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Dibakar Goswami - One of the best experts on this subject based on the ideXlab platform.
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Triphenylphosphonium-desferrioxamine as a candidate mitochondrial Iron Chelator
BioMetals, 2017Co-Authors: Roxana Yesenia Pastrana Alta, Hector Aguilar Vitorino, Dibakar Goswami, M. Teresa Machini, Breno Pannia EspósitoAbstract:Cell-impermeant Iron Chelator desferrioxamine (DFO) can have access to organelles if appended to suitable vectors. Mitochondria are important targets for the treatment of Iron overload-related neurodegenerative diseases. Triphenylphosphonium (TPP) is a delocalized lipophilic cation used to ferry molecules to mitochondria. Here we report the synthesis and characterization of the conjugate TPP–DFO as a mitochondrial Iron Chelator. TPP–DFO maintained both a high affinity for Iron and the antioxidant activity when compared to parent DFO. TPP–DFO was less toxic than TPP alone to A2780 cells (IC50 = 135.60 ± 1.08 and 4.34 ± 1.06 μmol L−1, respectively) and its native fluorescence was used to assess its mitochondrial localization (Rr = +0.56). These results suggest that TPP–DFO could be an interesting alternative for the treatment of mitochondrial Iron overload e.g. in Friedreich’s ataxia.
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Deferasirox-TAT(47–57) peptide conjugate as a water soluble, bifunctional Iron Chelator with potential use in neuromedicine
BioMetals, 2015Co-Authors: Dibakar Goswami, M. Teresa Machini, Hector A. Vitorino, Roxana Y. P. Alta, Daniel M. Silvestre, Cassiana S. Nomura, Breno P. EspósitoAbstract:Deferasirox (DFX), an orally active and clinically approved Iron Chelator, is being used extensively for the treatment of Iron overload. However, its water insolubility makes it cumbersome for practical use. In addition to this, the low efficacy of DFX to remove brain Iron prompted us to synthesize and evaluate a DFX-TAT(47–57) peptide conjugate for its Iron chelation properties and permeability across RBE4 cell line, an in vitro model of the blood–brain barrier. The water-soluble conjugate was able to remove labile Iron from buffered solution as well as from Iron overloaded sera, and the permeability of DFX-TAT(47–57) conjugate into RBE4 cells was not affected compared to parent deferasirox. The Iron bound conjugate was also able to translocate through the cell membrane.
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deferasirox tat 47 57 peptide conjugate as a water soluble bifunctional Iron Chelator with potential use in neuromedicine
Biometals, 2015Co-Authors: Roxana Yesenia Pastrana Alta, Hector Aguilar Vitorino, Dibakar Goswami, Daniel M. Silvestre, Cassiana S. Nomura, Teresa M Machini, Breno Pannia EspósitoAbstract:Deferasirox (DFX), an orally active and clinically approved Iron Chelator, is being used extensively for the treatment of Iron overload. However, its water insolubility makes it cumbersome for practical use. In addition to this, the low efficacy of DFX to remove brain Iron prompted us to synthesize and evaluate a DFX-TAT(47–57) peptide conjugate for its Iron chelation properties and permeability across RBE4 cell line, an in vitro model of the blood–brain barrier. The water-soluble conjugate was able to remove labile Iron from buffered solution as well as from Iron overloaded sera, and the permeability of DFX-TAT(47–57) conjugate into RBE4 cells was not affected compared to parent deferasirox. The Iron bound conjugate was also able to translocate through the cell membrane.
Joshua L Dunaief - One of the best experts on this subject based on the ideXlab platform.
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oral administration of the Iron Chelator deferiprone protects against loss of retinal ganglion cells in a mouse model of glaucoma
Experimental Eye Research, 2020Co-Authors: Albert Bargoud, Ying Song, Ahmara Ross, Joshua L DunaiefAbstract:Abstract Glaucoma is a progressive neurodegenerative process affecting the retinal ganglion cells (RGCs) and the optic nerve. Oxidative stress has been implicated in glaucoma pathogenesis, and Iron is a potent generator of oxidative stress. The oral Iron Chelator deferiprone (DFP) is protective against retinal degenerations associated with oxidative stress. To test whether DFP could be protective in glaucoma, we used microbead injections to induce elevated intraocular pressure (IOP) in a cohort of 3-month old C57BL/6J mice. One eye of each animal was injected with magnetic microbeads resulting in ocular hypertension for >7 weeks while the fellow eye was injected with saline and served as a normotensive internal control. While half of the cohort received oral DFP (1 mg/ml in the drinking water), the other half did not and served as controls. After 8 weeks, Brn3a immunolabeling of flat-mounted retinas was used for manual RGC quantification. Axon counts were obtained from thin sections of optic nerves using the AxonJ plugin for ImageJ. DFP administration was protective against RGC and optic nerve loss in the setting of elevated IOP. These results suggest that Iron chelation by DFP may provide glaucoma neuroprotection.
