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The Journal of Neuroscience, October 15, 1998, 18(20):8236-8246
Induction of NF- B Activity during Haloperidol-Induced
Oxidative Toxicity in Clonal Hippocampal Cells: Suppression of NF-B
and Neuroprotection by Antioxidants
Anke
Post,
Florian
Holsboer, and
Christian
Behl
Max Planck Institute of Psychiatry, 80804 Munich, Germany
Haloperidol (HP), a dopamine receptor antagonist, is cytotoxic to
mouse clonal hippocampal HT22 cells in a concentration-dependent manner
and causes cell death by oxidative stress. The addition of HP to HT22
cells led to an increase in intracellular peroxides and a
time-dependent drop in the intracellular glutathione levels. HP-induced
oxidative cell death was prevented by the pineal hormone melatonin, its
precursor N-acetyl serotonin, and most effectively by
vitamin E ( -tocopherol). These antioxidants inhibited the intracellular peroxide accumulation and stabilized the glutathione content of HT22 cells after the challenge with HP. At the molecular level, HP specifically induced the DNA binding activity and the transcriptional activity of the redox-sensitive transcription factor
NF- B. This enhanced NF-B activity could be blocked by the
neuroprotective antioxidants. The specific suppression of NF-B by
its inhibitor IB partially protected the cells against HP,
indicating that the activation of NF-B may be involved in HP-induced
oxidative cell death in vitro.
Key words:
haloperidol; oxidative stress; glutathione; NF-B; melatonin; vitamin E
Copyright © 1998 Society for Neuroscience 0270-6474/98/18208236-11$05.00/0
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