Effects of alpha-santalol on proapoptotic caspases and p53 expression in UVB irradiated mouse skin

Anticancer Res. 2008 Jan-Feb;28(1A):129-32.

Abstract

Background: Cancer chemoprevention by naturally occurring agents, especially phytochemicals, minerals and vitamins has shown promising results against various malignancies in a number of studies both under in vitro and in vivo conditions. One such phytochemical, alpha-santalol, a major component of sandalwood oil, is effective in preventing skin cancer in both chemically and UVB-induced skin cancer development in CD-1, SENCAR and SKH-1 mice; however, the mechanism of its efficacy is not fully understood. The objective of the present investigation was to study the effects of alpha-santalol on apoptosis proteins and p53 in UVB-induced skin tumor development in SKH-1 mice to elucidate the mechanism of action.

Materials and methods: Female SKH-1 mice were divided into two groups: Group 1, which served as control received topical application of acetone (0.1 ml) one hour before UVB treatment; Group 2 received alpha-santalol (0.1 ml, 5% w/v in acetone, topical) one hour prior to UVB treatment. UVB-induced promotion was continued for 30 weeks.

Results: Pre-treatment with alpha-santalol one hour prior to UVB exposure significantly (p < 0.05) reduced tumor incidence and multiplicity, and resulted in a significant (p < 0.05) increase in apoptosis proteins, caspase-3 and -8 levels and tumor suppressor protein, p53.

Conclusion: These results suggest that alpha-santalol prevents skin cancer development by inducing proapoptotic proteins via an extrinsic pathway and increasing p53.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Apoptosis / radiation effects
  • Caspase 3 / biosynthesis
  • Caspase 8 / biosynthesis
  • Female
  • Mice
  • Mice, Inbred SENCAR
  • Neoplasms, Radiation-Induced / etiology
  • Neoplasms, Radiation-Induced / prevention & control*
  • Polycyclic Sesquiterpenes
  • Sesquiterpenes / pharmacology*
  • Skin / drug effects*
  • Skin / enzymology
  • Skin / metabolism*
  • Skin / radiation effects
  • Skin Neoplasms / etiology
  • Skin Neoplasms / prevention & control*
  • Tumor Suppressor Protein p53 / biosynthesis*
  • Ultraviolet Rays

Substances

  • Polycyclic Sesquiterpenes
  • Sesquiterpenes
  • Tumor Suppressor Protein p53
  • santalol
  • Caspase 3
  • Caspase 8