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• W4377029110 abstract "<b>Abstract ID 22389</b> <b>Poster Board 340</b> Iron is an essential nutrient for multiple biological functions, including oxygen transport, redox action, and DNA synthesis. However, excess iron in the brain is neurotoxic due to its ability to produce reactive oxygen species (ROS) and resultant oxidative stress, which can further increase the risk of neurodegeneration diseases such as Parkinson’s Disease and Alzheimer’s Disease. We have previously demonstrated that impulsivity and hyperactivity behavior of mice with brain iron accumulation were associated with increased labile iron, and not with total iron, in the brain, suggesting a causative relationship between labile iron-induced oxidative stress and abnormal emotional behavior. Deferiprone (DFP) is a commonly used oral iron chelator to remove excess iron from the body in patients with secondary iron overload, such as thalassemia and sickle cell disease. DFP is capable of transporting iron across cell membranes and across the blood-brain barrier, making it a potential clinical treatment for patients with neurodegeneration associated with brain iron accumulation. In particular, DFP has demonstrated the ability <i>ex vivo</i> to oxidize iron from its ferrous (toxic, labile) form to ferric (physiologic) form, thus removing toxic iron and preventing oxidative stress. However, the efficacy of DFP on <i>in vivo</i> labile iron chelation and affective disorder has not been tested. To examine the labile iron chelation potential of DFP, we first treated iron overloaded SH-SY5Y neuroblastoma cells with DFP and found that DFP decreased intracellular labile iron levels, as determined by Calcein-AM assay, as well as ROS production, as determined by DCF-DA fluorescence assay. We then evaluated if DFP reverses excess labile iron from the iron-loaded brain and ameliorates iron-induced oxidative stress using Hfe H67D mutant mice, a mouse model of brain iron accumulation. While oral gavage of DFP to H67D mice for 6 weeks showed significant decrease in systemic iron overload, as determined by liver non-heme iron, non-heme iron levels in the brain did not decrease. Notably, DFP treatment decreased labile iron in the cortex along with decreased oxidative stress, as determined by isoprostane levels. In addition, H67D mice showed increased impulsivity and hyperactivity and decreased anxiety-like behavior, as assessed by Elevated Plus Maze (EPM) task, which was corrected by DFP treatment. Taken together, our results provide a potential therapeutic option for psychiatric disorders that are associated with increased labile iron and oxidative stress." @default.
• W4377029110 created "2023-05-19" @default.
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• W4377029110 date "2023-05-18" @default.
• W4377029110 modified "2023-09-26" @default.
• W4377029110 title "Deferiprone Decreases Labile Iron in Brain and Ameliorates Abnormal Emotional Behavior in Mice with Brain Iron Accumulation" @default.
• W4377029110 doi "https://doi.org/10.1124/jpet.122.223890" @default.
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