Influence of selenium on 3-methylcholanthrene induced skin carcinogenesis in mice

M P Bansal1, G Gupta

  • 1Department of Biophysics, Panjab University, Chandigarh, India.

Insights

Selenium treatment reduced skin tumor incidence and burden in mice exposed to 3-methylcholanthrene (MCA). This suggests selenium enhances detoxification pathways, not carcinogen metabolism, to suppress cancer development.

Area of Science:

  • Oncology
  • Toxicology
  • Biochemistry

Background:

  • 3-methylcholanthrene (MCA) is a known carcinogen used to induce skin tumors in experimental models.
  • Selenium is a trace element with potential chemopreventive properties against various cancers.

Purpose of the Study:

  • To investigate the effect of selenium treatment on the incidence and development of skin papillomas/tumors induced by MCA in male ICRC mice.
  • To explore the underlying mechanisms by which selenium may exert its protective effects.

Main Methods:

  • Male ICRC mice were treated with selenium.
  • Skin tumors were induced by topical application of 3-methylcholanthrene (MCA).
  • Tumor incidence, burden, and latent period were assessed. Aryl hydrocarbon hydroxylase (AHH) and glutathione S-transferase (GST) activities were measured in skin and liver tissues.

Main Results:

  • Selenium treatment significantly decreased the percentage incidence and tumor burden of skin papillomas/tumors.
  • The latent period for tumor induction was significantly increased in selenium-treated mice.
  • No significant influence of selenium was observed on aryl hydrocarbon hydroxylase (AHH) activity in skin and liver.
  • A significant increase in glutathione S-transferase (GST) activity was observed in selenium-treated mice.

Conclusions:

  • Selenium treatment demonstrates chemopreventive effects against MCA-induced skin carcinogenesis in mice.
  • The protective mechanism of selenium likely involves the enhancement of detoxication pathways, specifically via increased glutathione S-transferase (GST) activity.
  • Selenium does not appear to suppress carcinogenesis by altering the activation or inactivation of the carcinogen (MCA).