Cellular and sub-cellular responses to UVA in relation to carcinogenesis

UVA radiation (315-400 nm) contributes to skin aging and carcinogenesis. The aim of this review is to consider the mechanisms that underlie UVA-induced cellular damage, how this damage may be prevented or repaired and the signal transduction processes that are elicited in response to it.

Exposure to ultraviolet (UV) light is well-established as the causative factor in skin cancer. Until recently, most work on the mechanisms that underlie skin carcinogenesis focused on shorter wavelength UVB radiation (280-315 nm), however in recent years there has been increased interest in the contribution made by UVA. UVA is able to cause a range of damage to cellular biomolecules including lipid peroxidation, oxidized protein and DNA damage, such as 8-oxoguanine and cyclobutane pyrimidine dimers. Such damage is strongly implicated in both cell death and malignant transformation and cells have a number of mechanisms in place to mitigate the effects of UVA exposure, including antioxidants, DNA repair, and stress signalling pathways.

The past decade has seen a surge of interest in the biological effects of UVA exposure as its significance to the process of photo-carcinogenesis has become increasingly evident. However, unpicking the unique complexity of the cellular response to UVA, which is only now becoming apparent, will be a major challenge for the field of photobiology in the 21st century.