scholarly journals Research development in tumor therapy: role of iron-related nanoparticles

2021 ◽  
Vol 251 ◽  
pp. 02051
Author(s):  
Dai Peipei
Keyword(s):  
Iron Homeostasis ◽  
Tumor Therapy ◽  
Critical Role ◽  
Regulatory Proteins ◽  
Nutrient Element ◽  
Biochemical Activity ◽  
Body Tissues ◽  
Metal Organic ◽  
Essential Nutrient

As an essential nutrient element for life, iron’s metabolic balance in body tissues is crucial to sustaining normal physiological functions, and it is inextricably related to tumors. Nanotechnology is gaining much attention around the world for cancer treatment. Considering the critical role of iron metabolism, nanocarriers’ toxicity and biocompatibility, novel nanomaterials based on the biochemical activity of iron and the regulatory proteins of iron homeostasis-metabolism show broad application prospects in the field of tumor diagnosis and treatment. In this review, the role of iron-related nanocarriers for tumor therapy, such as iron oxide nanoparticles, Fe-based metal-organic frameworks, ferritin, and transferrin, was reviewed, aiming to help people better understand their tremendous potential in tumor therapy.

The critical role of the coordination sphere in the high-efficiency blue-light emission from aminopyrazine metal-organic polymers

2021 ◽  
Vol 186 ◽  
pp. 109025
Author(s):  
João Humberto Dias Campos ◽  
Meiry Edivirges Alvarenga ◽  
Maykon Alves Lemes ◽  
José Antônio do Nascimento Neto ◽  
Freddy Fernandes Guimarães ◽  
...  
Keyword(s):  
Blue Light ◽  
Coordination Sphere ◽  
High Efficiency ◽  
Light Emission ◽  
Critical Role ◽  
Organic Polymers ◽  
Blue Light Emission ◽  
Metal Organic

Critical role of water stability in metal–organic frameworks and advanced modification strategies for the extension of their applicability

2020 ◽  
Vol 7 (5) ◽  
pp. 1319-1347 ◽  
Author(s):  
Botao Liu ◽  
Kumar Vikrant ◽  
Ki-Hyun Kim ◽  
Vanish Kumar ◽  
Suresh Kumar Kailasa
Keyword(s):  
Drug Delivery ◽  
Water Purification ◽  
Gas Adsorption ◽  
Critical Role ◽  
Metal Organic Frameworks ◽  
Water Stability ◽  
Metal Organic

Metal–organic frameworks (MOFs) are well known for their versatile applications in diverse fields (e.g., gas adsorption, water purification, sensing, drug delivery, and catalysis).

scholarly journals The Role of the Liver in Iron Homeostasis and What Goes Wrong?

2021 ◽  
Vol 5 (2) ◽  
pp. 26-33
Author(s):  
Ernesto Robalino Gonzaga ◽  
Irene Riestra Guiance ◽  
Richard Henriquez ◽  
Gerri Mortimore ◽  
Jan Freeman
Keyword(s):  
Iron Overload ◽  
Iron Homeostasis ◽  
The Body ◽  
Body Tissues ◽  
Hepatic Iron Overload ◽  
Common Causes ◽  
Physiologic Function ◽  
Normal Cellular Function ◽  
Synthesis Of Hormones

Iron is an essential mineral that is vital for growth development, normal cellular function, synthesis of hormones and connective tissue, and most importantly, serves as a component of hemoglobin to carry oxygen to body tissues. The body finely regulates the amount of circulating and stored iron within the body to maintain concentration levels within range for optimal physiologic function. Without iron, the ability for cells to participate in electron transport and energy metabolism decreases. Furthermore, hemoglobin synthesis is altered, which leads to anemia and decreased oxygen delivery to tissue. Problems arise when there is too little or too much iron. This review explores the role of the liver in iron physiology, iron overload and discusses the most common causes of primary and secondary hepatic iron overload.

