deferoxamine

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デフェロキサミン

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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/10/09 15:57:55」(JST)

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英文文献

  • Therapeutic effect of deferoxamine on iron overload-induced inhibition of osteogenesis in a zebrafish model.
  • Chen B, Yan YL, Liu C, Bo L, Li GF, Wang H, Xu YJ.Author information Department of Orthopaedics, The Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.AbstractOsteoporosis results from an imbalance in bone remodeling, in which osteoclastic bone resorption exceeds osteoblastic bone formation. Iron has recently been recognized as an independent risk factor for osteoporosis. Reportedly, excess iron could promote osteoclast differentiation and bone resorption through the production of reactive oxygen species (ROS). We evaluated the effect of iron on osteoblast differentiation and bone formation in zebrafish and further investigated the potential benefits of deferoxamine (DFO), a powerful iron chelator, in iron-overloaded zebrafish. The zebrafish model of iron overload described in this study demonstrated an apparent inhibition of bone formation, accompanied by decreased expression of osteoblast-specific genes (runx2a, runx2b, osteocalcin, osteopontin, ALP, and collagen type I). The negative effect of iron on osteoblastic activity and bone formation could be attributed to increased ROS generation and oxidative stress. Most importantly, we revealed that DFO was capable of removing whole-body iron and attenuating oxidative stress in iron-overloaded larval zebrafish, which facilitated larval recovery from the reductions in bone formation and osteogenesis induced by iron overload.
  • Calcified tissue international.Calcif Tissue Int.2014 Mar;94(3):353-60. doi: 10.1007/s00223-013-9817-4. Epub 2014 Jan 12.
  • Osteoporosis results from an imbalance in bone remodeling, in which osteoclastic bone resorption exceeds osteoblastic bone formation. Iron has recently been recognized as an independent risk factor for osteoporosis. Reportedly, excess iron could promote osteoclast differentiation and bone resorption
  • PMID 24414856
  • Impact of antioxidants on the ability of phenolic phytochemicals to kill HCT116 colon cancer cells.
  • Murphy A, Testa K, Berkelhammer J, Hopkins S, Loo G.Author information Department of Nutrition, Cellular and Molecular Nutrition Research Laboratory, University of North Carolina at Greensboro , Greensboro, NC , USA.AbstractAbstract Certain phenolic phytochemicals can kill cancer cells. Possible interference from antioxidants is a concern, and this issue has not been studied appreciably. Therefore, the effect of ascorbate and N-acetylcysteine on the ability of epigallocatechin gallate (EGCG) and curcumin to kill HCT116 colon cancer cells was examined. EGCG and curcumin each caused DNA damage in the cells. The DNA-damaging ability of EGCG, but not curcumin, was hindered by either ascorbate or NAC, which was also shown in HT29 and SW480 colon cancer cells. Also, iron chelators (deferoxamine and 2,2'-dipyridyl) inhibited the ability of EGCG, but not curcumin, to cause damage to the DNA in HCT116 cells. Interestingly, curcumin, but not EGCG, increased the expression of growth arrest and DNA damage-inducible gene 153 and also heme oxygenase-1, and this stress gene upregulation by curcumin was antioxidant-insensitive. With prolonged incubation of HCT116 cells with either EGCG or curcumin, cell shrinkage, membrane blebbing, apoptotic bodies, and chromatin condensation/fragmentation were observed. These morphological changes were not apparent in EGCG-treated cells that had been pretreated with either ascorbate or NAC. However, the ascorbate and NAC pretreatments did not prevent the occurrence of the morphological changes in curcumin-treated cells. Thus, these findings suggest that ascorbate and NAC interfere with the ability of EGCG, but not curcumin, to kill HCT116 cells. This basic knowledge may help to better plan and optimize strategies for chemoprevention or chemotherapy.
  • Free radical research.Free Radic Res.2014 Mar;48(3):313-21. doi: 10.3109/10715762.2013.867958. Epub 2013 Dec 16.
  • Abstract Certain phenolic phytochemicals can kill cancer cells. Possible interference from antioxidants is a concern, and this issue has not been studied appreciably. Therefore, the effect of ascorbate and N-acetylcysteine on the ability of epigallocatechin gallate (EGCG) and curcumin to kill HCT116
  • PMID 24256565
  • Abnormal differentiation of dopaminergic neurons in zebrafish trpm7 mutant larvae impairs development of the motor pattern.
  • Decker AR1, McNeill MS2, Lambert AM3, Overton JD4, Chen YC5, Lorca RA6, Johnson NA7, Brockerhoff SE7, Mohapatra DP6, Macarthur H8, Panula P5, Masino MA3, Runnels LW4, Cornell RA9.Author information 1Department of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, United States.2Interdisciplinary Graduate Program in Neuroscience, University of Iowa, Iowa City, IA 52242, United States.3Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, United States.4UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ 08854, United States.5Neuroscience Center and Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland.6Department of Pharmacology, University of Iowa, Iowa City, IA 52245, United States.7Department of Biochemistry, University of Washington, Seattle, WA 98195, United States.8Department of Pharmacological and Physiological Science, St. Louis University, St. Louis, MO 63104, United States.9Department of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, United States; Interdisciplinary Graduate Program in Neuroscience, University of Iowa, Iowa City, IA 52242, United States. Electronic address: robert-cornell@uiowa.edu.AbstractTransient receptor potential, melastatin-like 7 (Trpm7) is a combined ion channel and kinase implicated in the differentiation or function of many cell types. Early lethality in mice and frogs depleted of the corresponding gene impedes investigation of the functions of this protein particularly during later stages of development. By contrast, zebrafish trpm7 mutant larvae undergo early morphogenesis normally and thus do not have this limitation. The mutant larvae are characterized by multiple defects including melanocyte cell death, transient paralysis, and an ion imbalance that leads to the development of kidney stones. Here we report a requirement for Trpm7 in differentiation or function of dopaminergic neurons in vivo. First, trpm7 mutant larvae are hypomotile and fail to make a dopamine-dependent developmental transition in swim-bout length. Both of these deficits are partially rescued by the application of levodopa or dopamine. Second, histological analysis reveals that in trpm7 mutants a significant fraction of dopaminergic neurons lack expression of tyrosine hydroxylase, the rate-limiting enzyme in dopamine synthesis. Third, trpm7 mutants are unusually sensitive to the neurotoxin 1-methyl-4-phenylpyridinium, an oxidative stressor, and their motility is partially rescued by application of the iron chelator deferoxamine, an anti-oxidant. Finally, in SH-SY5Y cells, which model aspects of human dopaminergic neurons, forced expression of a channel-dead variant of TRPM7 causes cell death. In summary, a forward genetic screen in zebrafish has revealed that both melanocytes and dopaminergic neurons depend on the ion channel Trpm7. The mechanistic underpinning of this dependence requires further investigation.
  • Developmental biology.Dev Biol.2014 Feb 15;386(2):428-39. doi: 10.1016/j.ydbio.2013.11.015. Epub 2013 Nov 27.
  • Transient receptor potential, melastatin-like 7 (Trpm7) is a combined ion channel and kinase implicated in the differentiation or function of many cell types. Early lethality in mice and frogs depleted of the corresponding gene impedes investigation of the functions of this protein particularly duri
  • PMID 24291744

