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Carcinogenesis Advance Access published online on May 5, 2006
Carcinogenesis, doi:10.1093/carcin/bgl058
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received November 29, 2005
Revised April 10, 2006
Accepted April 18, 2006

CARCINOGENESIS

Chemopreventive effects of {alpha}-santalol on ultraviolet B radiation-induced skin tumor development in SKH-1 hairless mice

Chandradhar Dwivedi 1 *, Hima B. Valluri 1, Xiangming Guan 1, and Rajesh Agarwal 2

1 Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007, USA
2 Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Health Sciences Center, Denver, CO 80202, USA

* To whom correspondence should be addressed.
Chandradhar Dwivedi, E-mail: Chandradhar.Dwivedi{at}sdstate.edu


  Abstract

Recent studies from our laboratory have shown the chemopreventive effects of {alpha}-santalol against 7,12-dimethylbenzanthracene (DMBA)-initiated and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin tumor development in mice. The objective of the present investigation was to study the effects of {alpha}-santalol on ultraviolet B (UVB) radiation-induced skin tumor development and UVB-caused increase in epidermal ornithine decarboxylase (ODC) activity in female hairless SKH-1 mice. For the tumor studies, 180 mice were divided into three groups of 60 mice in each, and each group was divided into two subgroups of 30 mice. The first subgroup served as control and treated topically on the dorsal skin with acetone. The second subgroup served as experimental and treated topically on the dorsal skin with {alpha}-santalol (5%, w/v in acetone). The tumorigenesis in the first group was initiated with UVB-radiation and promoted with TPA, in the second group was initiated with DMBA and promoted with UVB radiation, and in the third group was both initiated and promoted with UVB radiation. In each case, the study was terminated at 30 weeks. Topical application of {alpha}-santalol significantly (P<0.05) decreased tumor incidence and multiplicity in all the three protocols suggesting its chemopreventive efficacy against UVB radiation-caused tumor initiation, tumor promotion and complete carcinogenesis. In a short-term biochemical study, topical application of {alpha}-santalol also significantly (P<0.05) inhibited UVB-induced epidermal ODC activity. Together, for the first time, our findings suggest that {alpha}-santalol could be a potential chemopreventive agent against UVB-induced skin tumor development and, therefore, warrants further investigations.

Keywords: {alpha}-santalol; photocarcinogenesis; chemoprevention; Ultraviolet radiation; skin cancer.
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