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the oral Iron Chelator deferiprone protects against systemic Iron overload induced retinal degeneration in hepcidin knockout mice
Investigative Ophthalmology & Visual Science, 2014Co-Authors: Delu Song, Majda Hadziahmetovic, Michael Spino, Yafeng Li, Ying Song, L Zhao, John T Connelly, Joshua L DunaiefAbstract:To investigate the retinal-protective effects of the oral Iron Chelator deferiprone (DFP) in mice lacking the Iron regulatory hormone hepcidin (Hepc). These Hepc knockout (KO) mice have age-dependent systemic and retinal Iron accumulation leading to retinal degeneration.Hepc KO mice were given DFP in drinking water from age 6 to 18 months. They were then compared to Hepc KO mice not receiving DFP by fundus imaging, electroretinography (ERG), histology, immunofluorescence, and quantitative PCR to investigate the protective effect of DFP against retinal and retinal pigment epithelial (RPE) degeneration.In Hepc KO mice, DFP diminished RPE depigmentation and autofluorescence on fundus imaging. Autofluorescence in the RPE layer in cryosections was significantly diminished by DFP, consistent with the fundus images. Immunolabeling with L-ferritin and transferrin receptor antibodies showed a decreased signal for L-ferritin in the inner retina and RPE cells and an increased signal for transferrin receptor in the inner retina, indicating diminished retinal Iron levels with DFP treatment. Plastic sections showed that photoreceptor and RPE cells were well preserved in Hepc KO mice treated with DFP. Consistent with photoreceptor protection, the mRNA level of rhodopsin was significantly higher in retinas treated with DFP. The mRNA levels of oxidative stress-related genes heme oxygenase-1 and catalase were significantly lower in DFP-treated Hepc KO retinas. Finally, ERG rod a- and b- and cone b-wave amplitudes were significantly higher in DFP-treated mice.Long-term treatment with the oral Iron Chelator DFP diminished retinal and RPE Iron levels and oxidative stress, providing significant protection against retinal degeneration caused by chronic systemic Iron overload in Hepc KO mice. This indicates that Iron chelation could be a long-term preventive treatment for retinal disease involving Iron overload and oxidative stress.
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the oral Iron Chelator deferiprone protects against systemic Iron overload induced retinal degeneration in hepcidin knockout mice
Investigative Ophthalmology & Visual Science, 2014Co-Authors: Delu Song, Majda Hadziahmetovic, Michael Spino, Ying Song, L Zhao, John T Connelly, Joshua L DunaiefAbstract:PURPOSE To investigate the retinal-protective effects of the oral Iron Chelator deferiprone (DFP) in mice lacking the Iron regulatory hormone hepcidin (Hepc). These Hepc knockout (KO) mice have age-dependent systemic and retinal Iron accumulation leading to retinal degeneration. METHODS Hepc KO mice were given DFP in drinking water from age 6 to 18 months. They were then compared to Hepc KO mice not receiving DFP by fundus imaging, electroretinography (ERG), histology, immunofluorescence, and quantitative PCR to investigate the protective effect of DFP against retinal and retinal pigment epithelial (RPE) degeneration. RESULTS In Hepc KO mice, DFP diminished RPE depigmentation and autofluorescence on fundus imaging. Autofluorescence in the RPE layer in cryosections was significantly diminished by DFP, consistent with the fundus images. Immunolabeling with L-ferritin and transferrin receptor antibodies showed a decreased signal for L-ferritin in the inner retina and RPE cells and an increased signal for transferrin receptor in the inner retina, indicating diminished retinal Iron levels with DFP treatment. Plastic sections showed that photoreceptor and RPE cells were well preserved in Hepc KO mice treated with DFP. Consistent with photoreceptor protection, the mRNA level of rhodopsin was significantly higher in retinas treated with DFP. The mRNA levels of oxidative stress-related genes heme oxygenase-1 and catalase were significantly lower in DFP-treated Hepc KO retinas. Finally, ERG rod a- and b- and cone b-wave amplitudes were significantly higher in DFP-treated mice. CONCLUSIONS Long-term treatment with the oral Iron Chelator DFP diminished retinal and RPE Iron levels and oxidative stress, providing significant protection against retinal degeneration caused by chronic systemic Iron overload in Hepc KO mice. This indicates that Iron chelation could be a long-term preventive treatment for retinal disease involving Iron overload and oxidative stress.
