing, reflecting, or scattering UV radiation. However, their effectiveness is constrained by the production of potentially harmful photodegradation products for the skin.10-13
Previous research has shown that the dinucleotide pTpT, isolated from DNA, offers protection against UV-induced skin tumors in mice, including melanoma and non-melanoma skin cancer.14-16 However, these molecules have notable drawbacks, including instability, high production cost, and the complexity involved in their preparation and purification. We created a biomimetic
UV-exposed cells generate mutagenic photoproducts, primarily from absorbing radiation in the UVB range (280-320 nm). These include cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) photoproducts within the DNA of cells in the epidermal skin layers. CPDs, being slower to repair compared to (6-4) photoproducts, emerge as the key contributors to mutations in mammals.9 Current photoprotective agents work by absorbing, reflecting, or scattering UV radiation. However, their effectiveness is constrained by the production of potentially harmful photodegradation products for the skin.10-13
Previous research has shown that the dinucleotide pTpT, isolated from DNA, offers protection against UV-induced skin tumors in mice, including melanoma and non-melanoma skin cancer.14-16 However, these molecules have notable drawbacks, including instability, high production cost, and the complexity involved in their preparation and purification. We created a biomimetic
