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Sixto Malato - One of the best experts on this subject based on the ideXlab platform.
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photo fenton treatment of saccharin in a solar pilot compound parabolic collector use of olive mill wastewater as Iron Chelating Agent preliminary results
Journal of Hazardous Materials, 2019Co-Authors: Konstantina Davididou, Efthalia Chatzisymeon, Leonidas Perezestrada, Izabell Oller, Sixto MalatoAbstract:Abstract The aim of this work was to investigate the treatment of the artificial sweetener saccharin (SAC) in a solar compound parabolic collector pilot plant by means of the photo-Fenton process at pH 2.8. Olive mill wastewater (OMW) was used as Iron Chelating Agent to avoid acidification of water at pH 2.8. For comparative purposes, Ethylenediamine-N, N-disuccinic acid (EDDS), a well-studied Iron chelator, was also employed at circumneutral pH. Degradation products formed along treatment were identified by LC-QTOF-MS analysis. Their degradation was associated with toxicity removal, evaluated by monitoring changes in the bioluminescence of Vibrio fischeri bacteria. Results showed that conventional photo-Fenton at pH 2.8 could easily degrade SAC and its intermediates yielding k, apparent reaction rate constant, in the range of 0.64–0.82 L kJ−1, as well as, eliminate effluent’s chronic toxicity. Both OMW and EDDS formed Iron-complexes able to catalyse H2O2 decomposition and generate HO . OMW yielded lower SAC oxidation rates (k = 0.05–0.1 L kJ−1) than EDDS (k = 2.21–7.88 L kJ−1) possibly due to its higher TOC contribution. However, the degradation rates were improved (k = 0.13 L kJ−1) by increasing OMW dilution in the reactant mixture. All in all, encouraging results were obtained by using OMW as Iron Chelating Agent, thus rendering this approach promising towards the increase of process sustainability.
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microcontaminant degradation in municipal wastewater treatment plant secondary effluent by edds assisted photo fenton at near neutral ph an experimental design approach
Catalysis Today, 2015Co-Authors: S Papoutsakis, S Mirallescuevas, I Oller, J Garcia L Sanchez, Cesar Pulgarin, Sixto MalatoAbstract:This work aims to evaluate the applicability of EDDS (ethylenediamine-N,N'-disuccinic acid) as an Iron Chelating Agent for photo-Fenton treatment of municipal wastewater spiked with organic contaminants at near-neutral pH. A series of laboratory scale experiments are conducted under simulated sunlight in accordance with a central composite experimental design in order to define the most favorable conditions in terms of initial Iron concentration (maintaining a molar ratio 1:2 of Fe:EDDS), H2O2 and pH. The system is evaluated in terms of degradation efficiency, H2O2 consumption and Iron availability. The simulated system has been compared in terms of degradation efficiency with a 60 L compound parabolic collector (CPC), and significant correlation has been observed. An approach for estimating near-optimal regions of operability is also demonstrated. (C) 2015 Elsevier B.V. All rights reserved.
Hyeong-cheol Yang - One of the best experts on this subject based on the ideXlab platform.
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Effects of the Iron-Chelating Agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity.
Journal of biomedical materials research. Part B Applied biomaterials, 2011Co-Authors: Tingting Zhu, Heechul Park, Bum-soon Lim, Kyung Mi Son, Hyeong-cheol YangAbstract:Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (·OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts, and L929 mouse fibroblasts. Deferoxamine (DFO), an Iron Chelating Agent, effectively protected MC3T3-E1 cells from resin monomer-induced cytotoxicity, indicating that cytotoxicity was caused primarily by hydroxyl radicals. However, DFO only had a protective effect against relatively high concentrations of TEGDMA and HEMA in HDPCs and human gingival fibroblasts, and resin monomer-induced cytotoxicity in L929 was not attenuated by DFO. A labile Iron pool (LIP) was detectable only in MC3T3-E1 cells among the four cell types. This indicates that the generation of hydroxyl radicals induced by resin monomers is likely dependent on LIP levels. In contrast to resin monomers, hydrogen peroxide (H2O2)-induced cytotoxicity was not prevented by DFO in any of the cell types examined, although hydroxyl radicals were detected in MC3T3-E1 cells and HDPCs on exposure to exogenous H2O2. This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H2O2-treated cells. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2012.
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Effects of the Iron-Chelating Agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity.
