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Nitric oxide, nitrosyl iron complexes, ferritin and frataxin: A well equipped team to preserve plant iron homeostasis 总被引:2,自引:0,他引:2
Iron is a key element in plant nutrition. Iron deficiency as well as iron overload results in serious metabolic disorders that affect photosynthesis, respiration and general plant fitness with direct consequences on crop production.More than 25% of the cultivable land possesses low iron availability due to high pH (calcareous soils). Plant biologists are challenged by this concern and aimed to find new avenues to ameliorate plant responses and keep iron homeostasis under control even at wide range of iron availability in various soils. For this purpose, detailed knowledge of iron uptake, transport, storage and interactions with cellular compounds will help to construct a more complete picture of its role as essential nutrient. In this review, we summarize and describe the recent findings involving four central players involved in keeping cellular iron homeostasis in plants: nitric oxide, ferritin, frataxin and nitrosyl iron complexes. We attempt to highlight the interactions among these actors in different scenarios occurring under iron deficiency or iron overload, and discuss their counteracting and/or coordinating actions leading to the control of iron homeostasis. 相似文献
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Roberta J. Ward Stephanie Wilmet Rachida Legssyer Daniel Leroy Louise Toussaint Robert R. Crichton Christophe Pierreux Louis Hue Jacques Piette Surjit Kaila Srai Nita Solanky Dominique Klein Karl Summer 《Biometals》2009,22(2):211-223
The effects of changes in macrophage iron status, induced by single or multiple iron injections, iron depletion or pregnancy,
on both immune function and mRNA expression of genes involved in iron influx and egress have been evaluated. Macrophages isolated
from iron deficient rats, or pregnant rats at day 21 of gestation, either supplemented with a single dose of iron dextran,
10 mg, at the commencement of pregnancy, or not, showed significant increases of macrophage ferroportin mRNA expression, which was paralleled by significant decreases in hepatic Hamp mRNA expression. IRP activity in macrophages was not significantly altered by iron status or the inducement of pregnancy
± a single iron supplement. Macrophage immune function was significantly altered by iron supplementation and pregnancy. Iron
supplementation, alone or combined with pregnancy, increased the activities of both NADPH oxidase and nuclear factor kappa
B (NFκB). In contrast, the imposition of pregnancy reduced the ability of these parameters to respond to an inflammatory stimuli.
Increasing iron status, if only marginally, will reduce the ability of macrophages to mount a sustained response to inflammation
as well as altering iron homeostatic mechanisms. 相似文献
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Perception and response to nutritional iron by bacteria is essential for viability, and for the ability to adapt to the environment.
The iron response regulator (Irr) is part of a novel regulatory scheme employed by Rhizobium and other Alpha-Proteobacteria to control iron-dependent gene expression. Bradyrhizobium japonicum senses iron through the status of heme biosynthesis to regulate gene expression, thus it responds to an iron-dependent process
rather than to iron directly. Irr mediates this response by interacting directly with ferrochelatase, the enzyme that catalyzes
the final step in heme biosynthesis. Irr is expressed under iron limitation to both positively and negatively modulate gene
expression, but degrades in response to direct binding to heme in iron-sufficient cells. Studies with Rhizobium reveal that the regulation of iron homeostasis in bacteria is more diverse than has been generally assumed. 相似文献
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Iron deficiency is a common micronutrient deficiency associated with metabolic changes in the levels of iron regulatory proteins, hepcidin and ferroportin. Studies have associated dysregulation of iron homeostasis to other secondary and life-threatening diseases including anaemia, neurodegeneration and metabolic diseases. Iron deficiency plays a critical role in epigenetic regulation by affecting the Fe2+/α-ketoglutarate-dependent demethylating enzymes, Ten Eleven Translocase 1–3 (TET 1–3) and Jumonji-C (JmjC) histone demethylase, which are involved in epigenetic erasure of the methylation marks on both DNA and histone tails, respectively. In this review, studies involving epigenetic effects of iron deficiency associated with dysregulation of TET 1–3 and JmjC histone demethylase enzyme activities on hepcidin/ferroportin axis are discussed. 相似文献
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Zhongping Deng Lisa A. Dailey Joleen Soukup Jacqueline Stonehuerner Judy D. Richards Kimberly D. Callaghan Funmei Yang Andrew J. Ghio 《Biometals》2009,22(5):803-815
Despite recurrent exposure to zinc through inhalation of ambient air pollution particles, relatively little information is
known about the homeostasis of this metal in respiratory epithelial cells. We describe zinc uptake and release by respiratory
