ABSTRACT
Exposure of human or mouse skin to UVB radiation is reported to induce an accelerated generation of reactive oxygen species (ROS) (Bickers and Athar 2006), which are an inherent cellular metabolism. Through a series of one-electron subtractions, molecular oxygen is converted to superoxide anion, hydrogen peroxide, hydroxyl radical, and, finally, water. Most of these reactions occur in the mitochondria and are related to energy production. Cellular enzymes and controlled metabolic processes ordinarily keep oxidative damage to cells at a minimum
(Bergendi et al. 1999). However, in times of increased oxidative stress, including high metabolic demands and external injuries, such as sunlight, smoking, and pollution, oxidative damage may occur. Previous observations suggest that a ROS can act as both an initiator as well as a promoter of tumors by damaging critical cellular macromolecules, such as DNA, proteins, and lipids, and by acting as a stimulator or inducer of cell-signaling molecules. Skin-related disorders, such as photoaging and photocarcinogenesis, are believed to be mediated, at least in part, by ROS generation. Furthermore, UV irradiation results in the induction of matrix metalloproteinases (MMPs), which degrade the collagen and connective tissue components of the skin and block the transforming growth factor-beta type II (TGF-β2) receptor/ Smad signaling and also activate an activator protein (AP)-l, which, in turn, is triggered by a series of mitogen-activated protein kinases (MAPKs) (Quan et al. 2004). In addition, nuclear factor kappa B (NF-κB), a transcription factor, is also activated by UV irradiation. It is suggested that both AP-1 and NF-κB, which are activated by ROS, may provide the complex driving force that results in a series of complex biological interactions, resulting in skin diseases (Bowden 2004) (Figure 14.1).
