Carcinogenesis Advance Access published online on December 23, 2004
Carcinogenesis, doi:10.1093/carcin/bgi008
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1 Department of Health Sciences, University of Genoa, Via A. Pastore 1, I-16132 Genoa, Italy
* To whom correspondence should be addressed. The light emitted by halogen quartz bulbs contains a broad spectrum of UV wavelengths, is strongly genotoxic, and is a potent inducer of skin tumors in hairless mice. By using an UV-C filter, this light mimics solar radiation and induces a variety of genomic and transcriptional alterations in mouse skin. UV-related carcinogenesis involves depletion of antioxidants and glutathione in skin cells. On this basis, we evaluated modulation of carcinogenicity of UV-C-covered halogen lamps in SKH-1 hairless mice by the antioxidants N-acetyl-L-cysteine (NAC) and ascorbic acid (AsA). Both agents were given in the drinking water, either individually or in combination. The earliest skin lesions were detected after 300 days of exposure to light and became confluent in a number of mice after 480 days. NAC administration prolonged the latency time by 90 days. Moreover, NAC considerably and significantly decreased both incidence and multiplicity of light-induced skin tumors, prevented the occurrence of malignant lesions (squamocellular carcinomas), and reduced the tumor size. In contrast, AsA, which may behave as a prooxidant rather than an antioxidant, increased the multiplicity of total skin tumors, carcinomas in situ, and squamocellular carcinomas. Co-administration of NAC with AsA significantly attenuated the negative effect of AsA, presumably due to the ability of this thiol to maintain a reduced environment. Therefore, in agreement with our previous in vitro findings, oral NAC is able to attenuate the detrimental effects of AsA.
Received October 19, 2004
Revised December 14, 2004
Accepted December 15, 2004
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
Modulation of light-induced skin tumors by N-acetylcysteine and/or ascorbic acid in hairless mice
Silvio De Flora, E-mail: sdf{at}unige.it
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