epithelial cells and test the postulate that Zn2+ transport interacts with iron homeostasis in these same cells. Zn2+ uptake after 4 and 8 h of exposure to zinc sulfate was concentration- and time-dependent. A majority of Zn2+ release occurred in the 4 h immediately following cell exposure to ZnSO4. Regarding metal importers, mRNA for Zip1 and Zip2 showed no change after respiratory epithelial cell exposure to zinc while
mRNA for divalent metal transporter (DMT)1 increased. Western blot assay for DMT1 protein supported an elevated expression
of this transport protein following zinc exposure. RT-PCR confirmed mRNA for the metal exporters ZnT1 and ZnT4 with the former
increasing after ZnSO4. Cell concentrations of ferritin increased with zinc exposure while oxidative stress, measured as lipid peroxides, was decreased
supporting an anti-oxidant function for Zn2+. Increased DMT1 expression, following pre-incubations of respiratory epithelial cells with TNF-α, IFN-γ, and endotoxin, was
associated with significantly decreased intracellular zinc transport. Finally, incubations of respiratory epithelial cells
with both zinc sulfate and ferric ammonium citrate resulted in elevated intracellular concentrations of both metals. We conclude
that exposure to zinc increases iron uptake by respiratory epithelial cells. Elevations in cell iron can possibly affect an
increased expression of DMT1 and ferritin which function to diminish oxidative stress. Comparable to other metal exposures,
changes in iron homeostasis may contribute to the biological effects of zinc in specific cells and tissues. 相似文献
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The biological relevance of each of the three inorganic species – iron, oxygen, and nitric oxide (NO) – is crucial. Moreover,
their metabolic pathways cross each other and thus create a complex network of connections responsible for the regulation
of many essential biological processes. The iron storage protein ferritin, one of the main regulators of iron homeostasis,
influences oxygen and NO metabolism. Here, examples are given of the biological interactions of the ferritin molecule (ferritin
iron and ferritin shell) with reactive oxygen species (ROS) and NO. The focus is the regulation of ferritin expression by
ROS and NO. From these data, ferritin emerges as an important cytoprotective component of the cellular response to ROS and
NO. Also, by its ability to alter the amount of intracellular "free" iron, ferritin may affect the metabolism of ROS and NO.
It is proposed that this putative activity of ferritin may constitute a missing link in the regulatory loop between iron,
ROS, and NO.
Received: 2 January 1997 / Accepted: 9 June 1997 相似文献
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Synergism of nitric oxide and iron in killing the transformed murine oligodendrocyte cell line N20.1
Nitric oxide (NO) produced in inflammatory lesions may play a major role in the destruction of oligodendrocytes in multiple sclerosis and experimental allergic encephalomyelitis. The transformed murine oligodendroglial line N20.1 is much more resistant than primary oligodendrocytes to killing by the NO generator S-nitroso-N-acetyl-DL-penicillamine (SNAP). This observation prompted investigation of the mechanisms leading to cell death in the N20.1 cells and comparison of SNAP with another NO donor, sodium nitroprusside (SNP). We observed that N20.1 cells were 30 times more sensitive to SNP than to SNAP. The specific NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) protected against SNP only, not against SNAP. However, dithiothreitol protected against both SNAP and SNP, indicating that S-nitrosylation of cysteines plays a major role in the cytotoxicity of both NO donors. We did not observe any formation of peroxynitrite or increase of Ca2+ concentration with either SNAP or SNP, thus excluding their involvement in the mechanisms leading to N20.1 cell death. Based on two observations, (a) potentiation of the cytotoxic effect of SNP when coincubated with ferricyanide or ferrocyanide, but not sodium cyanide, and (b) protection by deferoxamine, an iron cyanide chelator, we conclude that the greater sensitivity of N20.1 cells to SNP compared with SNAP is due to synergism between NO released and the iron cyanide portion of SNP, with the cyanide accounting for very little of the cytotoxicity. Finally, SNP but not SNAP induces some apoptosis, as shown by DNA laddering and protection by a caspase-3 inhibitor. These results suggest that low levels of NO in combination with increased iron content lead to apoptotic cell death rather than the necrotic cell death seen with higher levels of NO generated by SNAP. 相似文献
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M. Claire Kennedy William E. Antholine Wenbao Li Qunkai Mao David H. Petering 《Inorganica chimica acta》1995,240(1-2):535-540
During the ESR spectroscopic titration of nitrosyl-iron bleomycin, ON---Fe(II)Blm, with DNA, its metal domain undergoes a change in environment as the DNA base pair to drug ratio increases to 50 to 1. The 15N---O stretching frequency of ON---Fe(II)Blm occurs at 1589 cm−1, similar to that for nitrosyl hemoglobin and myoglobin. Upon addition of DNA (3 base pairs per drug molecule), this vibration is substantially broadened. Injection of O2 into a solution of ON---Fe(II)BlmDNA converts the ESR signal of the nitrosyl species to low spin Fe(III) BlmDNA. NO is largely oxidized to NO2−. The combination of these products suggests that the initial reaction of ON---Fe(II)Blm with O2 generates Fe(III)Blm and peroxynitrite, O2NO−. If peroxynitrite is formed in the reaction, it does not cause detectable DNA damage. The structural integrity of a supercoiled DNA plasmid, pBR322, is not compromised and no base propenals are produced during this reaction. 相似文献
