Protection of cells from nitric oxide-mediated apoptotic death by glutathione C₆₀ derivative

Cell Biol Int. 2012 Jul;36(7):677-81. doi: 10.1042/CBI20110566.

Abstract

The influence of the glutathione C₆₀ derivative on the cytotoxicity of a highly reactive free radical NO (nitric oxide) has been investigated. Consistent with its cytoprotective abilities, the derivative scavenges ROS (reactive oxygen species) and RNS (reactive nitrogen species) both in vitro and under cell-free conditions. Moreover, the glutathione C₆₀ derivative protected PC12 cells from the cytotoxic effect of the NO-releasing compound, SNP (sodium nitroprusside). Addition of glutathione C₆₀ derivative alone did not induce apoptosis and necrosis. The results suggest that the glutathione C₆₀ derivative has the potential to prevent NO-mediated cell death without evident toxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Free Radical Scavengers / pharmacology
  • Fullerenes / pharmacology*
  • Glutathione / analogs & derivatives*
  • Glutathione / pharmacology
  • Nitric Oxide / metabolism*
  • Nitroprusside / toxicity
  • PC12 Cells
  • Rats
  • Reactive Nitrogen Species / metabolism
  • Reactive Oxygen Species / metabolism

Substances

  • Free Radical Scavengers
  • Fullerenes
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • glutathione C(60)-fullerene complex
  • Nitroprusside
  • Nitric Oxide
  • Glutathione