Over-expression of α-synuclein 98 triggers intracellular oxidative stress and enhances susceptibility to rotenone

Neurosci Lett. 2011 Mar 17;491(2):148-52. doi: 10.1016/j.neulet.2011.01.026. Epub 2011 Jan 14.

Abstract

The α-synuclein protein is a major component of Lewy bodies found in the brains of patients with Parkinson's disease (PD). Recently, α-synuclein 98 (α-syn98), a small isoform of the wild type protein was isolated. The neurotoxicity of this protein was assessed by over-expressing α-syn98 in dopaminergic cells. Enhanced expression of α-syn98 was insufficient to adversely affect the survival of neurons or to promote aggregation of the protein. However, when exposed to rotenone, α-syn98 over-expressing dopaminergic cells demonstrated significantly increased cytotoxicity and aggregate formation. Furthermore, we found enhanced basal ROS production and MDA levels in α-syn98 over-expressing neurons. High basal oxidative stress induced by α-syn98, combined with oxidative stress caused by rotenone treatment, promoted aggregate formation and significantly decreased cell viability. These data indicate that α-syn98 can enhance the susceptibility of dopaminergic neurons to oxidative insults by raising steady-state levels of oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Cell Line
  • Cell Survival / drug effects
  • Humans
  • Malondialdehyde / metabolism
  • Neurons / drug effects
  • Neurons / metabolism*
  • Oxidative Stress / physiology*
  • Protein Isoforms / biosynthesis
  • Rats
  • Reactive Oxygen Species / metabolism
  • Rotenone / toxicity*
  • Uncoupling Agents / toxicity*
  • alpha-Synuclein / biosynthesis*

Substances

  • Protein Isoforms
  • Reactive Oxygen Species
  • Uncoupling Agents
  • alpha-Synuclein
  • Rotenone
  • Malondialdehyde