Induction of apoptosis by capsaicin in A172 human glioblastoma cells

Cancer Lett. 2000 Dec 8;161(1):121-30. doi: 10.1016/s0304-3835(00)00608-x.

Abstract

Capsaicin induced apoptosis of A172 human glioblastoma cells in a time- and dose-dependent manner. Neither capsazepine, a vanilloid receptor antagonist, nor bis-(o-aminophenoxy)-ethane-N,N,N', N'-tetraacetic acid/acetoxymethyl ester (BAPTA/AM), an intracellular Ca(2+) chelator, significantly inhibited the capsaicin-induced apoptosis, although capsaicin increased intracellular Ca(2+) level. Capsaicin markedly reduced the basal generation of reactive oxygen species (ROS) and lipid peroxidation. Exogenous application of H(2)O(2) significantly prevented the cells from the apoptosis by capsaicin. Treatment with N-acetyl cysteine alone induced both reduction of the basal production of ROS and apoptosis. Taken together, these results suggest that capsaicin induced apoptosis in A172 cells and that vanilloid receptors and intracellular Ca(2+) may not be involved in the apoptotic mechanism of capsaicin. Reduction of the basal generation of ROS may play a role in the induction of apoptosis by capsaicin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Brain Neoplasms / drug therapy
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / pathology*
  • Calcium / metabolism
  • Capsaicin / analogs & derivatives*
  • Capsaicin / pharmacology*
  • Dose-Response Relationship, Drug
  • Glioblastoma / drug therapy
  • Glioblastoma / metabolism
  • Glioblastoma / pathology*
  • Humans
  • Kinetics
  • Lipid Peroxidation / drug effects
  • Reactive Oxygen Species / metabolism
  • Receptors, Drug / physiology
  • Tumor Cells, Cultured / drug effects

Substances

  • Reactive Oxygen Species
  • Receptors, Drug
  • capsazepine
  • Capsaicin
  • Calcium