Aluminium perturbs oscillatory phosphoinositide-mediated calcium signalling in hormone-stimulated hepatocytes

Biochem J. 1990 Jul 15;269(2):547-50. doi: 10.1042/bj2690547.

Abstract

Aluminium is known to be toxic to cells from bone, brain and bone marrow but the molecular target(s) affected by Al3+ are not known. We show here that Al3+ disrupts the oscillatory free Ca2+ responses of hepatocytes exposed to the Ca2(+)-mobilizing agonist phenylephrine. Al3+ initially increases the frequency of the oscillations and later induces broad Ca2+ spikes lasting several minutes. These broad spikes persist after removal of both agonist and Al3+ from the medium. In the absence of agonist, Al3+ has no effect on free Ca2+. The data suggest that some component(s) of the receptor-phosphoinositide-Ca2+ signalling pathway might be the site at which Al3+ exerts toxic effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Citrates / pharmacology*
  • Citric Acid
  • Deferoxamine / pharmacology
  • Kinetics
  • Liver / drug effects
  • Liver / metabolism*
  • Periodicity
  • Phenylephrine / pharmacology*
  • Phosphatidylinositols / metabolism*
  • Rats
  • Signal Transduction / drug effects*

Substances

  • Citrates
  • Phosphatidylinositols
  • Phenylephrine
  • Citric Acid
  • Deferoxamine
  • Calcium