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Protective effect of histidine on MPP+-induced hydroxyl radical generation in rat striatum

T Obata1, T Inada

  • 1Department of Pharmacology, Oita Medical University, 1-1, Hasama-machi, Oita 879-5593, Japan.tobata@oita-med.ac.jp

Brain Research
|January 16, 1999
PubMed

Insights

Histidine effectively reduced hydroxyl radical (.OH) formation in rat brains caused by MPP+. This suggests histidine acts as a neuroprotective agent against oxidative stress in the striatum.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Oxidative stress, specifically hydroxyl radical (.OH) formation, is implicated in neurodegenerative processes.
  • The neurotoxin MPP+ is known to induce oxidative damage in the brain.

Purpose of the Study:

  • To investigate the neuroprotective effect of histidine against MPP+-induced hydroxyl radical (.OH) formation.
  • To determine if histidine can mitigate oxidative stress in the rat striatum.

Main Methods:

  • Utilized in vivo microdialysis in anesthetized rats to measure extracellular hydroxyl radical (.OH) formation.
  • Assessed .OH generation by quantifying 2,3-dihydroxybenzoic acid (DHBA) formation, a nonenzymatic product.
  • Administered MPP+ and histidine to the striatum and monitored .OH levels.

Main Results:

  • MPP+ administration significantly increased hydroxyl radical (.OH) formation in the rat striatum.
  • Co-administration of histidine (25 mM) markedly reduced the MPP+-induced increase in .OH formation.
  • Histidine demonstrated a protective effect against MPP+-induced oxidative stress.

Conclusions:

  • Histidine exhibits neuroprotective properties by inhibiting hydroxyl radical (.OH) generation.
  • The findings suggest histidine may be a potential therapeutic agent for conditions involving MPP+-related oxidative neurotoxicity.

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