Cadmium induces reactive oxygen species generation and lipid peroxidation in cortical neurons in culture

Free Radic Biol Med. 2006 Mar 15;40(6):940-51. doi: 10.1016/j.freeradbiomed.2005.10.062. Epub 2005 Nov 21.

Abstract

Cadmium is a toxic agent that it is also an environmental contaminant. Cadmium exposure may be implicated in some humans disorders related to hyperactivity and increased aggressiveness. This study presents data indicating that cadmium induces cellular death in cortical neurons in culture. This death could be mediated by an apoptotic and a necrotic mechanism. The apoptotic death may be mediated by oxidative stress with reactive oxygen species (ROS) formation which could be induced by mitochondrial membrane dysfunction since this cation produces: (a) depletion of mitochondrial membrane potential and (b) diminution of ATP levels with ATP release. Necrotic death could be mediated by lipid peroxidation induced by cadmium through an indirect mechanism (ROS formation). On the other hand, 40% of the cells survive cadmium action. This survival seems to be mediated by the ability of these cells to activate antioxidant defense systems, since cadmium reduced the intracellular glutathione levels and induced catalase and SOD activation in these cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Cadmium / toxicity*
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Cerebral Cortex / embryology
  • Glutathione / metabolism
  • Lipid Peroxidation / drug effects*
  • Membrane Potentials / drug effects
  • Models, Biological
  • Neurons / drug effects*
  • Rats
  • Reactive Oxygen Species / metabolism*

Substances

  • Reactive Oxygen Species
  • Cadmium
  • Adenosine Triphosphate
  • Glutathione