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In the present study, the role of ethylene in nitric oxide (NO)-mediated protection by modulating ion homeostasis in Arabidopsis callus under salt stress was investigated. Results showed that the ethylene-insensitive mutant etr1-3 was more sensitive to salt stress than the wild type (WT). Under 100 mM NaCl, etr1-3 callus displayed a greater electrolyte leakage and Na+/K+ ratio but a lower plasma membrane (PM) H+-ATPase activity compared to WT callus. Application of exogenous 1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor)
or sodium nitroprusside (SNP, a NO donor) alleviated NaCl-induced injury by maintaining a lower Na+/K+ ratio and an increased PM H+-ATPase activity in WT callus but not in etr1-3 callus. The SNP actions in NaCl stress were attenuated by a specific NO scavenger or an ethylene biosynthesis inhibitor in
WT callus. Under 100 mM NaCl, the NO accumulation and ethylene emission appeared at early time, and NO production greatly
stimulated ethylene emission in WT callus. In addition, ethylene induced the expression of PM H+-ATPase genes under salt stress. The recovery experiment showed that NaCl-induced injury was reversible, as signaled by the
similar recovery of Na+/K+ ratio and PM H+-ATPase activity in WT callus. Taken together, the results indicate that ethylene and NO cooperate in stimulating PM H+-ATPase activity to modulate ion homeostasis for salt tolerance, and ethylene may be a part of the downstream signal molecular
in NO action. 相似文献
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The nicotinamide adenine dinucleotide phosphate (NADPH) and reduced glutathione (GSH) molecules play important roles in the redox homeostasis of plant cells. Using tomato (Solanum lycopersicum) plants grown with 120 mM NaCl, we studied the redox state of NADPH and GSH as well as ascorbate, nitric oxide (NO) and S-nitrosoglutathione (GSNO) content and the activity of the principal enzymes involved in the metabolism of these molecules in roots. Salinity caused a significant reduction in growth parameters and an increase in oxidative parameters such as lipid peroxidation and protein oxidation. Salinity also led to an overall decrease in the content of these redox molecules and in the enzymatic activities of the main NADPH-generating dehydrogenases, S-nitrosoglutathione reductase and catalase. However, NO content as well as gluthahione reductase and glutathione peroxidase activity increased under salinity stress. These findings indicate that salinity drastically affects redox and NO homeostasis in tomato roots. In our view, these molecules, which show the interaction between ROS and RNS metabolisms, could be excellent parameters for evaluating the physiological conditions of plants under adverse stress conditions. 相似文献
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Anatoly F. Vanin Xiaoping Liu Alexandre Samouilov Reonald A. Stukan Jay L. Zweier 《Biochimica et Biophysica Acta (BBA)/General Subjects》2000,1474(3):365-377
While the Fe2+–dithiocarbamate complexes have been commonly used as NO traps to estimate NO production in biological systems, these complexes can undergo complex redox chemistry. Characterization of this redox chemistry is of critical importance for the use of this method as a quantitative assay of NO generation. We observe that the commonly used Fe2+ complexes of N-methyl-D-glucamine dithiocarbamate (MGD) or diethyldithiocarbamate (DETC) are rapidly oxidized under aerobic conditions to form Fe3+ complexes. Following exposure to NO, diamagnetic NO–Fe3+ complexes are formed as demonstrated by the optical, electron paramagnetic resonance and gamma-resonance spectroscopy, chemiluminescence and electrochemical methods. Under anaerobic conditions the aqueous NO–Fe3+–MGD and lipid soluble NO–Fe2+–DETC complexes gradually self transform by reductive nitrosylation into paramagnetic NO–Fe2+–MGD complexes with yield of up to 50% and the balance is converted to Fe3+–MGD and nitrite. In dimethylsulfoxide this process is greatly accelerated. More efficient transformation of NO–Fe3+–MGD into NO–Fe2+–MGD (60–90% levels) was observed after addition of reducing equivalents such as ascorbate, hydroquinone or cysteine or with addition of excess Fe2+–MGD. With isotope labeling of the NO–Fe3+–MGD with 57Fe, it was shown that these complexes donate NO to Fe2+–MGD. NO–Fe3+–MGD complexes were also formed by reversible oxidation of NO–Fe2+–MGD in air. The stability of NO–Fe3+–MGD and NO–Fe2+–MGD complexes increased with increasing the ratio of MGD to Fe. Thus, the iron–dithiocarbamate complexes and their NO derivatives exhibit complex redox chemistry that should be considered in their application for detection of NO in biological systems. 相似文献
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Eric A. Johnson Miranda M. Russo Dillon B. Nye Jamie L. Schlessman Juliette T.J. Lecomte 《Biochimica et Biophysica Acta (BBA)/General Subjects》2018,1862(12):2660-2673