管道输液滴干对苹果缺铁失绿症的影响

为探索防止果树缺铁失绿症方案,该研究以Fe-N为铁肥品种,以管道输液滴干的方式对中秋王苹果树输入不同浓度的溶液,测定叶片的叶绿素相对含量(SPAD值)、百叶重、百叶厚、全铁和活性铁含量及荧光参数等指标。结果表明:Fe-N管道输液滴干处理显著提高了苹果叶片的SPAD值、百叶重、百叶厚、全铁以及活性铁的含量,发现叶片SPAD值与活性铁含量之间呈现良好的线性关系(相关系数为0.899),表明叶片SPAD值可以作为苹果缺铁诊断指标,同时也说明了苹果树体叶片黄化主要是由于活性铁含量低所致。16.4×10~(-3)mol·L~(-1)Fe-N溶液处理的叶片SPAD值、百叶重、百叶厚、全铁及活性铁含量显著高于其它处理,分别比对照提高了89.66%、20.42%、9.26%、158.0%、277.4%,该处理荧光参数也达到了较优水平。该研究结果为管道输液滴干防止苹果缺铁失绿症的应用奠定了基础。     

H2O2 mediates nitrate‐induced iron chlorosis by regulating iron homeostasis in rice

The uptake of nitrate by plant roots causes a pH increment in rhizosphere and leads to iron (Fe) deficiency in rice. However, little is known about the mechanism how the nitrate uptake‐induced high rhizosphere pH causes Fe deficiency. Here, we found that rice showed severe leaf chlorosis and large amounts of Fe plaque were aggregated on the root surface and intercellular space outside the exodermis in a form of ferrihydrite under alkaline conditions. In this case, there was significantly decreased Fe concentration in shoots, and the Fe deficiency responsive genes were strongly induced in the roots. The high rhizosphere pH induced excess hydrogen peroxide (H₂O₂) production in the epidermis due to the increasing expression of NADPH‐oxidase respiratory burst oxidase homolog 1, which enhanced root oxidation ability and improved the Fe plaque formation in rhizosphere. Further, the concentrated H₂O₂ regulated the phenylpropanoid metabolism with increased lignin biosynthesis and decreased phenolics secretion, which blocked apoplast Fe mobilization efficiency. These factors coordinately repressed the Fe utilization in rhizosphere and led to Fe deficiency in rice under high pH. In conclusion, our results demonstrate that nitrate uptake‐induced rhizosphere alkalization led to Fe deficiency in rice, through H₂O₂‐dependent manners of root oxidation ability and phenylpropanoid metabolism.     

Juncus bulbosus as a pioneer species in acidic lignite mining lakes: interactions, mechanism and survival strategies

Bulbous rush ( Juncus bulbosus ) initiates plant colonization in extremely acid lakes resulting from coal mining operations. Various analytical techniques (methylene blue/agar method, Ti³⁺-citrate solution) X-ray diffraction (XRD), scanning electron microscopy (SEM), and Energy-dispersive X-ray (EDX) were used to assess the mechanisms and strategies employed by J. bulbosus to overcome the extreme conditions. The plant releases oxygen into the rhizosphere in turn increasing the redox potential and inducing iron oxide plaque formation. XRD showed that the iron oxide of the plaque is mainly goethite that has been developed in the presence of CO₂; SEM showed that there is a micro-space between the roots and sand grains which is inhabited by microorganisms. Furthermore, SEM-EDX studies on internal iron distribution demonstrate that iron toxicity is delayed by the physiological and biochemical structure of the plant. It is suggested that J. bulbosus uses a variety of mechanisms and strategies (morphological, physiological and biochemical adaptation) which are mainly complementary and which interact with each other to help J. bulbosus to manage its growth and survival in an extreme environment.     

Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat

Managanese (Mn) is an essential trace element at low concentrations, but at higher concentrations is neurotoxic. It has several chemical and biochemical properties similar to iron (Fe), and there is evidence of metabolic interaction between the two metals, particularly at the level of absorption from the intestine. The aim of this investigation was to determine whether Mn and Fe interact during the processes involved in uptake from the plasma by the brain and other organs of the rat. Dams were fed control (70 mg Fe/kg), Fe-deficient (5–10 mg Fe/kg), or Fe-loaded (20 g carbonyl Fe/kg) diets, with or without Mn-loaded drinking water (2 g Mn/L), from day 18–19 of pregnancy, and, after weaning the young rats, were continued on the same dietary regimens. Measurements of brain, liver, and kidney Mn and nonheme Fe levels, and the uptake of⁵⁴Mn and⁵⁹Fe from the plasma by these organs and the femurs, were made when the rats were aged 15 and 63 d. Organ nonheme Fe levels were much higher than Mn levels, and in the liver and kidney increased much more with Fe loading than did Mn levels with Mn loading. However, in the brain the increases were greater for Mn. Both Fe depletion and loading led to increased brain Mn concentrations in the 15-d/rats, while Fe loading also had this effect at 63 d. Mn loading did not have significant effects on the nonheme Fe concentrations.⁵⁴Mn, injected as MnCl₂ mixed with serum, was cleared more rapidly from the circulation than was⁵⁹Fe, injected in the form of diferric transferrin. In the 15-d-rats, the uptake of⁵⁴Mn by brain, liver, kidneys, and femurs was increased by Fe loading, but this was not seen in the 63-d rats. Mn supplementation led to increased⁵⁹Fe uptake by the brain, liver, and kidneys of the rats fed the control and Fe-deficient diets, but not in the Fe-loaded rats. It is concluded that Mn and Fe interact during transfer from the plasma to the brain and other organs and that this interaction is synergistic rather than competitive in nature. Hence, excessive intake of Fe plus Mn may accentuate the risk of tissue damage caused by one metal alone, particularly in the brain.     

Influence of dietary iron deficiency on acute metal intoxication

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal and intestinal metallothionein (MT), disposition of the metals, and alterations in hematological parameters was investigated in rats. The administration of cadmium induced the hepatic, renal and intestinal MT while that of nickel or lead induced hepatic MT only. However, dietary iron deficiency did not influence the cadmium induced tissue MT but enhanced the ability of nickel or lead to restore the normal synthesis of renal and intestinal MT lowered under the influence of reduced body iron status. The accumulation of lead in liver and kidney and that of cadmium enhanced in liver only, while tissue deposition of nickel remained unaffected by iron deficiency. The induction of hepatic MT by three metals appears related to the concomitant rise in the hepatic zinc, calcium and iron levels in normal rats. However, dietary iron deficiency increased the hepatic zinc in response to nickel or cadmium and that of heptic calcium in response to lead.     

Genetics of tolerance to iron chlorosis in rice

Genetics of tolerance to iron chlorosis was investigated in eight crosses involving parents distinctly different in their level of tolerance. The segregating populations with parents and F₁s were screened under actual stress conditions in the field. Also, selected crosses were studied for Fe³⁺ uptake capacity. Tolerance/moderate tolerance to Fe chlorosis was dominant over susceptibility and it was controlled by two sets of nonallelic genes with complementary interaction. Gene Ic ₁ has been found to be basic and in complementation with Ic ₃ it confers tolerance. Likewise, Ic ₂ with Ic ₄ confers tolerance. The basic genes Ic ₁ and Ic ₂ are nonallelic and, in the absence of their respective complementary genes Ic ₃ and ₄ , ineffective, which results in susceptibility. Of tolerant cultivars, ARC 10372 and Cauvery have been tentatively assigned the genotype of Ic ₁ , Ic ₂ , Ic ₃ , Ic ₄ , and moderately tolerant IET 7613, Prasanna and Akashi Ic ₁ , ₂ Ic ₃ Ic ₄ . The susceptible ARC 5723 has been assigned Ic ₁ , ₂ , Ic ₃ , Ic ₄ , and IET 9829, Ic ₁ , ₂ Ic ₃ Ic ₄ . IET 7614 is susceptible, due to the presence of inhibitory genes I-Ic ₁ , I-Ic ₂ together with ic ₁ pt>, ic ₂ , Ic ₃ , Ic ₄ . Further, the gene Pc for purple coleoptile shows linkage with one of the complementary genes with a crossover value of 15.26%, while the gene(s) for seedling height Ts with Ic ₁ with a crossover value of 1.7%. It is possible that the gene(s) for iron chlorosis tolerance might belong to the second linkage group, where genes for purple leaf were located.     

