Bioavailability and intestinal absorption of aluminum in rats

In the present investigation, the deposition of aluminum in intestinal fragment and the appearance in blood were studied in a perfused rat intestine in situ for 1 h with several aluminum forms (16 mM). We observed that aluminum absorption was positively correlated with the theoretic affinity of aluminum and the functional groups of the chelating agent. The absorption of aluminum after ingestion of organic compounds is more important than after ingestion of mineral compounds, with the following order: Al citrate > Al tartrate, Al gluconate, Al lactate > Al glutamate, Al chloride, Al sulfate, Al nitrate. Absorption depends on the nature of the ligands associated with the Al3+ ion in the gastrointestinal fluid. The higher the aluminum retention in intestinal fragment, the lower the absorption and appearance in blood. However, the higher aluminum concentration is always in the jejunal fragment because of the influence of pH variation on this fragment. Another objective of the present study was to determine the influence of several parameters on aluminum citrate absorption: with or without 0.1 mmol dinitrophenol/L, with aluminum concentration from 3.2, 16, 32, and 48, to 64 mmol/L, media containing 0, 3, or 6 mmol Ca/L, with or without phosphorus or glucose. It is concluded that aluminum is absorbed from the gastrointestinal tract by (1) a paracellular energy independent and nonsaturable route, mainly used for high aluminum concentration, which is modified by extracellular calcium, and (2) a transcellular and saturable route, the aluminum level was not modified with enhancement of aluminum quantity in intestinal lumen. This pathway can be similar with calcium transfer through the intestine and is energy dependent because of a decrease of aluminum absorption that follows the removal of glucose and phosphorus.     

Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions

Aluminum (Al), oxidative stress and impaired cholinergic functions have all been related to Alzheimer's disease (AD). The present study evaluates the effect of aluminum on acetylcholinesterase (AChE) and lipid peroxidation in the mouse brain. Mice were loaded by gavage with Al 0.1 mmol/kg/day 5 days per week during 12 weeks. The mice were divided into four groups: (1) control; (2) 10 mg/mL of citrate solution; (3) 0.1 mmol/kg of Al solution; (4) 0.1 mmol/kg of Al plus 10 mg/mL of citrate solution. AChE activity was determined in the hippocampus, striatum, cortex, hypothalamus and cerebellum and lipid peroxidation was determined in the hippocampus, striatum and cortex. An increase of AChE activity was observed in the fourth group (Al + Ci) in the hippocampus (36%), striatum (54%), cortex (44%) and hypothalamus (22%) (p<0.01). The third group (Al) presented a decrease of AChE activity in the hypothalamus (20%) and an enhancement in the striatum (27%). Lipid peroxidation, measured by TBARS (thiobarbituric acid reactive substances), was elevated in the hippocampus and cerebral cortex when compared with the control (p < 0.01). The effect of aluminum on AChE activity may be due to a direct neurotoxic effect of the metal or perhaps a disarrangement of the plasmatic membrane caused by increased lipid peroxidation.     

Effect of oral aluminum and aluminum citrate on blood level and short-term tissue distribution of aluminum in the rat

Aluminum (Al) absorption seems to be very low, but many factors can enhance it in animals and humans. In the present study, we investigated the acute effect of Na citrate on Al absorption by monitoring Al levels in blood and several tissues. For this purpose, 18 Wistar male rats were divided into 3 groups: control, Al, and Al + Na citrate. After a 14-h fasting period, animals were dosed orally with deionized water, or 2 mmol Al chloride, or 2 mmol Al chloride plus 2 mmol Na citrate. Blood samples were taken before and 1, 2, 4, and 6 h after the gavage. Al concentrations in blood, liver, tibia, kidney, and intestinal wall were determined by ICP-OES. In the Al and Al + citrate groups, Al blood concentrations peaked at 1 h and 2 h with higher levels in the Al + citrate group. Al gavage resulted in an increase in Al level in intestinal wall, but not in the other investigated tissues. Simultaneous gavage of citrate with Al significantly increased its tissue levels in tibia, kidney, and in intestinal wall. Our data show clearly that Al as chloride can be absorbed, but not well retained by the organism tissues. Furthermore, the model used in the present study is appropriate for acute studies to investigate the effect of various compounds on Al absorption in the rat.     

