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dc.contributor.authorJirapas Sripetchwandeeen_US
dc.contributor.authorJantira Saniten_US
dc.contributor.authorNipon Chattipakornen_US
dc.contributor.authorSiriporn C. Chattipakornen_US
dc.description.abstractAims Although iron overload induces oxidative stress and brain mitochondrial dysfunction, and is associated with neurodegenerative diseases, brain mitochondrial iron uptake has not been investigated. We determined the role of mitochondrial calcium uniporter (MCU) in brain mitochondria as a major route for iron entry. We hypothesized that iron overload causes brain mitochondrial dysfunction, and that the MCU blocker prevents iron entry into mitochondria, thus attenuating mitochondrial dysfunction. Main methods Isolated brain mitochondria from male Wistar rats were used. Iron (Fe2 +and Fe3 +) at 0-286 μM were applied onto mitochondria at various incubation times (5-30 min), and the mitochondrial function was determined. Effects of MCU blocker (Ru-360) and iron chelator were studied. Key findings Both Fe2 +and Fe3 +entered brain mitochondria and caused mitochondrial swelling in a dose- and time-dependent manner, and caused mitochondrial depolarization and increased ROS production. However, Fe2 +caused more severe mitochondrial dysfunction than Fe3 +. Although all drugs attenuated mitochondrial dysfunction caused by iron overload, only an MCU blocker could completely prevent ROS production and mitochondrial depolarization. Significance Our findings indicated that iron overload caused brain mitochondrial dysfunction, and that an MCU blocker effectively prevented this impairment, suggesting that MCU could be the major portal for brain mitochondrial iron uptake. © 2013 Elsevier Inc.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleMitochondrial calcium uniporter blocker effectively prevents brain mitochondrial dysfunction caused by iron overloaden_US
article.title.sourcetitleLife Sciencesen_US
article.volume92en_US Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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