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systemic administration of the Iron Chelator deferiprone protects against light induced photoreceptor degeneration in the mouse retina
Free Radical Biology and Medicine, 2012Co-Authors: Majda Hadziahmetovic, Delu Song, Ying Song, Yong Zhong, Joshua L DunaiefAbstract:Abstract Oxidative stress plays a key role in a light-damage (LD) model of retinal degeneration as well as in age-related macular degeneration (AMD). Since Iron can promote oxidative stress, the Iron Chelator deferiprone (DFP) was tested for protection against light-induced retinal degeneration. To accomplish this, A/J mice were treated with or without oral DFP and then were placed in constant bright white fluorescent light (10,000 lx) for 20 h. Retinas were evaluated at several time points after light exposure. Photoreceptor apoptosis was assessed using the TUNEL assay. Retinal degeneration was assessed by histology 10 days after exposure to damaging white light. Two genes upregulated by oxidative stress, heme oxygenase 1 ( Hmox1 ) and ceruloplasmin ( Cp ), as well as complement component 3 ( C3 ) were quantified by RT-qPCR. Cryosections were immunolabeled for an oxidative stress marker (nitrotyrosine), a microglial marker (Iba1), as well as both heavy (H) and light (L) ferritin. Light exposure resulted in substantial photoreceptor-specific cell death. Dosing with DFP protected photoreceptors, decreasing the numbers of TUNEL-positive photoreceptors and increasing the number of surviving photoreceptors. The retinal mRNA levels of oxidative stress-related genes and C3 were upregulated following light exposure and diminished by DFP treatment. Immunostaining for nitrotyrosine indicated that DFP reduced the nitrative stress caused by light exposure. Robust H/L-ferritin-containing microglial activation and migration to the outer retina occurred after light exposure and DFP treatment reduced microglial invasion. DFP is protective against light-induced retinal degeneration and has the potential to diminish oxidative stress in the retina.
Fernando Tricta - One of the best experts on this subject based on the ideXlab platform.
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safety and effectiveness of long term therapy with the oral Iron Chelator deferiprone
Blood, 2003Co-Authors: Alan R Cohen, Renzo Galanello, Vitaliana De Sanctis, Antonio Piga, Fernando TrictaAbstract:The identification of a safe, orally active Iron Chelator is critically important for the prevention of morbidity and early death in patients receiving regular red cell transfusions. Based on our findings in a 1-year multicenter, prospective study of the safety and efficacy of deferiprone in patients with thalassemia major, we have extended the treatment period to 4 years. The mean dose of the Chelator was 73 mg/kg per day during 531 patient-years. The rates of agranulocytosis (absolute neutrophil count [ANC] < 500 × 109/L) and milder forms of neutropenia (ANC, 500-1500 × 109/L) were 0.2 and 2.8 per 100 patient-years, respectively. Neutropenia occurred significantly more commonly in patients with intact spleens. Gastrointestinal and joint symptoms decreased significantly after the first year of therapy, and led to discontinuation of deferiprone in only one patient in years 2 to 4. The mean alanine aminotransferase (ALT) value of 71 U/L after 4 years of therapy was significantly higher than the baseline value of 61 U/L. Trend analysis showed no increase in the ALT levels or the percentage of patients with ALT levels greater than twice the upper limit of the reference range. Ferritin levels did not change significantly from the values at the time of change from deferoxamine to deferiprone in either the intention-to-treat analysis or in the 84 patients who completed 4 years of therapy. Because of concerns regarding the effectiveness of the studied dose of deferiprone, 47 patients discontinued therapy, whereas 15 patients interrupted therapy because of concerns regarding low Iron levels. The results of this study help to define the safety and effectiveness of long-term therapy with deferiprone.