Effects of aluminum and deferoxamine on concentration of essential elements in animals experimentally intoxicated with aluminum]

To assess the effect of aluminium intoxication in tissues of experimental animals on Ca, Mg, Zn, Cu, and Fe concentration, aluminium nitrate was administered intraperitoneally to mice at a daily dose of 0.27 mMol/kg for 5 weeks. Concentration of Al, Ca, Mg, Zn, Cu, and Fe were analyzed by atomic absorption spectrometry. The Al content in liver and tibia was significantly higher in treated mice in comparison with control group. In Al loaded tissues the significant increase of all tested essential elements was found. To evaluate the results of DFO treatment on essential elements, mice received 6 times intraperitoneally 3.5 mMol/kg of DFO. This treatment had generally no effect on reduction of Al concentration in tibia and liver, as well as on changes in essential elements concentration.     

Accumulation of aluminum in rat brain: does it lead to behavioral and electrophysiological changes?

The present study was undertaken to examine possible aluminum (Al) accumulation in the brain of rats and to investigate whether subchronic exposure to the metal leads to behavioral and neurophysiological changes in both treated and control groups. Each of the groups consisted of 10 animals. Aluminum chloride (AlCl₃) at a low (50 mg/kg/d) or high (200 mg/kg/d) dose was applied to male Wistar rats by gavage for 8 wk. Al-free water by gavage was given to the control group throughout the experiment. Behavioral effects were evaluated by open-field (OF) motor activity and by acoustic startle response (ASR). Electrophysiological examination was done by recording spontaneous activity and sensory-evoked potentials from the visual, somatosensory, as well as auditory cortex. The Al content of each whole brain was determined by electrothermal atomic absorption spectrophotometry. Subchronic Al exposure slightly caused some changes in the evoked potentials and electrocorticograms and in the OF and ASR performance, but these results were not statistically significant. The brain Al levels of the control and the low and high dose of Al-exposed groups were measured as 0.717±0.208 μg/g (wet weight), 0.963±0.491 μg/g (wet weight) and 1.816±1.157 μg/g (wet weight), respectively.     

铝对秋茄幼苗生理特性的影响

为探讨铝对秋茄幼苗生理特性的影响,实验研究了不同浓度铝盐(0-100 mmol/L AlCl3)处理后秋茄的各种生理反应,对幼苗的生长、净光合效率、膜脂过氧化作用、游离脯氨酸含量等生理指标与胁迫程度及时间的关系作了对比研究,特别分析了高浓度(25-100 mmol/L Al3+)胁迫下,秋茄叶片和根部活性氧清除系统保护酶活性的变化趋势。研究发现,在10 mmol/L浓度以下,秋茄在生理特性上表现出对铝胁迫的最大适应性,能维持正常生命生长过程。当浓度增加至25-100 mmol/L,秋茄的生理反应较为敏感,膜脂过氧化加重,MDA含量及保护酶活性随铝浓度增加的变化趋势与其在海莲中的表现基本相似。高浓度铝胁迫的极端环境使植物体内产生过量的活性氧自由基,诱导了细胞膜系统的氧化损伤,最终导致秋茄植株衰老甚至死亡。抗氧化保护酶系统SOD、CAT、POD的协同作用,在一定时间内可以维持细胞内活性氧代谢平衡;特别是POD被激活的程度最大,且持续时间最长,可以考虑作为秋茄幼苗抗铝胁迫的生理标志。秋茄叶片和根部的游离脯氨酸含量在25和100 mmol/L Al3+胁迫下均显著增加。       

Aluminum effect on the activity of superoxide dismutase and of other antioxygenic enzymes in vitro