Journal of biomedical materials research. Part B Applied biomaterials, 2011Co-Authors: Tingting Zhu, Heechul Park, Bum-soon Lim, Kyung Mi Son, Hyeong-cheol YangAbstract:Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (·OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts, and L929 mouse fibroblasts. Deferoxamine (DFO), an Iron Chelating Agent, effectively protected MC3T3-E1 cells from resin monomer-induced cytotoxicity, indicating that cytotoxicity was caused primarily by hydroxyl radicals. However, DFO only had a protective effect against relatively high concentrations of TEGDMA and HEMA in HDPCs and human gingival fibroblasts, and resin monomer-induced cytotoxicity in L929 was not attenuated by DFO. A labile Iron pool (LIP) was detectable only in MC3T3-E1 cells among the four cell types. This indicates that the generation of hydroxyl radicals induced by resin monomers is likely dependent on LIP levels. In contrast to resin monomers, hydrogen peroxide (H(2)O(2))-induced cytotoxicity was not prevented by DFO in any of the cell types examined, although hydroxyl radicals were detected in MC3T3-E1 cells and HDPCs on exposure to exogenous H(2)O(2). This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H(2)O(2)-treated cells.
Alison Curnow - One of the best experts on this subject based on the ideXlab platform.
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Enhancing Protoporphyrin IX induced Photodynamic Therapy with a Topical Iron Chelating Agent in a Normal Skin Model
Journal of Heavy Metal Toxicity and Diseases, 2016Co-Authors: Alison Curnow, A. J. Macrobert, Sg BownAbstract:Protoporphyrin IX (PpIX)-induced photodynamic therapy (PDT) is being utilised within dermatological practice as a topical method of localised ablation of nonmelanoma skin cancer/precancer. Standardised protocols have been implemented to good effect when the disease remains superficial but improvement is required to widen the application of this light activated drug therapy to treat thicker or acrally located conditions. As innate haem biosynthesis is exploited to accumulate the light sensitive PpIX from a topically applied inert prodrug (aminolaevulinic acid; ALA), this pathway can be further manipulated through the concurrent administration of an Iron Chelating Agent to hyper-accumulate PpIX by temporarily reducing its Iron dependent conversion to haem. A topical preparation of ALA was applied to normal rat skin with or without the hydroxypyridinone Iron chelator, CP94. Image analysis quantification of tissue fluorescence following excision indicated that ALA plus CP94 produced 29.0% more fluorescence than ALA alone (p < 0.09), peaking at 5 hours. Furthermore, fluorescence spectroscopy of frozen skin samples from each treatment group were characteristic of PpIX (maxima 636 +/- 2 nm), indicating that topical CP94 administration elevated PpIX levels without significantly producing any other fluorescent species. When PDT efficacy was considered post irradiation, a substantial three-fold increase in effect was observed 4 days after treatment when the Iron chelator CP94 was co-administered topically with the prodrug (p < 0.07). It has therefore been established that the hydroxypyridinone CP94, is topically active within normal rat skin, effectively Chelating Iron to elevate PpIX accumulation and thus improve PDT efficacy.
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Enhancing protoporphyrin IX-induced PDT
Photodynamic Therapy: Back to the Future, 2009Co-Authors: Alison Curnow, Andrew Pye, Sandra CampbellAbstract:Photodynamic therapy (PDT) using porphyrin precursors is commonly used in dermatology. Evidence indicates that good clinical outcomes (associated with excellent cosmesis) can be achieved in superficial precancers and basal cell carcinoma (BCC), however, efficacy appears less favorable for thicker nodular BCC (nBCC) unless multiple PDT treatment cycles are performed. Enhancement is therefore required if nBCC lesions are to be treated effectively with a single PDT treatment. The most common technique currently being routinely employed clinically is the use of aminolevulinic acid (ALA) esters (usually methyl (MAL) or hexyl (HAL)). Standard dermatological PDT employing these porphyrin precursors already manipulates the normal heme biosynthesis pathway resulting in a temporary accumulation of the natural photosensitizer, protoporphyrin IX (PpIX). Further manipulation using Iron Chelating Agents is possible however. In normal and malignant human cells in vitro, the novel Iron Chelating Agent CP94 produced greater PPIX fluorescence when administered with ALA or MAL than either congener produced alone. CP94 was also significantly more effective than the clinically established Iron Chelating Agent desferrioxamine (DFO). Topical application of ALA+CP94 to clinical nBCC lesions was a simple and safe treatment modification which produced a significant increase in clinical clearance when CP94 was included in the cream.
