Objectives: To examine how the amount, subtype and distribution of melanin in skin can affect how the skin photoages.
Introduction: Casual comparison of the appearance and texture of unprotected photo-exposed hand and face skin versus skin of the secluded body sites reveals a striking impact of accumulated solar radiation on skin aging, particularly after the 3rd or 4th decades of life. The basis of this change is revealed in anatomical, histological, and ultrastructural changes in the epidermis and dermis of the skin, which result from alterations at the cellular and molecular levels. Principal among these is the marked flattening of the dermal-epidermal junction with consequent loss of rete ridges.
Materials / method: Examination of skin from normal healthy individuals of different ages and comparison to conditions with pigment loss (e.g., vitiligo) at tissue, protein and cell culture levels.
Results: Actinic skin aging-associated changes remains largely unexplained in terms of mechanism, but are underpinned by key interactions between functional units in the skin, including the epidermal-melanin- and epidermal-dermal cell-units. Some of these solar-light driven changes involve phenotype switching in dermal fibroblasts, including via their adoption of senescent phenotype with associated dysfunctional secretomes. There is increasing evidence that environmental pollution and even certain wavelengths of visible light can also contribute to the global ‘photo-aging’ response.
Conclusion: Human skin is equipped at least partially with effective protective devices against actinic damage; principal among them includes the synthesis of copious amounts melanin that acts as a near-universal stress absorber. This enigmatic indole biopolymer acts as a ‘sink’ for toxins, pollutants, drugs, as well as a redox buffer against a host of reactive oxygen species. Brown/black (or wild-type) melanin far outperforms the photo-labile red/yellow pheomelanin, which increases the vulnerability of the of the skin to photo-damage and so photo-carcinogenesis.
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