The effect of Al on superoxide dismutase (SOD) and on other antioxygenic enzymes: horseradish peroxidase, catalase, and glutathione peroxidase, has been investigated in vitro. In the case of SOD, the effect of metal chelators (EDTA and deferoxamine) and a possible synergistic effect with iron salts have also been tested using the pyrogallol assay. There is no significant inhibitory effect of Al on the activity of any of the above-mentioned enzymes. Noticeable increases in SOD activity were observed when metal chelators were added to the medium, but not when high concentrations of Al were present too, in the case of deferoxamine (DFO). The former fact seems to be a consequence of the chelation of transition metal ions that catalyze pyrogallol autoxidation by a mechanism not inhibitable by SOD, interfering in its action, which may account for part of the DFO antioxidant effect observed in vivo. The latter phenomenon could be owing to a saturation of the chelating capacity of DFO by an excess of Al present in the medium, which should bring the system back to the interfering conditions explained above. It can be concluded that Al, either in the presence or in the absence of iron salts, does not inhibit SOD activity in vitro. Moreover, no significant binding of Al to SOD was demonstrated, and the amounts of its metal constituents, Cu and Zn, were not affected by preincubation of the enzyme with Al. The effect of the different compounds tested on the rate of autoxidation of the indicating scavenger, pyrogallol, and a suitable hypothesis on their role in the oxidation process are also discussed.     

Desferoxamine protects against glucocorticoid-induced osteonecrosis of the femoral head via activating HIF-1α expression

Glucocorticoid-induced osteonecrosis of the femoral head (GIOFH) is one of the most common complications of glucocorticoid administration. By chelating Fe²⁺, desferoxamine (DFO) was reported to be able to activate the HIF-1α/VEGF pathway and promote angiogenesis. In the present study, we examined whether DFO administration could promote angiogenesis and bone repair in GIOFH. GIOFH was induced in rats by methylprednisolone in combination with lipopolysaccharide. Bone repair was assessed by histologic analysis and microcomputed tomography (micro-CT). Vascularization was assessed by Microfil perfusion and micro-CT analysis. Immunohistochemical staining was performed to analyze the expression of HIF-1α, VEGF, and CD31. Our in vivo study revealed that DFO increased HIF-1α/VEGF expression and promoted angiogenesis and osteogenesis in GIOFH. Moreover, our in vitro study revealed that DFO restored dexamethone-induced HIF-1α downregulation and angiogenesis inhibition. Besides, our in vitro study also demonstrated that DFO could protect bone marrow-derived stem cells from dexamethone-induced apoptosis and mitochondrial dysfunction by promoting mitophagy and mitochondrial fission. In summary, our data provided useful information for the development of novel therapeutics for management of GIOFH.     

The Effects of Glutamate and Citrate on Absorption and Distribution of Aluminum in Rats