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clinical investigation of the novel Iron Chelating Agent cp94 to enhance topical photodynamic therapy of nodular basal cell carcinoma
British Journal of Dermatology, 2008Co-Authors: Sandra Campbell, C A Morton, R Alyahya, S Horton, Alison CurnowAbstract:Summary Background Photodynamic therapy (PDT) involves the activation of a photosensitizer by visible light to produce activated oxygen species within target cells, resulting in their destruction. Evidence-based guidelines support the efficacy of PDT using topical 5-aminolaevulinic acid (ALA-PDT) in actinic keratoses, Bowen disease and basal cell carcinoma (BCC). Efficacy for nodular BCC appears inferior to that for superficial BCC unless prior debulking or repeat treatments are performed. Objectives The aim of this study was to assess the safety and efficacy of adding a novel Iron-Chelating Agent, CP94 (1,2-diethyl-3-hydroxypyridin-4-one hydrochloride), to topical ALA, to temporarily increase the accumulation of the photosensitizer in the tumour. Methods A mixed topical formulation of ALA + increasing concentrations of CP94 was used to carry out PDT on previously biopsied nodular BCC with no prior lesion preparation using standard light delivery. The area was assessed clinically and surgically excised 6 weeks later for histological examination. Results Enhanced PDT using 40% CP94 resulted in significantly greater clearance rates in nodular BCC than with ALA-PDT alone, in our protocol of single-treatment PDT with no lesion preparation. Conclusions The results of this study demonstrate the safe and effective use of an enhanced ALA-PDT protocol for nodular BCC using CP94, with no adverse reactions to this modification. This is the first time this formulation has been used in patients. This formulation is now the focus of further study.
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Enhancement of 5-aminolaevulinic acid-induced photodynamic therapy in normal rat colon using hydroxypyridinone Iron-Chelating Agents
British journal of cancer, 1998Co-Authors: Alison Curnow, A. J. Macrobert, B.w. Mcilroy, Matthew J. Postle-hacon, John B. Porter, Sg BownAbstract:Currently, the clinical use of 5-aminolaevulinic acid (ALA)-induced protoporphyrin IX (PPIX) for photodynamic therapy (PDT) is limited by the maximum tolerated oral ALA dose (60 mg kg(-1)). This study investigates whether hydroxypyridinone Iron-Chelating Agents can be used to enhance the tissue levels of PPIX, without increasing the administered dose of ALA. Quantitative charge-coupled device (CCD) fluorescence microscopy was employed to study PPIX fluorescence pharmacokinetics in the colon of normal Wistar rats. The Iron chelator, CP94, when administered with ALA was found to produce double the PPIX fluorescence in the colonic mucosa, compared with the same dose of ALA given alone and to be more effective than the other Iron chelator studied, CP20. Microspectrofluorimetric studies demonstrated that PPIX was the predominant porphyrin species present. PDT studies conducted on the colonic mucosa showed that the simultaneous administration of 100 mg kg(-1) CP94 i.v. and 50 mg kg(-1) ALA i.v. produced an area of necrosis three times larger than similar parameters without the Iron-Chelating Agent with the same light dose. It is possible, therefore, to increase the amount of necrosis produced by ALA-induced PDT substantially, without increasing the administered dose of ALA, through the simultaneous administration of the Iron-Chelating Agent, CP94.
Tingting Zhu - One of the best experts on this subject based on the ideXlab platform.
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Effects of the Iron-Chelating Agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity.
Journal of biomedical materials research. Part B Applied biomaterials, 2011Co-Authors: Tingting Zhu, Heechul Park, Bum-soon Lim, Kyung Mi Son, Hyeong-cheol YangAbstract:Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (·OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts, and L929 mouse fibroblasts. Deferoxamine (DFO), an Iron Chelating Agent, effectively protected MC3T3-E1 cells from resin monomer-induced cytotoxicity, indicating that cytotoxicity was caused primarily by hydroxyl radicals. However, DFO only had a protective effect against relatively high concentrations of TEGDMA and HEMA in HDPCs and human gingival fibroblasts, and resin monomer-induced cytotoxicity in L929 was not attenuated by DFO. A labile Iron pool (LIP) was detectable only in MC3T3-E1 cells among the four cell types. This indicates that the generation of hydroxyl radicals induced by resin monomers is likely dependent on LIP levels. In contrast to resin monomers, hydrogen peroxide (H2O2)-induced cytotoxicity was not prevented by DFO in any of the cell types examined, although hydroxyl radicals were detected in MC3T3-E1 cells and HDPCs on exposure to exogenous H2O2. This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H2O2-treated cells. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2012.
