作者: Jirapas Sripetchwandee , Noppamas Pipatpiboon , Nipon Chattipakorn , Siriporn Chattipakorn
DOI: 10.1371/JOURNAL.PONE.0085115
关键词:
摘要: Background Excessive iron accumulation leads to toxicity in the brain; however underlying mechanism is unclear. We investigated effects of overload induced by high iron-diet consumption on brain mitochondrial function, synaptic plasticity and learning memory. Iron chelator (deferiprone) antioxidant (n-acetyl cysteine) iron-overload brains were also studied. Methodology Male Wistar rats fed either normal diet or for 12 weeks, after which each group treated with vehicle deferiprone (50 mg/kg) n-acetyl cysteine (100 both another 4 weeks. High caused accumulation, dysfunction, impaired cognition, blood-brain-barrier breakdown, apoptosis. Although attenuated these deleterious effects, combined therapy provided more robust results. Conclusion In conclusion, this first study demonstrating that anti-oxidant completely restored function overload.