Glyphosate induced cell death through apoptotic and autophagic mechanisms

Neurotoxicol Teratol. May-Jun 2012;34(3):344-9. doi: 10.1016/j.ntt.2012.03.005. Epub 2012 Apr 4.

Abstract

Herbicides have been recognized as the main environmental factor associated with human neurodegenerative disorders such as Parkinson's disease(PD). Previous studies indicated that the exposure to glyphosate, a widely used herbicide, is possibly linked to Parkinsonism, however the underlying mechanism remains unclear. We investigated the neurotoxic effects of glyphosate in differentiated PC12 cells and discovered that it inhibited viability of differentiated PC12 cells in dose-and time-dependent manners. Furthermore, the results showed that glyphosate induced cell death via autophagy pathways in addition to activating apoptotic pathways. Interestingly, deactivation of Beclin-1 gene attenuated both apoptosis and autophagy in glyphosate treated differentiated PC12 cells, suggesting that Beclin-1 gene is involved in the crosstalk between the two mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins / genetics
  • Autophagy / drug effects*
  • Beclin-1
  • Blotting, Western
  • Cell Culture Techniques
  • Cell Differentiation / drug effects
  • Cell Survival / drug effects
  • Dose-Response Relationship, Drug
  • Gene Silencing
  • Glycine / analogs & derivatives*
  • Glycine / toxicity
  • Herbicides / toxicity*
  • PC12 Cells
  • Rats
  • Time Factors

Substances

  • Apoptosis Regulatory Proteins
  • Beclin-1
  • Becn1 protein, rat
  • Herbicides
  • glyphosate
  • Glycine