Helicobacter pylori-related iron deficiency anemia: a review

Several clinical reports have demonstrated that Helicobacter pylori gastric infection has emerged as a new cause of refractory iron deficiency anemia, unresponsive to iron therapy, and not attributable to usual causes such as intestinal losses or poor intake, malabsorption or diversion of iron in the reticulo-endothelial system. Although the interaction between infection and iron metabolism is now well consolidated, our understanding of the pathogenetic mechanism underlying the anemia is still wanting. Microbiological and ferrokinetic studies seem to suggest that Helicobacter pylori infected antrum could act as a sequestering focus for serum iron by means of outer membrane receptors of the bacterium, that in vitro are able to capture and utilize for growth iron from human lactoferrin. The proposed hypothesis does not answer why this complication is such a rare disease outcome in a common human infection but it may be used as a template for further controlled studies to determine the mechanisms of this atypical, medically important putative sequelae of H. pylori infection.     

Foliar fertilization to control iron chlorosis in pear (Pyrus communis L.) trees

The effectiveness of foliar fertilization to re-green chlorotic leaves in iron-deficient pear trees has been studied. Trials were made to assess the influence of (i) the level of Fe deficiency, (ii) the leaf surface treated (adaxial or abaxial), and (iii) two different surfactants, L-77 and Mistol. Treatments were ferrous sulphate alone, ascorbic, citric and sulphuric acids, applied either alone or in combination with ferrous sulphate, Fe-DTPA and water as a control. Solutions were applied with a brush and leaves were treated twice each year. None of the treatments caused a full recovery from Fe deficiency chlorosis. Treatments containing Fe caused the largest re-greening effects, and FeSO₄ had a similar re-greening effect to Fe(III)-DTPA. Increases in leaf Chl were more pronounced with abaxial leaf surface applications and in severely deficient leaves. Using Fe(III)-DTPA in foliar sprays does not seem to be justified, since their effects are not better than those of FeSO₄. The joint use of Fe(III)-DTPA and L-77 and that of FeSO₄ and citric acid do not seem to be suitable. With a single foliar application, FeSO₄ combined with acids gave slightly better results than FeSO₄ alone. Acidic solution applications without Fe may be effective in alleviating chlorosis in some cases, especially in the case of citric acid. In the current state of knowledge, foliar fertilization cannot offer yet a good alternative for full control of Fe chlorosis, although its low environmental impact and cost make this technique a good complementary measure to soil Fe-chelate applications and other chlorosis alleviation management techniques. Abbreviations: Chl – chlorophyll; EDDCHA – ethylenediamine di(5-carboxy-2-hydroxyphenylacetic) acid; EDDHA – ethylenediamine di(o-hydroxyphenylacetic) acid; EDDHMA – ethylenediamine di(o-hydroxy-p-methylphenylacetic) acid; EDDHSA – ethylenediamine di(2-hydroxy-5-sulfophenylacetic) acid     

Structural and functional integrity of Sulla carnosa photosynthetic apparatus under iron deficiency conditions

• The abundance of calcareous soils makes bicarbonate‐induced iron (Fe) deficiency a major problem for plant growth and crop yield. Therefore, Fe‐efficient plants may constitute a solution for use on calcareous soils.
• We investigated the ability of the forage legume Sulla carnosa (Desf.) to maintain integrity of its photosynthetic apparatus under Fe deficiency conditions. Three treatments were applied: control, direct Fe deficiency and bicarbonate‐induced Fe deficiency.
• At harvest, all organs of deficient plants showed severe growth inhibition, the effect being less pronounced under indirect Fe deficiency. Pigment analysis of fully expanded leaves revealed a reduction in concentrations of chlorophyll a, chlorophyll b and carotenoids under Fe deficiency. Electron transport rate, maximum and effective quantum yield of photosystem II (PSII), photochemical quenching (qP), non‐photochemical quenching (qN) as well as P700 activity also decreased significantly in plants exposed to direct Fe deficiency, while qN was not affected. The effects of indirect Fe deficiency on the same parameters were less pronounced in bicarbonate‐treated plants. The relative abundances of thylakoid proteins related to PSI (PsaA, Lhca1, Lhca2) and PSII (PsbA, Lhcb1) were also more affected under direct than indirect Fe deficiency.
• We conclude that S. carnosa can maintain the integrity of its photosynthetic apparatus under bicarbonate‐induced Fe deficiency, preventing harmful effects to both photosystems under direct Fe deficiency. This suggests a high capacity of this species not only to take up Fe in the presence of bicarbonate (HCO₃^?) but also to preferentially translocate absorbed Fe towards leaves and prevent its inactivation.

