Literature DB >> 9163689

Carcinogenesis induced by UVA (365-nm) radiation: the dose-time dependence of tumor formation in hairless mice.

A de Laat1, J C van der Leun, F R de Gruijl.   

Abstract

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.

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Year:  1997        PMID: 9163689     DOI: 10.1093/carcin/18.5.1013

Source DB:  PubMed          Journal:  Carcinogenesis        ISSN: 0143-3334            Impact factor:   4.944


  27 in total

Review 1.  UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer.

Authors:  Gerd P Pfeifer; Ahmad Besaratinia
Journal:  Photochem Photobiol Sci       Date:  2011-08-01       Impact factor: 3.982

2.  Ultraviolet A does not induce melanomas in a Xiphophorus hybrid fish model.

Authors:  David L Mitchell; André A Fernandez; Rodney S Nairn; Rachel Garcia; Lakshmi Paniker; David Trono; Howard D Thames; Irma Gimenez-Conti
Journal:  Proc Natl Acad Sci U S A       Date:  2010-05-03       Impact factor: 11.205

Review 3.  Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.

Authors:  Aiman Q Khan; Jeffrey B Travers; Michael G Kemp
Journal:  Environ Mol Mutagen       Date:  2018-02-21       Impact factor: 3.216

4.  Silibinin is a potent sensitizer of UVA radiation-induced oxidative stress and apoptosis in human keratinocyte HaCaT cells.

Authors:  Sreekanth Narayanapillai; Chapla Agarwal; Cynthia Tilley; Rajesh Agarwal
Journal:  Photochem Photobiol       Date:  2012-01-10       Impact factor: 3.421

5.  Activation of p38 MAP kinase and JNK pathways by UVA irradiation.

Authors:  Jack Zhang; G Tim Bowden
Journal:  Photochem Photobiol Sci       Date:  2011-08-22       Impact factor: 3.982

6.  The role of JNK and p38 MAPK activities in UVA-induced signaling pathways leading to AP-1 activation and c-Fos expression.

Authors:  Amy L Silvers; Michael A Bachelor; G Timothy Bowden
Journal:  Neoplasia       Date:  2003 Jul-Aug       Impact factor: 5.715

7.  Nucleolin stabilizes Bcl-X L messenger RNA in response to UVA irradiation.

Authors:  Jack Zhang; George Tsaprailis; G Tim Bowden
Journal:  Cancer Res       Date:  2008-02-15       Impact factor: 12.701

8.  Inhibition of UVA-induced apoptotic signaling pathway by polypeptide from Chlamys farreri in human HaCaT keratinocytes.

Authors:  Jin-Lian Li; Ning Liu; Xue-Hong Chen; Mi Sun; Chun-Bo Wang
Journal:  Radiat Environ Biophys       Date:  2007-05-09       Impact factor: 1.925

Review 9.  Cancer prevention research - then and now.

Authors:  Ann M Bode; Zigang Dong
Journal:  Nat Rev Cancer       Date:  2009-06-18       Impact factor: 60.716

10.  UVA causes dual inactivation of cathepsin B and L underlying lysosomal dysfunction in human dermal fibroblasts.

Authors:  Sarah D Lamore; Georg T Wondrak
Journal:  J Photochem Photobiol B       Date:  2013-03-28       Impact factor: 6.252

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