UVA radiation generates a significant oxidative stress in skin cells which is further enhanced by the release of the pro-oxidant catalysts iron and heme, and exacerbated by UVA-mediated destruction of cellular reducing equivalents and the antioxidant enzyme catalase. An important consequence of this altered redox state is the generation of oxidized membrane components in the form of 4-hydroxynonenal, ceramides and oxidized phospholipids, all of which are potent signalling molecules which lead to modulation of the expression of many genes. Transcription factors (such as nuclear factor kappa-light-chain-enhancer of activated B cells) and several genes (e.g. interleukins, intercellular adhesion molecule and 1, hemeoxygenase 1) involved in the inflammatory response are dramatically modified by UVA. Levels of both antioxidant and pro-oxidant proteins, including manganese-dependent superoxide dismutase, glutathione peroxidase, hemeoxygenase 1, NADPH oxidase, ferritin, and methionine-S-sulfoxidereductase, are increased by UVA treatment and following moderate dose levels these will contribute to either the restoration or a further perturbation of redox homeostasis. Finally, UVA induces a whole set of matrix metalloproteinases and proteases, primarily in cells of dermal origin, which can contribute to the long-term consequences of UVA exposure of skin.