Department of Dermatology, Heinrich Heine, University Düsseldorf, Germany.
- Page(s) : 170-1
- Published in: 2001
Chronic sun exposure causes photoaging of human skin, a process that is characterized by clinical, histological and biochemical changes which differ from alterations in chronologically aged but sun-protected skin. Within recent years substantial progress has been made in unraveling the underlying mechanisms of photoaging . A question of great importance has been: Which parts of the sunlight cause which feature of photoaging? Ultraviolet rays penetrate into the skin and according to their wavelength interact with different cells that are located at different depths. Ultraviolet radiation of the shorter wavelength (UVB; 290-320 nm) is mostly absorbed in the epidermis and affects predominantly epidermal cells, i.e. keratinocytes, while longer wavelengths (UVA; 320-400 nm) penetrate deeper and can interact with both epidermal keratinocytes and dermal fibroblasts. Once UV light has reached the cells of the skin, the different wavelengths exert their specific effects. UVA rays mostly act indirectly through generation of reactive oxygen species (ROS) which subsequently can exert a multitude of effects such as lipidperoxidation, activation of transcription factors and generation of DNA-strand breaks. While UVB light can also generate ROS, its main action is the direct interaction with DNA via induction of DNA damage .
Exposure of human skin to UVA rays has been shown to trigger two of the major pathways leading to photoaging: (i) induction of matrixmetalloproteinases and (ii) of mutations in mitochondrial DNA.