Effects of cadmium on lymphocyte activation

Biochim Biophys Acta. 1989 Mar 28;1011(1):25-32. doi: 10.1016/0167-4889(89)90073-6.

Abstract

The effects of cadmium (Cd) on phytohemoagglutinin or phorbol myristate acetate-induced lymphocyte activation were investigated and a dose-dependent inhibition of cell proliferation was found. Kinetic studies revealed that the Cd-sensitive step is an early event of T cell stimulation. Failure of IL2 secretion and reduction of IL2 receptor expression in the Cd-treated cells are also reported. Regardless of which mechanism is responsible for Cd effects, our studies show that the inhibition of lymphocyte activation is associated with reduced [3H]phorbol dibutyrate binding to Ca2+-phospholipid-dependent protein kinase and altered breakdown of phosphatidylinositols. Thus, Cd interferes with two biochemical events which play a critical role in lymphocyte signal transduction and activation.

MeSH terms

  • Adult
  • Cadmium / pharmacology*
  • Cadmium Chloride
  • Cadmium Radioisotopes
  • Calcium / pharmacology
  • Cell Division / drug effects
  • Cell Membrane / metabolism
  • Dose-Response Relationship, Drug
  • Humans
  • Interleukins / metabolism
  • Kinetics
  • Lymphocyte Activation / drug effects*
  • Lymphocytes / cytology
  • Lymphocytes / drug effects
  • Lymphocytes / physiology
  • Phorbol 12,13-Dibutyrate / metabolism
  • Phosphatidylinositols / metabolism
  • Phospholipids / pharmacology
  • Phytohemagglutinins / pharmacology
  • Protein Kinases / metabolism
  • Receptors, Interleukin-2 / metabolism
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Cadmium Radioisotopes
  • Interleukins
  • Phosphatidylinositols
  • Phospholipids
  • Phytohemagglutinins
  • Receptors, Interleukin-2
  • Cadmium
  • Phorbol 12,13-Dibutyrate
  • Protein Kinases
  • Cadmium Chloride
  • Tetradecanoylphorbol Acetate
  • Calcium