Thiram and ziram stimulate non-selective cation channel and induce apoptosis in PC12 cells

Neurotoxicology. 2003 Jun;24(3):425-34. doi: 10.1016/S0161-813X(03)00013-5.

Abstract

The neurotoxicity of dithiocarbamates has been previously reported, however, the detailed mechanism underlying the neurotoxicity is still not fully understood. Among the dithiocarbamates, we investigated thiram and ziram in a neuronal-like pheochromocytoma (PC12) cells. Thiram and ziram strongly induced cell death in both dose- and time-dependent manners with the LC(50) of 0.3 and 2 microM, respectively. The cell death showed typical apoptotic features, such as DNA fragmentation and an increase of subdiploidy nuclei. Interestingly, both thiram and ziram induced rapid and sustained increases of intracellular Ca(2+) in PC12 cells, which were almost completely blocked by flufenamic acid (FFA), an inhibitor of non-selective cation channel. BAPTA-AM, an intracellular Ca(2+) chelator, inhibited the thiram- and ziram-induced apoptotic cell death. These results suggest that thiram and ziram induce apoptotic neuronal cell death by Ca(2+) influx through non-selective cation channels. The present study may provide a clue for understanding the mechanism of neurotoxicity of thiram and ziram.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Calcium / metabolism
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Dose-Response Relationship, Drug
  • Ion Channels / agonists
  • Ion Channels / antagonists & inhibitors
  • Ion Channels / metabolism*
  • PC12 Cells
  • Rats
  • Thiram / pharmacology*
  • Ziram / pharmacology*

Substances

  • Ion Channels
  • nonselective cation channel protein, rat
  • Thiram
  • Ziram
  • Calcium