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The Mechanisms of 6-Hydroxydopamine-Induced Astrocyte Death
 EVI aaaab
aInstitute for Biological Research "Sini  a Stankovi ," Belgrade, Serbia and MontenegrobInstitute of Microbiology and Immunology, School of Medicine, University of Belgrade, Belgrade, Serbia and Montenegro
Address for correspondence: Nevena Rai  evi, Institute for Biological Research, Bulevar Despota Stefana 142, Belgrade, Serbia and Montenegro. Voice: 381-11-20-78-339; fax: 381-11- 276-14-33. nevenar{at}ibiss.bg.ac.yu
Treatment with 6-hydroxydopamine significantly reduced the viability of cultured rat primary astrocytes, rat astrocytoma cell line C6, and human astrocytoma cell line U251. 6-Hydroxydopamine-treated astrocytes exhibited altered nuclear morphology, DNA fragmentation, and reduced intracellular esterase activity, which indicated apoptotic cell death. Astrocytes were protected by neutralization of 6-hydroxydopamine autooxidation products H2O2, O2•–, and •OH, but not by cell-derived or chemically generated anti-apoptotic free radical nitric oxide. Finally, 6-hydroxydopamine activated extracellular signal-regulated kinase in astrocytes and selective inhibitor of extracellular signal-regulated kinase activation partially prevented astrocyte death. Taken together, these data indicate that 6-hydroxydopamine-triggered oxidative stress induces extracellular signal-regulated kinase-dependent apoptotic death of astrocytes.
Key Words: 6-OHDA • Parkinson's disease • oxidative stress • apoptosis • astrocytes
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