TY - JOUR

T1 - Cellular and sub-cellular responses to UVA in relation to carcinogenesis

AU - Ridley, Andrew J.

AU - Whiteside, James R.

AU - McMillan, Trevor J.

AU - Allinson, Sarah L.

PY - 2009

Y1 - 2009

N2 - PURPOSE: 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. RESULTS: 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. CONCLUSIONS: 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

AB - PURPOSE: 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. RESULTS: 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. CONCLUSIONS: 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

KW - UVA

KW - antioxidants

KW - reactive oxygen species

KW - base excision repair

KW - ATM

KW - MAPK

KW - p53

U2 - 10.1080/09553000902740150

DO - 10.1080/09553000902740150

M3 - Journal article

VL - 85

SP - 177

EP - 195

JO - International Journal of Radiation Biology

JF - International Journal of Radiation Biology

SN - 0955-3002

IS - 3

ER -