     

The effect of Helicobacter pylori infection and dietary iron deficiency on host iron homeostasis: a study in mice

BACKGROUND: Helicobacter pylori, which requires iron to survive, may cause host iron deficiency by directly competing with the host for available iron or by impairing iron uptake as a consequence of atrophy-associated gastric hypochlorhydria. The aim of this study was to examine the effect of H. pylori infection and dietary iron deficiency on host iron homeostasis in a mouse model. MATERIALS AND METHODS: H. pylori SS1-infected and uninfected C57BL/6 mice, fed either a normal diet or an iron-deficient diet, were assessed for iron status and infection-associated gastritis over a 30-week period. RESULTS: After 10 weeks, serum ferritin values were higher in H. pylori-infected mice than in uninfected controls, irrespective of dietary iron intake (p = .04). The infection-related increase in body iron stores persisted in the iron-replete mice but diminished over time in mice with restricted dietary iron intake (p < .0001). At 30 weeks serum ferritin levels were lower in these animals (p = .063). No significant difference in bacterial numbers was detected at the 30-week time point (p > .05) and the histological changes observed were consistently associated with infection (p < .01) and not with the iron status of the mice (p = .771). CONCLUSIONS: Infection with H. pylori did not cause iron deficiency in iron-replete mice. However, diminished iron stores in mice as a result of limited dietary iron intake were further lowered by concurrent infection, thus indicating that H. pylori competes successfully with the host for available iron.     

Impaired iron status in rats as induced by copper deficiency

The hypothesis was tested that marginal copper deficiency affects iron status. Copper restriction (1 vs 5 mg Cu/kg diet) significantly lowered iron concentrations and transferrin saturation in plasma and reduced blood hemoglobin, hematocrit, and iron concentrations in tibia and femur, but raised iron concentrations in liver. Marginal copper deficiency did not affect feed intake and body-weight gain.     

Diagnosis of iron deficiency in groundnut,Arachis hypogaea L.

Summary Investigations into iron deficiency have been hindered by the lack of a satisfactory diagnostic tissue test, which in turn results from the total iron content of plant tissue commonly being an unreliable index of the iron status. Our measurements of chlorotic and normal leaves of field grown groundnut (Arachis hypogaea L.) showed that total iron was unsatisfactory as the measure of iron status of plant tissue. It was found that iron status was better assessed from an estimate of the ferrous iron content of fresh leaf materials obtained by extraction with o-phenanthroline. Extractable iron content increased with leaf age. Chlorotic buds or the first fully opened leaf always contained less than 6μg extractable-Fe/g fresh tissue. Approved for publication as ICRISAT Journal Article No. 307.     

Light-mediated release of phytosiderophores in wheat and barley under iron or zinc deficiency

The effect of varied light intensity (50 – 600 mol m-2 s-1) on the rate of phytosiderophore release was studied under zinc (Zn) deficiency using a bread (Triticum aestivum L. cv. Aroona) and a durum wheat cultivar (Triticum durum Desf. cv. Durati) differing in zinc (Zn) efficiency and under iron (Fe) deficiency using a barley cultivar (Hordeum vulgare L. Europe). Plants were grown under controlled environmental conditions in nutrient solution for 15 days (wheat plants) or 11 days (barley plants). Phytosiderophore release was determined by measuring capacity of root exudates to mobilize copper (Cu) from a Cu-loaded resin.With increasing light intensity visual Zn deficiency symptoms such as whitish-brown lesions on leaf blade developed rapidly and severely in wheat, particularly in the durum cultivar Durati. In wheat plants supplied well with Zn, increases in light intensity from 100 to 600 mol m-2 s-1 did not clearly affect the rate of phytosiderophore release. However, under Zn deficiency increases in light intensity markedly enhanced release of phytosiderophores in Zn-deficient Aroona, but not in Zn-inefficient Durati. When Fe-deficient barley cultivar Europe was grown first at 220 mol m-2 s-1 and then exposed to 600 mol m-2 s-1 for 24 and 48 h, the rate of release of phytosiderophores was enhanced about 4-fold and 7-fold, respectively. Transfer of Fe-deficient plants from 600 to 50 mol m-2 s-1 for 48 h reduced the rate of release of phytosiderophores by a factor of 7. The effect of light on phytosiderophore release was similar regardless of whether the rate of phytosiderophore release was expressed per plant or per unit dry weight of roots.The results demonstrate a particular role of light intensity in phytosiderophore release from roots under both Zn and Fe deficiency. It is suggested that in the studies concerning the role of phytosiderophore release in expression of Zn or Fe efficiency among and within cereals, a special attention should be given to the light conditions.     