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safety profile of the oral Iron Chelator deferiprone a multicentre study
British Journal of Haematology, 2000Co-Authors: Alan R Cohen, Calogero Vullo, A Dipalma, Renzo Galanello, Antonio Piga, Fernando TrictaAbstract:In previous trials, the orally active Iron Chelator deferiprone (L1) has been associated with sporadic agranulocytosis, milder forms of neutropenia and other side-effects. To determine the incidence of these events, we performed a multicentre prospective study of the Chelator. Blood counts were performed weekly, and confirmed neutropenia mandated discontinuation of therapy. Among 187 patients with thalassaemia major, the incidence of agranulocytosis (neutrophils 2500 μg/l. This study characterized the safety profile of deferiprone, and, under the specific conditions of monitoring, demonstrated that agranulocytosis is less common than previously predicted.
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A Multi‐Center Safety Trial of the Oral Iron Chelator Deferiprone
Annals of the New York Academy of Sciences, 1998Co-Authors: Alan R Cohen, Calogero Vullo, Renzo Galanello, Antonio Piga, Fernando TrictaAbstract:Abstract: Deferiprone, also known as L1, is an orally active Iron Chelator that has been studied extensively in clinical trials. The sporadic occurrence of agranulocytosis in association with deferiprone and the highly variable frequency of other possible side effects such as arthralgia have created uncertainty about the true incidence of deferiprone-related complications. A multi-center, 1-year trial was initiated to determine the safety profile of deferiprone. Using the Apotex formulation of deferiprone, 187 patients with thalassemia who were unable or unwilling to use deferoxamine were enrolled in four centers; 162 patients completed one year of therapy. Agranulocytosis (ANC < 500/mm3) occurred in one patient after 15 weeks of treatment, was not accompanied by infection and resolved following treatment with G-CSF. Nine other subjects developed less severe neutropenia (ANC 500-1500/mm3) with the lowest absolute neutrophil count reaching 500-1250/mm3. The neutropenia in these patients developed after 1-50 weeks of therapy, frequently accompanied febrile illnesses, and occurred predominantly in non-splenectomized patients. Reasons other than neutropenia for discontinuing use of deferiprone included nausea (4), voluntary withdrawal (3), high ALT (2), platelet count
Breno P. Espósito - One of the best experts on this subject based on the ideXlab platform.
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Deferasirox-TAT(47–57) peptide conjugate as a water soluble, bifunctional Iron Chelator with potential use in neuromedicine
BioMetals, 2015Co-Authors: Dibakar Goswami, M. Teresa Machini, Hector A. Vitorino, Roxana Y. P. Alta, Daniel M. Silvestre, Cassiana S. Nomura, Breno P. EspósitoAbstract:Deferasirox (DFX), an orally active and clinically approved Iron Chelator, is being used extensively for the treatment of Iron overload. However, its water insolubility makes it cumbersome for practical use. In addition to this, the low efficacy of DFX to remove brain Iron prompted us to synthesize and evaluate a DFX-TAT(47–57) peptide conjugate for its Iron chelation properties and permeability across RBE4 cell line, an in vitro model of the blood–brain barrier. The water-soluble conjugate was able to remove labile Iron from buffered solution as well as from Iron overloaded sera, and the permeability of DFX-TAT(47–57) conjugate into RBE4 cells was not affected compared to parent deferasirox. The Iron bound conjugate was also able to translocate through the cell membrane.
Michael Spino - One of the best experts on this subject based on the ideXlab platform.
