alpha-Bisabolol, a nontoxic natural compound, strongly induces apoptosis in glioma cells

Biochem Biophys Res Commun. 2004 Mar 12;315(3):589-94. doi: 10.1016/j.bbrc.2004.01.088.


In this study, alpha-bisabolol, a sesquiterpene alcohol present in natural essential oil, was found to have a strong time- and dose-dependent cytotoxic effect on human and rat glioma cells. After 24 h of treatment with 2.5-3.5 microM alpha-bisabolol, the viability of these cells was reduced by 50% with respect to untreated cells. Furthermore, the viability of normal rat glial cells was not affected by treatment with alpha-bisabolol at the same concentrations as above. Glioma cells treated with high concentration of alpha-bisabolol (10 microM) resulted in a 100% cell death. Judging from hypo-G1 accumulation, poly(ADP-ribose) polymerase cleavage, and DNA ladder formation, the cytotoxicity triggered by alpha-bisabolol resulted from apoptosis induction. Moreover, the dissipation of mitochondrial-inner transmembrane potential and the release of cytochrome c from mitochondria indicated that, in these glioma cells, apoptosis occurred through an intrinsic pathway. As pointed out by the experimental results, alpha-bisabolol may be considered a novel compound able to inhibit glioma cell growth and survival.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects*
  • Astrocytes / drug effects
  • Astrocytes / metabolism
  • Cell Line, Tumor
  • Cell Membrane Permeability / drug effects
  • Cell Survival / drug effects
  • Cytochromes c / metabolism
  • Cytoplasm / drug effects
  • Cytoplasm / metabolism
  • Cytosol / drug effects
  • Cytosol / metabolism
  • DNA Fragmentation / drug effects
  • DNA Fragmentation / physiology
  • Dose-Response Relationship, Drug
  • Drug Screening Assays, Antitumor / methods
  • Flow Cytometry
  • Glioma / drug therapy
  • Glioma / pathology*
  • Humans
  • Intracellular Membranes / drug effects
  • Intracellular Membranes / metabolism
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Monocyclic Sesquiterpenes
  • Poly(ADP-ribose) Polymerases / metabolism
  • Rats
  • Sesquiterpenes / pharmacology*


  • Antineoplastic Agents
  • Monocyclic Sesquiterpenes
  • Sesquiterpenes
  • bisabolol
  • Cytochromes c
  • Poly(ADP-ribose) Polymerases