Molecular basis of 6-hydroxydopamine-induced caspase activations due to increases in oxidative stress in the mouse striatum

Ken ichi Tanaka, Norio Ogawa, Masato Asanuma

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

To clarify the possible role of in the in vivo toxic effects of 6-hydroxydopamine (6-OHDA), especially caspase activations, we examined its effects on striatal lipid peroxidation (LPO) and caspase activations in 6-OHDA-lesioned mice. Both dopamine (DA) levels and DA turnover were significantly changed by the 6-OHDA i.c.v. injection compared with the pre-injection level in the striatum. In addition, the striatal glutathione (GSH) content fluctuated and was significantly decreased both at 3 and 14 days after 6-OHDA i.c.v. injection. Moreover, superoxide dismutase (SOD) activity at 7 days after 6-OHDA i.c.v. injection was transiently and significantly increased compared with the pre-injection level. The levels of thiobarbituric acid-reactive substances (TBA-RS) were significantly increased at 1, 3 and 14 days. 6-OHDA significantly increased the activities of all three caspases, except for the caspase-3 activity at 7 days throughout the experimental period compared with the pre-injection level. In conclusion, 6-OHDA-induced dopaminergic dysfunction is mainly due to caspase activations by increases in oxidative stress in the mouse striatum.

Original languageEnglish
Pages (from-to)85-89
Number of pages5
JournalNeuroscience Letters
Volume410
Issue number2
DOIs
Publication statusPublished - Dec 20 2006

Keywords

  • 6-Hydroxydopamine
  • Caspase
  • Glutathione
  • Mice
  • Oxidative stress
  • Parkinson's disease
  • Striatum

ASJC Scopus subject areas

  • Neuroscience(all)

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