The objective of this study was to evaluate the effect of glutamate (Glu) and citrate (Cit) on the absorption and distribution of aluminum in rats. In the in vitro experiment, 18 adult male Sprague-Dawley rats (average weight of 250 ± 15 g) were randomly divided into three groups. The entire intestine was rapidly removed and cultured in prediction samples of 20 mmol AlCl(3), 20 mmol AlCl(3)+20 mmol Cit, and 20 mmol AlCl(3)+20 mmol Glu, respectively. Liquid in different intestines and the intestines were obtained for Al determination. In the in vivo chronic study, 24 adult male Sprague-Dawley rats (average weight of 127 ± 10 g) were divided into four groups fed with the following diets: no Al and Glu added (control), AlCl(3) (1.2 mmol), AlCl(3) (1.2 mmol) + Cit (1.2 mmol), and AlCl(3) (1.2 mmol) + Glu (1.2 mmol) daily for 50 days, respectively. After rat sacrifice, blood samples were obtained for biochemical analyses, and organ samples like the brain, kidney, liver, and bone were rapidly taken for Al determination. The results showed that the absorption rate of Al with the following order: duodenum > jejunum > ileum in the in vitro study and the administration of AlCl(3)+Cit or AlCl(3)+Glu resulted in significant increases in Al absorption in the three parts of the gut (duodenum, jejunum, and ileum) compared to the AlCl(3) alone group based on wet weight (P < 0.05). There were no differences between the AlCl(3)+Cit and AlCl(3)+Glu groups. In the in vivo chronic study, supplementing either AlCl(3) alone or AlCl(3)+Glu decreased food consumption significantly (P < 0.05) compared with the control group. Compared with the control group, animals fed with the AlCl(3) diet monitored for red blood cell, kidney, and liver showed a higher level (P < 0.05), but did not significantly increase Al retention in the brain and bone (P > 0.05); animals fed with AlCl(3)+Cit diets were monitored for higher Al retention in the brain, kidney, bone, and liver (P < 0.05), while animals fed with AlCl(3)+Glu diets were monitored for red blood cell, brain, and kidney (P < 0.05). Compared with the AlCl(3) group, simultaneous administration of AlCl(3) and Glu led to a significant increase in Al retention in red blood cell, brain, and kidney (P < 0.01) while AlCl(3) and Cit in the kidney and bone (P < 0.01). Simultaneous administration of AlCl(3) and Cit significantly increases plasma malondialdehyde level (P < 0.05); both simultaneous administration of AlCl(3) and Glu or AlCl(3) and Cit led to significant decreases in superoxide dismutase level in the plasma (P < 0.05), while AlCl3 alone did not. The results indicated that both Cit and Glu enhanced Al absorption in the intestine in vitro, and Glu increased Al deposition in red blood cell, brain, and kidney in vivo.     

Effects of oral aluminum on essential trace elements metabolism during pregnancy

The present study was conducted to assess in rats the effects of oral aluminum (Al) exposure on calcium (Ca), magnesium (Mg), manganese (Mn), copper (Cu), zinc (Zn), and iron (Fe) accumulation and urinary excretion. Three groups of plug-positive Sprague-Dawley (SD) rats were given by gavage 0, 200, and 400 mg/kg/d of Al(OH)₃ on gestational days 1–20. Three groups of nonpregnant female SD rats of the same age received Al(OH)₃ by gavage at the same doses for 20 consecutive days. At the end of the treatment period, 24-h urine samples were collected for analysis of Al and essential elements. Subsequently, all animals were sacrificed and samples of liver, bone, spleen, kidneys, and brain were removed for metal analyses. With some exceptions, the urinary amounts of Al, Mn, and Cu excreted by pregnant animals as well as the urinary levels of Al excreted by nonpregnant rats were higher in the Al-treated groups than in the respective control groups. Although higher Al levels were found in the liver of pregnant rats, the concentrations of Al in the brain of these animals were lower than those found in the same tissues of nonpregnant rats. With regard to the essential elements, tissue accumulation was most affected in pregnant than in nonpregnant animals. In pregnant rats, the hepatic and renal concentrations of Ca, Mg, Mn, Cu, Zn, and Fe, as well as the levels of Ca in bone, and the concentrations of Cu in brain were significantly higher in the Al-exposed groups than in the control group. According to the current results, oral Al exposure during pregnancy can produce significant changes in the tissue distribution of a number of essential elements.     

Effects of chelating agent and environmental stresses on microbial biofilms: relevance to clinical microbiology