Abstract 98: Reducing Mitochondrial, But Not Cytosolic Iron, Protects The Heart Against Ischemia-reperfusion Injury

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Hsiang-Chun J Chang ◽  
Rongxue Wu ◽  
Hossein Ardehali
Keyword(s):  
Cardiac Function ◽  
Iron Homeostasis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Mitochondrial Iron

Introduction: Iron is essential for the activity of a large number of cellular proteins, but excess free iron can cause cellular damage through production of reactive oxygen species (ROS). Mitochondria are the major site of cellular iron homeostasis, and we recently showed the mitochondrial iron export is mediated by ATP-binding cassette protein-B8 (ABCB8). The role of mitochondrial iron in ischemia-reperfusion (I/R) injury in the heart has not been examined. We hypothesize that mitochondrial iron has a critical role in I/R damage and a reduction of mitochondrial iron is protective against I/R injury through a reduction in ROS. Results: Cardiomyocyte-specific ABCB8 transgenic (TG) mice had significantly lower mitochondrial iron in the heart than nontransgenic (NTG) littermates at baseline, but their cardiac function and the expression of key antioxidant systems were indistinguishable from NTG littermates. To study the role of mitochondrial iron in I/R injury, we subjected ABCB8 TG mice to I/R. TG mice displayed significantly less apoptosis compared to NTG littermates (11.76% vs. 17.63%, p<0.05, n=4-6) and had significantly reduced lipid peroxidation products 48 hours after I/R. To further confirm that our in vivo finding was due to reduced mitochondrial iron, we studied the effect of pharmacological reduction of mitochondrial iron in vitro. 2,2-bipyridyl (BPD) is a mitochondria-accessible iron chelator while deferoxamine (DFO) has poor penetrance into mitochondria. Treating rat cardiomyoblasts H9C2 with BPD but not DFO significantly reduced chelatable mitochondrial iron, as measured by staining cells with rhodamine B-[(1,10-phenanthrolin-5-yl)aminocarbonyl]benzyl ester. In addition, BPD but not DFO pretreatment protected cells against H2O2 induced cell death (p<0.05). BPD treatment in mice decreased baseline mitochondrial iron and significantly preserved cardiac function after I/R. Conclusions: Our findings demonstrate that selective reduction in mitochondrial iron is protective in I/R injury, and show that mitochondrial iron is a source of ROS and cellular damage in I/R. Thus, targeting mitochondrial iron with selective iron chelators, as studied in our system, may provide a novel approach for treatment of ischemic heart disease.

scholarly journals Reductive Iron Assimilation and Intracellular Siderophores Assist Extracellular Siderophore-Driven Iron Homeostasis and Virulence

2014 ◽  
Vol 27 (8) ◽  
pp. 793-808 ◽  
Author(s):  
Bradford J. Condon ◽  
Shinichi Oide ◽  
Donna M. Gibson ◽  
Stuart B. Krasnoff ◽  
B. Gillian Turgeon
Keyword(s):  
Iron Homeostasis ◽  
Iron Acquisition ◽  
Wild Type ◽  
Peptide Synthetases ◽  
Asexual Sporulation ◽  
High Affinity ◽  
Iron Assimilation ◽  
Genes Encoding ◽  
Essential Nutrient

Iron is an essential nutrient and prudent iron acquisition and management are key traits of a successful pathogen. Fungi use nonribosomally synthesized secreted iron chelators (siderophores) or reductive iron assimilation (RIA) mechanisms to acquire iron in a high affinity manner. Previous studies with the maize pathogen Cochliobolus heterostrophus identified two genes, NPS2 and NPS6, encoding different nonribosomal peptide synthetases responsible for biosynthesis of intra- and extracellular siderophores, respectively. Deletion of NPS6 results in loss of extracellular siderophore biosynthesis, attenuated virulence, hypersensitivity to oxidative and iron-depletion stress, and reduced asexual sporulation, while nps2 mutants are phenotypically wild type in all of these traits but defective in sexual spore development when NPS2 is missing from both mating partners. Here, it is reported that nps2nps6 mutants have more severe phenotypes than both nps2 and nps6 single mutants. In contrast, mutants lacking the FTR1 or FET3 genes encoding the permease and ferroxidase components, respectively, of the alternate RIA system, are like wild type in all of the above phenotypes. However, without supplemental iron, combinatorial nps6ftr1 and nps2nps6ftr1 mutants are less virulent, are reduced in growth, and are less able to combat oxidative stress and to sporulate asexually, compared with nps6 mutants alone. These findings demonstrate that, while the role of RIA in metabolism and virulence is overshadowed by that of extracellular siderophores as a high-affinity iron acquisition mechanism in C. heterostrophus, it functions as a critical backup for the fungus.

