Abstract
Photoaging and photocarcinogenesis are primarily due to solar ultraviolet (UV) radiation, which alters DNA, cellular antioxidant balance, signal transduction pathways, immunology, and the extracellular matrix (ECM). The DNA alterations include UV radiation induced thymine-thymine dimers and loss of tumor suppressor gene p53. UV radiation reduces cellular antioxidant status by generating reactive oxygen species (ROS), and the resultant oxidative stress alters signal transduction pathways such as the mitogen-activated protein kinase (MAPK), the nuclear factor-kappa beta (NF-κB)/p65, the janus kinase (JAK), signal transduction and activation of transcription (STAT) and the nuclear factor erythroid 2-related factor 2 (Nrf2). UV radiation induces pro-inflammatory genes and causes immunosuppression by depleting the number and activity of the epidermal Langerhans cells. Further, UV radiation remodels the ECM by increasing matrixmetalloproteinases (MMP) and reducing structural collagen and elastin. The photoprotective strategies to prevent/treat photoaging and photocarcinogenesis include oral or topical agents that act as sunscreens or counteract the effects of UV radiation on DNA, cellular antioxidant balance, signal transduction pathways, immunology and the ECM. Many of these agents are phytochemical derivatives and include polyphenols and non-polyphenols. The flavonoids are polyphenols and include catechins, isoflavones, proanthocyanidins, and anthocyanins, whereas the non-flavonoids comprise mono phenolic acids and stilbenes. The natural sources of polyphenols include tea, cocoa, grape/wine, soy, pomegranate, and Polypodium leucotomos. The non-phenolic phytochemicals include carotenoids, caffeine and sulphoraphance (SFN). In addition, there are other phytochemical derivatives or whole extracts such as baicalin, flavangenol, raspberry extract, and Photomorphe umbellata with photoprotective activity against UVB radiation, and thereby carcinogenesis.
Highlights
Premature skin aging and development of malignant cutaneous tumors, melanoma and non-melanoma, are interrelated issues that are increasingly important problems in the field of dermatology
We review the mechanisms of photoaging and photocarcinogenesis, the photoprotective strategies, and the phytochemicals that can provide photoprotection
The photoprotective strategies include the blockade of UV photon incidence, DNA repair, removal of reactive oxygen species (ROS), anti-inflammation, and immunomodulation
Summary
Premature skin aging and development of malignant cutaneous tumors, melanoma and non-melanoma, are interrelated issues that are increasingly important problems in the field of dermatology. Skin aging is important aesthetically, whereas skin cancer is a direct threat to the health of the patient. We review the mechanisms of photoaging and photocarcinogenesis, the photoprotective strategies, and the phytochemicals that can provide photoprotection. The photoaging and photocarcinogenic mechanisms are predominantly the effect of solar ultraviolet (UV) radiation that induces reactive oxygen species (ROS) and alters DNA/cellular homeostasis, which together alter signal transduction pathways and inflammatory cascade and induce immunosuppression and extracellular matrix (ECM). The photoprotective strategies include the blockade of UV photon incidence, DNA repair, removal of ROS (antioxidant), anti-inflammation, and immunomodulation. The photochemical derivatives that are effective for these photoprotective strategies are polyphenols, flavonoids and non-flavonoids, non-phenolic derivatives, and whole plant extracts
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