Aims: To determine the effect of pH, temperature, desiccation, ethylenediaminetetraacetic acid (EDTA) and desferrioxamine B (DFO) on Panton‐Valentine leukocidin‐positive community acquired methicillin‐susceptible Staphylococcus aureus (PVL +ve CA‐MSSA) biofilm formation. Methods and Results: Biofilms from PVL +ve CA‐MSSA (clinical isolate) were subjected to pH, temperature, desiccation, EDTA and DFO. PVL +ve CA‐MSSA were more resistant to pH and heat than their planktonic equivalents. Desiccation studies demonstrated that PVL +ve CA‐MSSA biofilms were more refractory to the treatment than planktonic cells. Significant inhibition of PVL +ve CA‐MSSA biofilm formation was observed in the presence of 1 mmol l^?1 EDTA. Low concentrations (2·5 μmol l^?1) of DFO enhanced the growth of PVL +ve CA‐MSSA biofilms. At higher concentrations (1 mmol l^?1), DFO did inhibit the growth but not as much as EDTA. A combination of EDTA and DFO inhibited PVL +ve CA‐MSSA biofilm formation at lower concentrations than either alone. Conclusions: This study demonstrates that PVL +ve CA‐MSSA biofilms are resistant to environmental stress but their growth can inhibited effectively by a mixture of EDTA and DFO. Significance and Impact of the Study: The inhibition of biofilm formation by PVL +ve CA‐MSSA using chelating agents has not been previously reported and provides a practical approach to achieve the disruption of these potentially important biofilms formed by an emerging pathogen.     

Evaluation of the protective activity of deferiprone, an aluminum chelator, on aluminum-induced developmental toxicity in mice

BACKGROUND: Since deferiprone can be an effective chelating agent for the treatment of aluminum (Al) overload, in the present study we investigated whether this chelator could protect against Al-induced maternal and developmental toxicity in mice. METHODS: A single oral dose of Al nitrate nonahydrate (1,327 mg/kg) was given on gestation day 12, the most sensitive time for Al-induced maternal and developmental toxic effects in mice. At 2, 24, 48, and 72 hr thereafter, deferiprone was given by gavage at 0 and 24 mg/kg. Cesarean sections were performed on day 18 of gestation and fetuses were examined for malformations and variations. RESULTS: Aluminum-induced maternal toxicity was evidenced by significant reductions in body weight gain, corrected body weight change, and food consumption. Developmental toxicity was evidenced by a significant decrease in fetal weight per litter and an increase in the total number of fetuses and litters showing bone retardation. No beneficial effects of deferiprone on these adverse effects could be observed. By contrast, a more pronounced decrease in maternal weight gain and corrected body weight change, as well as a higher number of litters with fetuses showing skeletal variations was noted in the group exposed to Al nitrate and treated with deferiprone at 24 mg/kg. CONCLUSIONS: According to the current results, deferiprone would not be effective to prevent Al-induced maternal and embryo/fetal toxicity in mice.     

Objectives and Methods of Iron Chelation Therapy

Recent developments in the understanding of the molecular control of iron homeostasis provided novel insights into the mechanisms responsible for normal iron balance. However in chronic anemias associated with iron overload, such mechanisms are no longer sufficient to offer protection from iron toxicity, and iron chelating therapy is the only method available for preventing early death caused mainly by myocardial and hepatic damage. Today, long-term deferoxamine (DFO) therapy is an integral part of the management of thalassemia and other transfusion-dependent anemias, with a major impact on well-being and survival. However, the high cost and rigorous requirements of DFO therapy, and the significant toxicity of deferiprone underline the need for the continued development of new and improved orally effective iron chelators. Within recent years more than one thousand candidate compounds have been screened in animal models. The most outstanding of these compounds include deferiprone (L1); pyridoxal isonicotinoyl hydrazone (PIH) and; bishydroxy- phenyl thiazole. Deferiprone has been used extensively as a substitute for DFO in clinical trials involving hundreds of patients. However, L1 treatment alone fails to achieve a negative iron balance in a substantial proportion of subjects. Deferiprone is less effective than DFO and its potential hepatotoxicity is an issue of current controversy. A new orally effective iron chelator should not necessarily be regarded as one displacing the presently accepted and highly effective parenteral drug DFO. Rather, it could be employed to extend the scope of iron chelating strategies in a manner analogous with the combined use of medications in the management of other conditions such as hypertension or diabetes. Coadministration or alternating use of DFO and a suitable oral chelator may allow a decrease in dosage of both drugs and improve compliance by decreasing the demand on tedious parenteral drug administration. Combined use of DFO and L1 has already been shown to result in successful depletion of iron stores in patients previously failing to respond to single drug therapy, and to lead to improved compliance with treatment. It may also result in a “shuttle effect” between weak intracellular chelators and powerful extracellular chelators or exploit the entero-hepatic cycle to promote fecal iron excretion. All of these innovative ways of chelator usage are now awaiting evaluation in experimental models and in the clinical setting.     