Induction of ferric reductase activity in response to iron deficiency in Arabidopsis

The response to iron deficiency was investigated in 16 ecotypes of Arabidopsis thaliana (L.) Heynh. and in Arabidopsis griffithiana. An increase in root ferric reductase activity was observed under conditions of iron deficiency in these ecotypes and in both species. This observation is consistent with a Strategy I response which is typical for dicot plants. A. griffithiana, however, showed a lower induction of ferric reductase activity in response to iron deficiency than that of the commonly studied A. thaliana Columbia ecotypes.     

Reduction of root iron in Plantago lanceolata during recovery from Fe deficiency

Changes in root-associated Fe(III) reductase activity and Fe concentration during recovery from temporary iron starvation were investigated in hydroponically grown Plantago lanceolata L. Within two days, interruption of the Fe supply resulted in enhanced rates of reduction by intact plant roots. Transfer of iron deficient plants to a solution containing various amounts of chelated Fe caused a transient increase in reduction activity before the rates declined to a level determined by the amount of Fe added. Repression of root-associated redox activity was independent of the Fe concentration in the preculture. When iron deficient plants were submitted to a supply of Fe localized to a part of the root system (split-root plants), the decrease in reduction rates was much more pronounced in the Fe-deprived portion of the roots than in the Fe-supplied one. No correlation was observed between root Fe concentration and Fe(III) reductase activity. Continued growth of split-root plants in the +Fe/-Fe regime increased the reduction rates of the +Fe-grown portion of the root system over the rates in iron sufficient plants with non-divided roots. The results are discussed in relation to putative factors mediating intra- and interorgan regulation of iron nutrition.     

Reduction of root iron in Plantago lanceolata during recovery from Fe deficiency

Changes in root-associated Fe(III) reductase activity and Fe concentration during recovery from temporary iron starvation were investigated in hydroponically grown Plantago lanceolata L. Within two days, interruption of the Fe supply resulted in enhanced rates of reduction by intact plant roots. Transfer of iron deficient plants to a solution containing various amounts of chelated Fe caused a transient increase in reduction activity before the rates declined to a level determined by the amount of Fe added. Repression of root-associated redox activity was independent of the Fe concentration in the preculture. When iron deficient plants were submitted to a supply of Fe localized to a part of the root system (split-root plants), the decrease in reduction rates was much more pronounced in the Fe-deprived portion of the roots than in the Fe-supplied one. No correlation was observed between root Fe concentration and Fe(III) reductase activity. Continued growth of split-root plants in the +Fe/-Fe regime increased the reduction rates of the +Fe-grown portion of the root system over the rates in iron sufficient plants with non-divided roots. The results are discussed in relation to putative factors mediating intra- and interorgan regulation of iron nutrition.     