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Effects of the Iron-Chelating Agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity.
Journal of biomedical materials research. Part B Applied biomaterials, 2011Co-Authors: Tingting Zhu, Heechul Park, Bum-soon Lim, Kyung Mi Son, Hyeong-cheol YangAbstract:Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (·OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts, and L929 mouse fibroblasts. Deferoxamine (DFO), an Iron Chelating Agent, effectively protected MC3T3-E1 cells from resin monomer-induced cytotoxicity, indicating that cytotoxicity was caused primarily by hydroxyl radicals. However, DFO only had a protective effect against relatively high concentrations of TEGDMA and HEMA in HDPCs and human gingival fibroblasts, and resin monomer-induced cytotoxicity in L929 was not attenuated by DFO. A labile Iron pool (LIP) was detectable only in MC3T3-E1 cells among the four cell types. This indicates that the generation of hydroxyl radicals induced by resin monomers is likely dependent on LIP levels. In contrast to resin monomers, hydrogen peroxide (H(2)O(2))-induced cytotoxicity was not prevented by DFO in any of the cell types examined, although hydroxyl radicals were detected in MC3T3-E1 cells and HDPCs on exposure to exogenous H(2)O(2). This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H(2)O(2)-treated cells.
Gideon Koren - One of the best experts on this subject based on the ideXlab platform.
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immune function in patients with β thalassaemia receiving the orally active Iron Chelating Agent deferiprone
British Journal of Haematology, 1997Co-Authors: Ronen Loebstein, Matitiahu Berkovitch, Gideon Koren, Ilan Dalal, Eric Nisbetbrown, Naftaly Meydan, David W Andrews, Michael Loubser, Chaim M Roifman, Nancy F OlivieriAbstract:Short-term deferiprone may reduce body Iron in some patients with thalassaemia major. Concerns regarding potential immunosuppressive effects of deferiprone have been raised from results of animal studies and case reports in humans. We studied immune function in 57 thalassaemia patients: 36 treated with deferiprone (L1; CP020) and 21 treated with desferrioxamine (DFO). Circulating B lymphocytes were increased in all patient groups. No differences were detected between treatment groups in percentages of circulating lymphocytes, concentrations of IgG, IgM or IgA, specific antibody titres, complement levels, or in vitro lymphocyte proliferation. No clinically important infections were observed in any patient. These data suggest that no clinical or laboratory changes consistent with immuno-suppression or immunodeficiency are observed during deferiprone therapy.
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Efficacy of Deferiprone in the Treatment of Acute Iron Intoxication in Rats
Clinical Toxicology, 1996Co-Authors: Frank F. Fassos, Lee Koren, Corrado Falcitelli, Patrick St. Louis, Richard Daneman, Ross G. Cameron, Matitiahu Berkovitch, Nick Daneman, Julia Klein, Gideon KorenAbstract:Background: Deferiprone [(1,2-dimethyl-3-hydroxypyrid-4-one) (L1)], is the first orally active Iron Chelating Agent to reach clinical trials in patients with chronic Iron overload. Its efficacy in preventing morbidity and mortality in acute Iron poisoning has not been tested. Objective: To determine whether deferiprone can reduce the mortality of rats following toxic oral doses of Iron. Methods: Rats were administered 612 mg/kg elemental Iron by gavage, corresponding to the LDS8. A parallel group received the same oral dose of Iron followed by deferiprone intraperitoneally at 400 mg/kg (loading dose), followed by additional intraperitoneal injections of 200 mg/kg, 100 mg/kg and 100 mg/kg of deferiprone at one hour intervals. Results: Coadministering deferiprone with the Iron decreased mortality from 58% (11/19) to 15% (3/20) (p = 0.013). The administration of deferiprone was associated with urinary excretion of Iron (which did not occur with Iron alone) and the production of the red deferiprone-Iron compl...