scholarly journals Ferroportin 3 is a dual-targeted mitochondrial/chloroplast iron exporter necessary for iron homeostasis in Arabidopsis

2020 ◽  
Author(s):  
Leah J. Kim ◽  
Kaitlyn M. Tsuyuki ◽  
Fengling Hu ◽  
Emily Y. Park ◽  
Jingwen Zhang ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Homeostasis ◽  
Critical Role ◽  
Physiological Role ◽  
Chloroplast Ultrastructure ◽  
Iron Regulation ◽  
Wild Type ◽  
Mitochondrial Ultrastructure ◽  
Iron Deficient

ABSTRACTMitochondria and chloroplasts are organelles with high iron demand that are particularly susceptible to iron-induced oxidative stress. Despite the necessity of strict iron regulation in these organelles, much remains unknown about mitochondrial and chloroplast iron transport in plants. Here, we propose that Arabidopsis Ferroportin 3 (FPN3) is an iron exporter dual-targeted to mitochondria and chloroplasts. FPN3 is expressed in shoots regardless of iron conditions, but its transcripts accumulate under iron deficiency in roots. fpn3 mutants cannot grow as well as wild type under iron-deficient conditions and shoot iron levels are reduced in fpn3 mutants compared to wild type. ICP-MS measurements show that iron levels in the mitochondria and chloroplasts are increased relative to wild type, consistent with the proposed role of FPN3 as a mitochondrial/plastid iron exporter. In iron deficient fpn3 mutants, abnormal mitochondrial ultrastructure was observed, whereas chloroplast ultrastructure was not affected, implying that FPN3 plays a critical role in the mitochondria. Overall, our study suggests that FPN3 is essential for optimal iron homeostasis.Significance statementIron homeostasis must be tightly controlled in the mitochondria and chloroplasts, but iron trafficking in these organelles is not fully understood. Our work suggests that FPN3 is an iron exporter required for maintaining proper iron levels in mitochondria and chloroplasts. Furthermore, FPN3 is necessary for the optimal growth and normal mitochondrial ultrastructure under iron deficiency. This study reveals the physiological role of FPN3 and advances our understanding of iron regulation in mitochondria and chloroplasts.

scholarly journals Role of Iron Metabolism-Related Genes in Prenatal Development: Insights from Mouse Transgenic Models

Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1382
Author(s):  
Zuzanna Kopeć ◽  
Rafał R. Starzyński ◽  
Aneta Jończy ◽  
Rafał Mazgaj ◽  
Paweł Lipiński
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Current Knowledge ◽  
Prenatal Development ◽  
Postnatal Life ◽  
Mammalian Development ◽  
Knock Out ◽  
Stage Of Development ◽  
Essential Nutrient

Iron is an essential nutrient during all stages of mammalian development. Studies carried out over the last 20 years have provided important insights into cellular and systemic iron metabolism in adult organisms and led to the deciphering of many molecular details of its regulation. However, our knowledge of iron handling in prenatal development has remained remarkably under-appreciated, even though it is critical for the health of both the embryo/fetus and its mother, and has a far-reaching impact in postnatal life. Prenatal development requires a continuous, albeit quantitatively matched with the stage of development, supply of iron to support rapid cell division during embryogenesis in order to meet iron needs for erythropoiesis and to build up hepatic iron stores, (which are the major source of this microelement for the neonate). Here, we provide a concise overview of current knowledge of the role of iron metabolism-related genes in the maintenance of iron homeostasis in pre- and post-implantation development based on studies on transgenic (mainly knock-out) mouse models. Most studies on mice with globally deleted genes do not conclude whether underlying in utero iron disorders or lethality is due to defective placental iron transport or iron misregulation in the embryo/fetus proper (or due to both). Therefore, there is a need of animal models with tissue specific targeted deletion of genes to advance the understanding of prenatal iron metabolism.

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