Hydrogen peroxide induces neurite degeneration: Prevention by tocotrienols

Free Radic Res. 2011 Jun;45(6):681-91. doi: 10.3109/10715762.2011.567984. Epub 2011 Mar 21.

Abstract

Reactive oxygen species (ROS) may attack several types of tissues and chronic exposure to ROS may attenuate various biological functions and increase the risk of several types of serious disorders. It is known that treatments with ROS attack neurons and induce cell death. However, the mechanisms of neuronal change by ROS prior to induction of cell death are not yet understood. Here, it was found that treatment of neurons with low concentrations of hydrogen peroxide induced neurite injury, but not cell death. Unusual bands located above the original collapsin response mediator protein (CRMP)-2 protein were detected by western blotting. Treatment with tocopherol or tocotrienols significantly inhibited these changes in neuro2a cells and cerebellar granule neurons (CGCs). Furthermore, prevention by tocotrienols of hydrogen peroxide-induced neurite degeneration was stronger than that by tocopherol. These findings indicate that neurite beading is one of the early events of neuronal degeneration prior to induction of death of hydrogen peroxide-treated neurons. Treatment with tocotrienols may protect neurite function through its neuroprotective function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Cell Death / drug effects
  • Cell Shape / drug effects
  • Cells, Cultured
  • Hydrogen Peroxide / pharmacology*
  • Intercellular Signaling Peptides and Proteins / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Nerve Tissue Proteins / metabolism*
  • Neurites / drug effects*
  • Neurites / pathology
  • Oxidants / pharmacology*
  • Oxidative Stress
  • Tocotrienols / pharmacology*

Substances

  • Antioxidants
  • Intercellular Signaling Peptides and Proteins
  • Nerve Tissue Proteins
  • Oxidants
  • Tocotrienols
  • collapsin response mediator protein-2
  • Hydrogen Peroxide