Mapping genetic loci for iron deficiency chlorosis in soybean

The objective of this study was to map genes controlling iron deficiency chlorosis in two intraspecific soybean [Glycine max (L.) Merrill] populations. Chlorosis symptoms were evaluated by visual scores and spectrometric chlorophyll determinations at the V4 stage (third trifoliolate leaf fully developed) in the field in 1993, and at V2 (first trifoliolate leaf fully developed) and V4 stages in 1994. A total of 89 RFLP and 10 SSR markers in the Pride B216 x A15 population, and 82 RFLP, 14 SSR and 1 morphological I (hilum color) markers in the Anoka x A7 population were used to map quantitative trait loci (QTL) affecting iron deficiency chlorosis. QTL with minor effects were detected on six linkage groups of the Pride B216 x A15 population, suggesting a typical polygene mechanism. In contrast, in the Anoka x A7 population, one QTL contributed an average of 72.7% of the visual score variation and 68.8% of the chlorophyll concentration variation and was mapped on linkage group N. Another QTL for visual score variation, and one for chlorophyll concentration variation were detected on linkage groups A1 and I, respectively. Due to the large LOD score and major genetic effect of the QTL on linkage group N, the quantitative data was reclassified into qualitative data fitting a one major gene model according to the means of the QTL genotypic classes. The major gene was mapped in the same interval of linkage group N using both visual scores and chlorophyll concentrations, thus verifying that one major gene is involved in segregation for iron chlorosis deficiency in the Anoka x A7 population. This study supported a previous hypothesis that two separate genetic mechanisms control iron deficiency in soybean.     

Effect of iron and/or vitamin A re-supplementation on vitamin A and iron status of rats after a dietary deficiency of both components

Iron and vitamin A deficiency are common nutritional problems in developing countries. From animal experiments and intervention studies, growing evidence is pointing to a possible influence of iron on vitamin A metabolism. We assessed the affects of an oral supplementation of vitamin A and/or iron on the recovery of rats from vitamin A and iron deficiency. Weanling male Wistar rats were kept for four weeks on an iron and vitamin A deficient diet. Thereafter, rats were repleted with iron 35 mg/kg feed, with vitamin A 4500 IU/kg feed both, or with iron 35 mg/kg and vitamin A 4500 IU/kg for five weeks. Retinol and retinyl esters in plasma and tissues were determined by HPLC. Iron was determined by atomic absorption spectrophotometry. The determination of haematological parameters showed that rats developed an anaemia during depletion. This was reversed by the re-supplementation with iron but not vitamin A alone. The simultaneous supplementation of vitamin A was of no additional benefit. When rats were resupplemented with iron alone a substantial further decrease in plasma retinol (P < 0.002) and liver vitamin A (P < 0.05) was observed. A similar but less pronounced decrease in plasma retinol was observed in the rats re-supplemented with vitamin A alone, despite a substantial increase in liver vitamin A (P < 0.002). Despite lower liver vitamin A levels compared to the group re-supplemented with vitamin A lone, the group re-supplemented with iron and vitamin A had substantial higher plasma levels compared to the one supplemented with iron alone (P < 0.002). In conclusion, the study supports an interaction of iron and vitamin A on the level of retinol transport in plasma. Despite a comparable availability of vitamin A as indicated by the comparable liver levels only the re-supplementation of both iron and vitamin A can normalize the retinol level in plasma. This might be of nutritional consequence in developing countries with regard to the supplementation regime of both nutrients iron and vitamin A to prevent a functional deficiency of vitamin A despite sufficient dietary availability.     

Nitric oxide and glutathione impact the expression of iron uptake- and iron transport-related genes as well as the content of metals in A. thaliana plants grown under iron deficiency

Mounting evidence indicate that nitric oxide (NO) acts as a signaling molecule mediating iron deficiency responses through the upregulation of the expression of iron uptake-related genes. Accordingly, NO donors such as nitrosoglutathione (GSNO) were reported to improve the fitness of plants grown under iron deficiency. Here, we showed that glutathione, a by-product of GSNO, triggered the upregulation of the expression of iron uptake- and transport-related gene and an increase of iron concentration in Arabidopsis thaliana seedlings facing iron deficiency. Furthermore, we provided evidence that under iron deficiency, NO released by GSNO did not improve the root iron concentration but impacted the content of copper. Collectively, our data highlight the complexity of interpreting data based on the use of NO donors when investigating the role of NO in iron homeostasis.     

Varietal response to iron chlorosis in upland rice

Summary In a study involving twenty upland rice genotypes, the induction of iron chlorosis was found to be more by superphosphate application than due to lime incorporation into an alfisol soil under greenhouse conditions in GI tray-grown seedlings as quantified by two parameters viz., total chlorphyll content and Fe²⁺ content. Of the two indices of iron chlorosis, Fe²⁺ was more sensitive than chlorophyll content. Genotypes were grouped into efficient and inefficient categories both in terms of absorption and utilization of iron based on the degree of reduction in response to added superphosphate.