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dc.contributor.authorJirapas Sripetchwandeeen_US
dc.contributor.authorNoppamas Pipatpiboonen_US
dc.contributor.authorNipon Chattipakornen_US
dc.contributor.authorSiriporn Chattipakornen_US
dc.description.abstractBackground: Excessive iron accumulation leads to iron toxicity in the brain; however the underlying mechanism is unclear. We investigated the effects of iron overload induced by high iron-diet consumption on brain mitochondrial function, brain synaptic plasticity and learning and memory. Iron chelator (deferiprone) and antioxidant (n-acetyl cysteine) effects on ironoverload brains were also studied. Methodology: Male Wistar rats were fed either normal diet or high iron-diet consumption for 12 weeks, after which rats in each diet group were treated with vehicle or deferiprone (50 mg/kg) or n-acetyl cysteine (100 mg/kg) or both for another 4 weeks. High iron-diet consumption caused brain iron accumulation, brain mitochondrial dysfunction, impaired brain synaptic plasticity and cognition, blood-brain-barrier breakdown, and brain apoptosis. Although both iron chelator and antioxidant attenuated these deleterious effects, combined therapy provided more robust results. Conclusion: In conclusion, this is the first study demonstrating that combined iron chelator and anti-oxidant therapy completely restored brain function impaired by iron overload. © 2014 Sripetchwandee et al.en_US
dc.subjectAgricultural and Biological Sciencesen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleCombined therapy of iron chelator and antioxidant completely restores brain dysfunction induced by iron toxicityen_US
article.title.sourcetitlePLoS ONEen_US
article.volume9en_US Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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