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We investigated the neuroprotective effect of D\u2010\u03b2\u2010hydroxybutyrate (bHB), a ketone body, against rotenone toxicity by using SH\u2010SY5Y dopaminergic neuroblastoma cells. SH\u2010SY5Y cells, differentiated by all\u2010trans\u2010retinoic acid, were exposed to rotenone at concentrations ranging from 0 to 1,000 nM. We evaluated cellular oxidation reduction by the alamarBlue assay, viability by lactate dehydrogenase (LDH) assay, and survival\/death ratio by live\/dead assays. Exposure to rotenone for 48 hr oxidized cells and decreased their viability and survival rate in a concentration\u2010dependent manner. Pretreatment of cells with 8 mM bHB provided significant protection to SH\u2010SY5Y cells. Whereas rotenone caused the loss of mitochondrial membrane potential, released cytochrome c into the cytosol, and reduced cytochrome c content in mitochondria, addition of bHB blocked this toxic effect. bHB also attenuated the rotenone\u2010induced activation of caspase\u20109 and caspase\u20103. Administration of 0\u201310 mM 3\u2010nitropropionic acid, a complex II inhibitor, also decreased the reducing power of SH\u2010SY5Y cells measured by alamarBlue assay. Pretreatment with 8 mM bHB attenuated the decrease of alamarBlue fluorescence. These data demonstrated that bHB had a neuroprotective effect that supported the mitochondrial respiration system by reversing the inhibition of complex I or II. Ketone bodies, the alternative energy source in the mammalian brain, appear to have therapeutic potential in PD. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21021","type":"journal-article","created":{"date-parts":[[2006,8,17]],"date-time":"2006-08-17T17:46:35Z","timestamp":1155836795000},"page":"1376-1384","source":"Crossref","is-referenced-by-count":88,"title":["D\u2010\u03b2\u2010hydroxybutyrate protects dopaminergic SH\u2010SY5Y cells in a rotenone model of Parkinson's 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