Glutathione-mediated effects of lithium in decreasing protein oxidation induced by mitochondrial complex I dysfunction

J Neural Transm (Vienna). 2015 Jun;122(6):741-6. doi: 10.1007/s00702-014-1318-8. Epub 2014 Sep 27.

Abstract

The aim of this study was to elucidate whether glutathione is involved in lithium's ability to decrease carbonylation and nitration produced by complex I inhibition, which is consistently found in BD. Neuroblastoma cells were treated with rotenone, a complex I inhibitor. Our results suggest that glutathione is essential for lithium's ability to ameliorate rotenone-induced protein carbonylation, but not nitration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Electron Transport Complex I / antagonists & inhibitors*
  • Glutathione / metabolism*
  • Humans
  • Immunohistochemistry
  • Lithium Compounds / pharmacology*
  • Neuroblastoma / metabolism
  • Protein Carbonylation / drug effects*
  • Rotenone / pharmacology
  • Tyrosine / analogs & derivatives*
  • Tyrosine / metabolism
  • Uncoupling Agents / pharmacology

Substances

  • Lithium Compounds
  • Uncoupling Agents
  • Rotenone
  • 3-nitrotyrosine
  • Tyrosine
  • Electron Transport Complex I
  • Glutathione