和文文献

  • フッ素によるアルミニウムに依存した Na, K-ATPase 活性の抑制
  • 石川 一郎,出山 義昭,吉村 善隆,鈴木 邦明
  • 北海道歯学雑誌 31(2), 44-51, 2010-12-15
  • … NaFとKFはNa,K-ATPase活性を濃度に依存して抑制し,50%阻害濃度(Ki0.5)は約1.4mMであった.0.25mMF存在下での活性抑制は約10%であり,2.5mMではほぼ完全に抑制された.FによるKi0.5はアルミニウム(A1)存在下でA1の濃度に依存して減少し,A1のキレーターであるdeferoxamine存在下では増加した. …
  • NAID 10028208506
  • Iron chelation therapy in the management of thalassemia : the Asian perspectives
  • VIPRAKASIT Vip,LEE-LEE Chan,CHONG Quah Thuan,LIN Kai-Hsin,KHUHAPINANT Archrob
  • International journal of hematology 90(4), 435-445, 2009-11-15
  • NAID 10026109273

関連リンク

デフェロキサミン(英: deferoxamine, desferrioxamine, desferoxamine, DFO, DFOA, desferal)とは体内から過剰な鉄を除去するために使用されるキレート剤の一つで、鉄 過剰症及び鉄中毒の治療薬。イギリスでは一般にメシル酸デフェロキサミンとして使用 ...
Deferoxamine (also known as desferrioxamine B, desferoxamine B, DFO-B, DFOA, DFB or desferal) is a bacterial siderophore produced by the actinobacteria Streptomyces pilosus. It has medical applications as a chelating agent used to ...

関連画像

Drugs reference index « deferoxamine »Deferoxamine (Desferrioxamine)Deferoxamine retinopathy - Retina Image Details of DEF; Ligand Name: DEFEROXAMINE Antidote: Deferoxamine (DFO)Deferoxamine Mesylate Powder, 500mg/Vial


★リンクテーブル★
リンク元デフェロキサミン」「desferrioxamine
拡張検索deferoxamine mesilate」「deferoxamine mesylate

デフェロキサミン」

  [★]

deferoxamine
メシル酸デフェロキサミン deferoxamine mesilate
デスフェラール Desferal
デスフェリオキサミンデスフェラール
  • キレート剤
  • CAS:138-14-7
  • C25H48N6O8・CH4SO3
http://www.genome.jp/kegg-bin/get_entry?dr+D01186

適応

  • 鉄中毒


desferrioxamine」

  [★]

デスフェリオキサミン

deferoxaminedeferoxamine mesilateDesferal


deferoxamine mesilate」

  [★] デフェロキサミン メシル酸デフェロキサミン

deferoxamineDesferaldesferrioxamine


deferoxamine mesylate」

  [★] デフェロキサミン deferoxamineメシル酸デフェロキサミン




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