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Inhibition of trifluoperazine-induced DNA fragmentation by cyclic AMP mediated signaling

U G Kang1, M J Kim, P G Suh

  • 1Department of Psychiatry, Seoul National University College of Medicine, Korea.

Molecules and Cells
|February 15, 2000
PubMed

Insights

Trifluoperazine (TFP) causes DNA fragmentation in PC12 cells. This process is not mediated by calcium but involves Gs and adenylate cyclase pathways, as shown by inhibition experiments.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Trifluoperazine (TFP) is a phenothiazine antipsychotic.
  • TFP exhibits calmodulin antagonist properties.
  • TFP induces DNA fragmentation in PC12 cells.

Purpose of the Study:

  • To investigate the intracellular signaling pathways involved in TFP-induced DNA fragmentation.
  • To determine the role of calcium and other signaling molecules in TFP's effect on DNA.

Main Methods:

  • PC12 cells were treated with TFP.
  • Various signaling modulators were used, including calcium chelators, ionopores, phospholipase C inhibitors, protein kinase C modulators, cholera toxin, forskolin, and dibutyryl cyclic AMP.
  • DNA fragmentation was assessed.

Main Results:

  • TFP induced DNA fragmentation in a dose- and time-dependent manner.
  • Agents affecting calcium signaling did not block TFP-induced DNA fragmentation.
  • Cholera toxin, forskolin, and dibutyryl cyclic AMP inhibited TFP-induced DNA fragmentation.

Conclusions:

  • Calcium-mediated signaling is not the primary pathway for TFP-induced DNA fragmentation.
  • The Gs and adenylate cyclase pathways play a significant role in TFP-induced DNA fragmentation in PC12 cells.

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