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We, therefore, investigated the effect of 3\u2010nitropropionic acid (NPA), a mitochondrial toxin and <jats:italic>in vitro<\/jats:italic> model of Huntington's disease (HD), on mitochondrial function and viability of primary striatal astrocytes. Although NPA is known as an irreversible inhibitor of succinate dehydrogenase, we observed an increase of astrocyte ATP levels after NPA treatment. This effect could be explained by NPA\u2010mediated alterations of cytochrome <jats:italic>c<\/jats:italic> oxidase subunit IV isoform (COX IV) expression. The up\u2010regulation of COX isoform IV\u20102 caused an increased enzyme activity at the expense of elevated mitochondrial peroxide production causing increased cell death. The application of a small interfering RNA against COX IV\u20102 revealed the causal implication of COX isoform IV\u20102 in NPA\u2010mediated elevation of oxidative stress and necrotic cell death. Thus, we propose a novel, additional mechanism of NPA\u2010induced cell stress and death which is based on structural and functional changes of astrocyte COX and which could indirectly impair neuronal survival. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.20864","type":"journal-article","created":{"date-parts":[[2009,3,20]],"date-time":"2009-03-20T17:56:47Z","timestamp":1237571807000},"page":"1480-1491","source":"Crossref","is-referenced-by-count":30,"title":["Cytochrome <i>c<\/i> oxidase isoform IV\u20102 is involved in 3\u2010nitropropionic acid\u2010induced toxicity in striatal 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