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the oral Iron Chelator deferiprone protects against systemic Iron overload induced retinal degeneration in hepcidin knockout mice
Investigative Ophthalmology & Visual Science, 2014Co-Authors: Delu Song, Majda Hadziahmetovic, Michael Spino, Yafeng Li, Ying Song, L Zhao, John T Connelly, Joshua L DunaiefAbstract:To investigate the retinal-protective effects of the oral Iron Chelator deferiprone (DFP) in mice lacking the Iron regulatory hormone hepcidin (Hepc). These Hepc knockout (KO) mice have age-dependent systemic and retinal Iron accumulation leading to retinal degeneration.Hepc KO mice were given DFP in drinking water from age 6 to 18 months. They were then compared to Hepc KO mice not receiving DFP by fundus imaging, electroretinography (ERG), histology, immunofluorescence, and quantitative PCR to investigate the protective effect of DFP against retinal and retinal pigment epithelial (RPE) degeneration.In Hepc KO mice, DFP diminished RPE depigmentation and autofluorescence on fundus imaging. Autofluorescence in the RPE layer in cryosections was significantly diminished by DFP, consistent with the fundus images. Immunolabeling with L-ferritin and transferrin receptor antibodies showed a decreased signal for L-ferritin in the inner retina and RPE cells and an increased signal for transferrin receptor in the inner retina, indicating diminished retinal Iron levels with DFP treatment. Plastic sections showed that photoreceptor and RPE cells were well preserved in Hepc KO mice treated with DFP. Consistent with photoreceptor protection, the mRNA level of rhodopsin was significantly higher in retinas treated with DFP. The mRNA levels of oxidative stress-related genes heme oxygenase-1 and catalase were significantly lower in DFP-treated Hepc KO retinas. Finally, ERG rod a- and b- and cone b-wave amplitudes were significantly higher in DFP-treated mice.Long-term treatment with the oral Iron Chelator DFP diminished retinal and RPE Iron levels and oxidative stress, providing significant protection against retinal degeneration caused by chronic systemic Iron overload in Hepc KO mice. This indicates that Iron chelation could be a long-term preventive treatment for retinal disease involving Iron overload and oxidative stress.
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the oral Iron Chelator deferiprone protects against systemic Iron overload induced retinal degeneration in hepcidin knockout mice
Investigative Ophthalmology & Visual Science, 2014Co-Authors: Delu Song, Majda Hadziahmetovic, Michael Spino, Ying Song, L Zhao, John T Connelly, Joshua L DunaiefAbstract:PURPOSE To investigate the retinal-protective effects of the oral Iron Chelator deferiprone (DFP) in mice lacking the Iron regulatory hormone hepcidin (Hepc). These Hepc knockout (KO) mice have age-dependent systemic and retinal Iron accumulation leading to retinal degeneration. METHODS Hepc KO mice were given DFP in drinking water from age 6 to 18 months. They were then compared to Hepc KO mice not receiving DFP by fundus imaging, electroretinography (ERG), histology, immunofluorescence, and quantitative PCR to investigate the protective effect of DFP against retinal and retinal pigment epithelial (RPE) degeneration. RESULTS In Hepc KO mice, DFP diminished RPE depigmentation and autofluorescence on fundus imaging. Autofluorescence in the RPE layer in cryosections was significantly diminished by DFP, consistent with the fundus images. Immunolabeling with L-ferritin and transferrin receptor antibodies showed a decreased signal for L-ferritin in the inner retina and RPE cells and an increased signal for transferrin receptor in the inner retina, indicating diminished retinal Iron levels with DFP treatment. Plastic sections showed that photoreceptor and RPE cells were well preserved in Hepc KO mice treated with DFP. Consistent with photoreceptor protection, the mRNA level of rhodopsin was significantly higher in retinas treated with DFP. The mRNA levels of oxidative stress-related genes heme oxygenase-1 and catalase were significantly lower in DFP-treated Hepc KO retinas. Finally, ERG rod a- and b- and cone b-wave amplitudes were significantly higher in DFP-treated mice. CONCLUSIONS Long-term treatment with the oral Iron Chelator DFP diminished retinal and RPE Iron levels and oxidative stress, providing significant protection against retinal degeneration caused by chronic systemic Iron overload in Hepc KO mice. This indicates that Iron chelation could be a long-term preventive treatment for retinal disease involving Iron overload and oxidative stress.
