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Oxidative stress-resistant cells are protected against haloperidol toxicity
C Behl1, F Lezoulac'h, M Widmann
1Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany. chris@komserv.mpipsykl.mpg.de
Brain Research
|April 22, 1996
Summary
High doses of haloperidol cause cell death through oxidative stress. Cells resistant to amyloid beta-protein toxicity were also resistant to haloperidol, suggesting free radicals mediate haloperidol-induced cell death.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Neuroleptic drugs like haloperidol can be cytotoxic at high concentrations.
- Haloperidol toxicity is hypothesized to involve oxidative stress and necrosis.
- Amyloid beta-protein (A beta) is a known oxidative stressor.
Purpose of the Study:
- To investigate the role of oxidative stress in haloperidol-induced cytotoxicity.
- To determine if resistance to oxidative stress confers resistance to haloperidol.
Main Methods:
- Utilized rat pheochromocytoma PC12 cell clones.
- Selected cell clones for resistance to amyloid beta-protein toxicity.
- Assessed the sensitivity of selected cell clones to haloperidol toxicity.
Main Results:
- Selected PC12 cell clones resistant to A beta toxicity also exhibited resistance to haloperidol.
- This cross-resistance indicates a shared mechanism of toxicity.
Conclusions:
- Free radicals are strongly implicated in haloperidol-induced cell death.
- Oxidative stress is a key mechanism underlying haloperidol's cytotoxic effects.