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While the neurotoxic mechanisms are vastly different for excitotoxins and 1\u2010methyl\u20104\u2010phenylpyridinium ion (MPP<jats:sup>+<\/jats:sup>), both are thought to involve free radical production, compromised mitochondrial activity and excessive lipid peroxidation. We show here that the levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) increased significantly after treatment of cultured cerebellar granule cells (CGCs) with 50 \u03bcM MPP<jats:sup>+<\/jats:sup>. Co\u2010treatment with antioxidants such as ascorbate (ASC), catalase, \u03b1\u2010tocopherol (\u03b1\u2010TOH), coenzyme Q<jats:sub>10<\/jats:sub> (CoQ<jats:sub>10<\/jats:sub>) or superoxide dismutase (SOD) rescued the cells from MPP<jats:sup>+<\/jats:sup>\u2010induced death. MPP<jats:sup>+<\/jats:sup>\u2010induced cell death was also abolished by co\u2010treatment with nitric oxide synthase (NOS) inhibitors such as 7\u2010nitroindazole (7\u2010NI), 2\u2010ethyl\u20102\u2010thiopseudourea hydrobromide (EPTU) or <jats:italic>S<\/jats:italic>\u2010methylisothiourea sulphate (MPTU). We also tested the protective effects of an iron chelator (deferoxamine mesylate, DFx) and a peroxynitrite scavenger (FeTTPS) and the results lend further support to the view that the free radical cytotoxicity plays an essential role in MPP<jats:sup>+<\/jats:sup>\u2010induced death in primary cultures of CGC.<\/jats:p>","DOI":"10.1016\/j.cellbi.2004.03.005","type":"journal-article","created":{"date-parts":[[2004,6,2]],"date-time":"2004-06-02T17:50:25Z","timestamp":1086198625000},"page":"373-380","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["Protection against MPP<sup>+<\/sup> neurotoxicity in cerebellar granule cells by antioxidants"],"prefix":"10.1002","volume":"28","author":[{"given":"Rosa 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