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the oral Iron Chelator deferiprone protects against Iron overload induced retinal degeneration
Investigative Ophthalmology & Visual Science, 2011Co-Authors: Majda Hadziahmetovic, Steven Grieco, Jared Iacovelli, Ying Song, John Connelly, Natalie Wolkow, Arkady Lyubarsky, Domenico Pratico, Jennifer D Lee, Michael SpinoAbstract:Purpose Iron-induced oxidative stress may exacerbate age-related macular degeneration (AMD). Ceruloplasmin/Hephaestin double-knockout (DKO) mice with age-dependent retinal Iron accumulation and some features of AMD were used to test retinal protection by the oral Iron Chelator deferiprone (DFP). Methods Cultured retinal pigment epithelial (ARPE-19) cells and mice were treated with DFP. Transferrin receptor mRNA (Tfrc), an indicator of Iron levels, was quantified by qPCR. In mice, retinal oxidative stress was assessed by mass spectrometry, and degeneration by histology and electroretinography. Results DFP at 60 μM decreased labile Iron in ARPE-19 cells, increasing Tfrc and protecting 70% of cells against a lethal dose of H(2)O(2). DFP 1 mg/mL in drinking water increased retinal Tfrc mRNA 2.7-fold after 11 days and also increased transferrin receptor protein. In DKOs, DFP over 8 months decreased retinal Iron levels to 72% of untreated mice, diminished retinal oxidative stress to 70% of the untreated level, and markedly ameliorated retinal degeneration. DFP was not retina toxic in wild-type (WT) or DKO mice, as assessed by histology and electroretinography. Conclusions Oral DFP was not toxic to the mouse retina. It diminished retinal Iron levels and oxidative stress and protected DKO mice against Iron overload-induced retinal degeneration. Further testing of DFP for retinal disease involving oxidative stress is warranted.
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the oral Iron Chelator deferiprone protects against Iron overload induced retinal degeneration
Investigative Ophthalmology & Visual Science, 2011Co-Authors: Majda Hadziahmetovic, Steven Grieco, Michael Spino, Jared Iacovelli, Ying Song, John Connelly, Natalie Wolkow, Arkady Lyubarsky, Domenico Pratico, Leah Z HarrisAbstract:Iron-induced oxidative stress may exacerbate age-related macular degeneration (AMD). Ceruloplasmin/Hephaestin double-knockout (DKO) mice with age-dependent retinal Iron accumulation and some features of AMD were used to test retinal protection by the oral Iron Chelator deferiprone (DFP).Cultured retinal pigment epithelial (ARPE-19) cells and mice were treated with DFP. Transferrin receptor mRNA (Tfrc), an indicator of Iron levels, was quantified by qPCR. In mice, retinal oxidative stress was assessed by mass spectrometry, and degeneration by histology and electroretinography.DFP at 60 μM decreased labile Iron in ARPE-19 cells, increasing Tfrc and protecting 70% of cells against a lethal dose of H(2)O(2). DFP 1 mg/mL in drinking water increased retinal Tfrc mRNA 2.7-fold after 11 days and also increased transferrin receptor protein. In DKOs, DFP over 8 months decreased retinal Iron levels to 72% of untreated mice, diminished retinal oxidative stress to 70% of the untreated level, and markedly ameliorated retinal degeneration. DFP was not retina toxic in wild-type (WT) or DKO mice, as assessed by histology and electroretinography.Oral DFP was not toxic to the mouse retina. It diminished retinal Iron levels and oxidative stress and protected DKO mice against Iron overload-induced retinal degeneration. Further testing of DFP for retinal disease involving oxidative stress is warranted.
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Pharmacokinetic Disposition of the Oral Iron Chelator Deferiprone in the Domestic Pigeon (Columba livia)
Journal of Avian Medicine and Surgery, 2007Co-Authors: Douglas P. Whiteside, Peter D. Conlon, Kay G Mehren, Angelo Tesoro, Ian K. Barker, Robert M Jacobs, Jake J. Thiessen, Michael SpinoAbstract:ABSTRACT Deferiprone is a bidentate oral Iron Chelator used for the treatment of Iron overload in people. The purpose of this study was to determine the pharmacokinetic disposition of deferiprone in the domestic pigeon (Columba livia) and to compare the results with a previous study in the white leghorn chicken. Deferiprone (DFP) was administered orally as a suspension at a single dose of 50 mg/kg to 10 Iron-loaded (IL-DFP) pigeons and 10 non–Iron-loaded controls (NIL-DFP). Six NIL-DFP birds were also administered deferiprone intravenously to determine the bioavailability of the drug after a 30-day washout period. To evaluate if deferiprone induces its own metabolism, the pharmacokinetic disposition of the drug was also studied in the IL-DFP group after oral therapy with deferiprone at a dosage of 50 mg/kg q12h for 30 days. For each phase, collected blood was analyzed for deferiprone by high-performance liquid chromatography to develop a plasma concentration versus time curve. Deferiprone was rapidly abso...
