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Premature Aging of Skin from Environmental Assaults

 Among all environmental factors, solar ultraviolet (UV) radiation is mostimportant for premature skin aging, a process accordingly also termed photoaging. Other factors include exposure to near-infrared radiation (IRA;760-1440 nm) from sunlight or artificial IRA radiation devices, tobaccosmoke, and particulate matter from airborne traffic pollution .

Within recent years substantial progress has been made in elucidating the molecular mechanisms underlying extrinsic skin aging. These studies have initially focused on photoaging of the skin. From this large body of researchit is now clear that both UVB (290-320 nm) and UVA(320-400 nm) radiation contribute to photoaging. 

UV-induced alterations at the level of thedermis are best studied and appear to be largely responsible for the phenotype of photoaged skin. It is also generally agreed that UVB acts preferentially on the epidermis, where it not only damages DNA in keratinocytes and melanocytes but also causes the production of soluble factors including proteolytic enzymes, which then in a second step affect the dermis. Incontrast, UVA radiation penetrates far more deeply on average and hence exerts direct effects on both the epidermal and the dermal compartment.UVA is also 10-100 times more abundant in sunlight than UVB, dependingon the season and time of day. It has therefore been proposed that, although UVA photons are individually far less biologically active than UVB photons, UVA radiation may be at least as important as UVB radiation for the pathogenesis of photoaging.

The exact mechanisms by which UV radiation causes premature skin agingare not yet clear, but a number of molecular pathways have been described to explain one or more of the key features of photoaged skin. Some of thes emodels are based on irradiation protocols, which use single or few UV exposures, whereas others take into account the fact that photoaging results from chronic UV damage and as a consequence employ chronic repetitive irradiation protocols. Still others rely on largely theoretic constructs rather than on experimental observations.

It should be noted that many if not most of the detrimental effects that are induced by UVB and UVA radiation also occur upon exposure of the skin to other environmental assaults, but that the molecular mechanisms and signaling pathways involved may differ substantially. As an example, UV radiation as well as IRA radiation cause collagen degradation in the skin (and thereby wrinkle formation) by upregulating the expression of collagen degrading proteases such as matrix metalloproteinase-l (MMP-l) in dermal fibroblasts and in both instances this effect is causally related to the intracellular generation of oxidative stress. 

In the case of IRA radiation, the oxidative stress is being generated within mitochondria (reactive species leak out of the mitochondrial respiratory chain as a consequence of IRA irradiation) and this intramitochondrial production of reactive oxygen species initiates a retrograde signaling response, which is directed from the mitochondria toward the cell nucleus. In marked contrast, UV radiation-induced MMP-l induction is not mediated by a retrograde mitochondrial signaling pathway, but involves a singlet oxygentriggered disturbance of cell membrane microdomains (in the case of UVA-I), or activation of intracytoplasmatic transcription factors such as the arylhydrocarbon receptor pathway (in the case of UVB) or the generation of cyclobutane pyrimidine dimers in nuclear DNA (in the case of UVB). In other words, all these environmental assaults may cause similar clinical, histological, and even molecular problems, but they are initiated and mediated through distinct intracellular pathways and thus are differentially susceptible to prevention strategies. 

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Indeed, effective prevention of UV versus IRA radiation-induced premature skin aging requires distinct antioxidants: in the case of IRA, antioxidants that preferentially localize within mitochondria work best, whereas for UV, antioxidants that accumulate in the cytoplasm or enzymes that are capable of repairing nuclear DNA will be more effective.

In this chapter we will focus on the most popular pathogenic concepts relevant for UV-induced skin aging, because photoaging is by far the best studied and probably also most relevant example of extrinsic skin aging. For more detailed information on IRA radiation and tobacco smoke-induced skin aging, interested readers should refer to a recent review.


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