Carcinogenesis, Vol 18, 1013-1020, Copyright © 1997 by Oxford University Press
A de Laat, JC van der Leun and FR de Gruijl
Although ultraviolet B (UVB wavelengths 280-315 nm) dominates the
carcinogenic effect of sunlight, ultraviolet A (UVA 315-400 nm) is
estimated to contribute 10-20% to the carcinogenic dose; a substantial
background that is not affected by a depletion of the ozone layer.
Furthermore, certain high-power modern tanning lamps emit mainly long wave
UVA (UVA1; 340-400 nm). For a proper risk estimate of UVA exposure its
carcinogenicity relative to that of UVB exposure needs to be determined
more accurately. To this end we determined the dose-time relationship for
skin tumor induction in hairless mice that were irradiated daily with
custom-made Philips 365-nm sources. Irradiation of the group exposed to the
highest of the four daily doses (430, 240, 140 and 75 kJ/m2) had to be
discontinued because severe scratching set in after 3 months (no tumors).
In the lower dose-groups the prevalence curves for skin carcinomas
(percentage of tumor-bearing mice versus logarithm of time) ran virtually
parallel, and were similar to those found with daily UVB exposure. However,
the relationship between the daily dose (D) and the median tumor induction
time (t50) appeared to differ: with UVB we found that t50 D(r) = constant,
with r = 0.6, whereas with UVA1 we found r approximately 0.4. This would
imply that 365-nm carcinogenesis shows less of a dose-dependency than UVB
carcinogenesis, and that 365-nm radiation becomes more carcinogenic,
relative to UVB, as the daily doses are lowered. This relative shift at low
doses complicates extrapolation of UVB to UVA risks in humans. Based on the
t50 from the lowest dose-group we found that the carcinogenicity at 365 nm
(per J/m2) is 0.9 x 10(-4) times that at 293 nm, the wavelength of maximum
carcinogenicity in hairless mice. This result for 365-nm carcinogenicity
falls well within the margins of error of the wavelength dependency that
was estimated earlier from experiments with broadband UV sources.
ARTICLES
Carcinogenesis induced by UVA (365-nm) radiation: the dose-time dependence of tumor formation in hairless mice
Department of Dermatology, University Hospital Utrecht, Utrecht University, The Netherlands.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  H. S. Choi, A. M. Bode, J.-H. Shim, S.-Y. Lee, and Z. Dong c-Jun N-Terminal Kinase 1 Phosphorylates Myt1 To Prevent UVA-Induced Skin Cancer Mol. Cell. Biol., April 15, 2009; 29(8): 2168 - 2180. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Zhang, G. Tsaprailis, and G. T. Bowden Nucleolin Stabilizes Bcl-XL Messenger RNA in Response to UVA Irradiation Cancer Res., February 15, 2008; 68(4): 1046 - 1054. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Mouret, C. Baudouin, M. Charveron, A. Favier, J. Cadet, and T. Douki From the Cover: Cyclobutane pyrimidine dimers are predominant DNA lesions in whole human skin exposed to UVA radiation PNAS, September 12, 2006; 103(37): 13765 - 13770. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Maeda, R. A. Espino, E. G. Chomey, L. Luong, A. Bano, D. Meakins, and V. A. Tron Loss of p21WAF1/Cip1 in Gadd45-deficient keratinocytes restores DNA repair capacity Carcinogenesis, October 1, 2005; 26(10): 1804 - 1810. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Crallan, E. Ingham, and M. N. Routledge Wavelength dependent responses of primary human keratinocytes to combined treatment with benzo[a]pyrene and UV light Mutagenesis, July 1, 2005; 20(4): 305 - 310. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Ikehata, H. Kudo, T. Masuda, and T. Ono UVA induces C->T transitions at methyl-CpG-associated dipyrimidine sites in mouse skin epidermis more frequently than UVB Mutagenesis, November 1, 2003; 18(6): 511 - 519. [Abstract] [Full Text] [PDF]
|
|