Determination of aluminum levels in the kidney,liver, and brain of mice treated with aluminum hydroxide

In the present study, aluminum (Al) accumulation has been examined after aluminum loading in mice. The kidney, liver, and brain aluminum levels for mice that had been treated orally with aluminum hydroxide for 105 d and for the control group were determined using graphite furnace atomic absorption spectrophotometry (GFAAS) following an acid digestion. Matrix modifier consisted of 2% Triton X-100 and 2% Mg (NO₃)₂. Al loaded mice showed a significant increase in tissue aluminum levels, relative to the control group.     

水杨酸调节决明根系铝诱导的氧化胁迫

水杨酸(Salicylicacid,SA)在调节生物和非生物胁迫,诱导植物氧化胁迫中起着重要的作用,但对铝诱导的氧化胁迫的调节作用尚不清楚。本文研究了SA对决明(CassiatoraL.)根系铝诱导的H2O2和O2-含量变化,包括抗氧化酶活性以及细胞质膜过氧化胁迫变化的影响。介质中20mmol/L铝处理增加质膜透性,导致MDA含量上升及根尖细胞Evansblue染色加重(测定细胞死亡),而外源供给5mmol/LSA能缓解铝诱导的氧化胁迫。SA处理能明显降低根尖H2O2和O2-的含量,但两者含量与CAT、APX和GR的活性变化没有相关性,而与POD活性增加有关。水杨酸诱导H2O2含量的下降与抑制O2-积累和SOD活性有关。结果表明,SA可能激活一条由H2O2介导的、依赖于POD的抗氧化机制来缓解脂质的过氧化作用。     

Novel near-infrared fluorescent integrin-targeted DFO analogue

Desferrioxamine (DFO), a siderophore initially isolated from Streptomyces pilosus, possesses extraordinary metal binding properties with wide biomedical applications that include chelation therapy, nuclear imaging, and antiproliferation. In this work, we prepared a novel multifunctional agent consisting of (i) a near-infrared (NIR) fluorescent probe-cypate; (ii) an integrin alpha vbeta3 receptor (ABIR)-avid cyclic RGD peptide, and (iii) a DFO moiety, DFO-cypate-cyclo[RGDfK(approximately)] (1, with approximately representing the cypate conjugation site at the side chain of lysine; f is d-phenylalanine). Compound 1 and two control compounds, cypate-cyclo[RGDfK(approximately)] ( 2) and cypate-DFO ( 3), were synthesized by modular assembly of the corresponding protected RGD peptide cyclo[R(Pbf)GD(OBut)fK] and DFO on the dicarboxylic acid-containing cypate scaffold in solution. The three compounds exhibited similar UV-vis and emission spectral properties. Metal binding analysis shows that DFO as well as 1 and 3 exhibited relatively high binding affinity with Fe(III), Al(III), and Ga(III). In contrast to Ga(III), the binding of Fe to 1 and 3 quenched the fluorescence emission of cypate significantly, suggesting an efficient metal-mediated approach to perturb the spectral properties of NIR fluorescent carbocyanine probes. In vitro, 1 showed a high ABIR binding affinity (10 (-7) M) comparable to that of 2 and the reference peptide cyclo(RGDfV), indicating that both DFO and cypate motifs did not interfere significantly with the molecular recognition of the cyclic RGD motif with ABIR. Fluorescence microscopy showed that internalization of 1 and 2 in ABIR-positive A549 cells at 1 h postincubation was higher than 3 and cypate alone, demonstrating that incorporating ABIR-targeting RGD motif could improve cellular internalization of DFO analogues. The ensemble of these findings demonstrate the use of multifunctional NIR fluorescent ABIR-targeting DFO analogues to modulate the spectral properties of the NIR fluorescent probe by the chelating properties of DFO and visualize intracellular delivery of DFO by receptor-specific peptides. These features provide a strategy to explore the potential of 1 in tumor imaging and treatment as well as some molecular recognition processes mediated by metal ions.     

The DNA damage-inducible C. elegans tankyrase is a nuclear protein closely linked to chromosomes

Liver-specific ZP domain-containing protein (LZP) was recently identified as a secreted protein that is specifically expressed in liver. However, the physiological effects of LZP are largely unknown. In this study, we found that LZP was detectable in mouse kidneys, testes, ovaries and heart, in addition to liver. LZP was localized in the spermatid cells of testes, corpus luteum cells of ovaries, and cardiac muscle cells of heart. But the protein mainly anchored on the apical membrane of the thick ascending limb of the loop of Henle (TAL) cell in mouse kidney. In rat kidney LZP and Tamm-Horsfall protein (THP) were co-localized in TAL. The in vivo interaction between LZP and THP was confirmed in kidney and urine by co-immunoprecipitation assay, and the in vitro interaction was detected by GST pull-down assay, implying that the interaction could be independent on N-linked glycosylated modification of LZP. Surprisingly, LZPs with intramolecular disulfide bridges could self-interact, and then self-aggregate into spheres of varying sizes, but not polymerize into filaments. The finding that LZP might act as a new partner of THP would provide novel insights into renal functions related to THP and LZP, such as the urothelial permeability barrier and the host defense against the adhesion of pathogens.     

Accumulation of heavy metals by some wood-rotting fungi

Accumulation of aluminum, cadmium, lead and calcium was studied in the wood-roting fungiDaedalea quercina, Ganoderma applanatum, Stereum hirsutum andSchizophyllum commune. The heavy metal content was measured in mycelia cultured in liquid media in the presence of either individual Al, Cd, Pb and Ca salts or of their mixtures. After 8-d cultivations in media containing 1 mmol/L concentration of individual heavy metals, the lead content was maximal in the mycelium ofStereum hirsutum (90.6 mmol/g) while the mycelium ofGanoderna applanatum contained maximal values of cadmium (272 mmol/g), aluminum (600 mmol/g) and calcium (602 mmol/g). When the mycelia were grown on mixtures of all metal salts, lead was the preferentially accumulated ion except inG. applanatum which had a higher affinity for aluminum.     

Involvement of putrescine and nitric oxide in aluminum tolerance by modulating citrate secretion from roots of red kidney bean

Background and Aims

Polyamines and nitric oxide (NO) are two important molecules modulating numerous environment stresses in plants. This study was to investigate the roles of polyamines and NO in aluminum (Al) tolerance in red kidney bean.

Methods

The interaction between putrescine (Put) and NO under Al stress was examined. NO donor and scavenger were used to further examine the role of NO in Al-induced citrate secretion from roots by high performance liquid chromatography.

Results

Al stress caused increase of endogenous free Put, and exogenous Put alleviated Al-induced inhibition of root elongation and Al accumulation. In addition, Put induced NO production and nitrate reductase (NR) activity under Al stress. Al- and Put-induced NO production could be reversed by NR inhibitor. Furthermore, Al stress stimulated citrate secretion from roots, and this response was stimulated by NO donor, whereas NO scavenger inhibited Al-induced citrate secretion from roots. Concomitantly, NO donor reduced Al accumulation in root apexes, while NO scavenger further enhanced Al accumulation. Al-induced inhibition of root growth was significantly improved by exogenous citrate treatment.

Conclusions

Put and NO enhanced Al tolerance by modulating citrate secretion from roots, and NO may act downstream of Put in red kidney bean under Al stress.