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Iron Toxicity (iron + toxicity)
Selected AbstractsDistinct physiological responses of two rice cultivars subjected to iron toxicity under field conditionsANNALS OF APPLIED BIOLOGY, Issue 2 2009R.J. Stein Abstract Iron toxicity is recognised as the most widely distributed nutritional disorder in lowland and irrigated rice, derived from the excessive amounts of ferrous ions generated by the reduction of iron oxides in flooded soils. Rice cultivars with variable degrees of tolerance to iron toxicity have been developed, and cultural practices such as water management and fertilisation can be used to reduce its negative impact. However, because of the complex nature of iron toxicity, few physiological data concerning tolerance mechanisms to excess iron in field conditions are available. To analyse the physiological responses of rice to iron excess in field conditions, two rice cultivars with distinct tolerance to iron toxicity [BR-IRGA 409 (susceptible) and IRGA 420 (tolerant)] were grown in two areas, with a well-established history of iron toxicity (in Camaquć, RS, Brazil) and without iron toxicity (in Cachoeirinha, RS, Brazil). Plants from the susceptible cultivar grown in the iron-toxic site showed lower levels of chlorophylls and soluble proteins (together with higher carbonyl levels) indicating photooxidative and oxidative damage. The toxic effects observed were because of the accumulation of high levels of iron and not because of any indirectly induced shoot deficiency of other nutrients. Higher activities of antioxidative enzymes were also observed in leaves of plants from the susceptible cultivar only in the iron-toxic site, probably as a result of oxidative stress rather than because of specific involvement in a tolerance mechanism. There was no difference between cultivars in iron accumulation in the symplastic and apoplastic space of leaves, with both cultivars accumulating 85,90% of total leaf iron in the symplast. However, susceptible plants accumulated higher levels of iron in low-molecular-mass fractions than tolerant plants. The accumulation of iron in the low-molecular-mass fraction probably has a direct influence on iron toxicity, and the adaptive strategy of tolerant plants may rely on their capacity to buffer the iron amounts present in the low mass fraction, a new parameter to be considered when evaluating tolerance to iron excess in field-cultivated rice plants. [source] Redox Properties of the Iron Complexes of Orally Active Iron Chelators CP20, CP502, CP509, and ICL670HELVETICA CHIMICA ACTA, Issue 12 2004Martin Merkofer Redox cycling of iron is a critical aspect of iron toxicity. Reduction of a low-molecular-weight iron(III)-complex followed by oxidation of the iron(II)-complex by hydrogen peroxide may yield the reactive hydroxyl radical (OH.) or an oxoiron(IV) species (the Fenton reaction). Complexation of iron by a ligand that shifts the electrode potential of the complex to either to far below ,350,mV (dioxygen/superoxide, pH=7) or to far above +320,mV (H2O2/HO., H2O pH=7) is essential for limitting Fenton reactivity. The oral chelating agents CP20, CP502, CP509, and ICL670 effectively remove iron from patients suffering from iron overload. We measured the electrode potentials of the iron(III) complexes of these drugs by cyclic voltammetry with a mercury electrode and determined the dependence on concentration, pH, and stoichiometry. The standard electrode potentials measured are ,620,mV, ,600,mV, ,535,mV, and ,535,mV with iron bound to CP20, ICL670, CP502, and CP509, respectively, but, at lower chelator concentrations, electrode potentials are significantly higher. [source] Curcumin reduces the toxic effects of iron loading in rat liver epithelial cellsLIVER INTERNATIONAL, Issue 1 2009Donald J. Messner Abstract Background/Aims: Iron overload can cause liver toxicity and increase the risk of liver failure or hepatocellular carcinoma in humans. Curcumin (diferuloylmethane), a component of the food spice turmeric, has antioxidant, iron binding and hepatoprotective properties. The aim of this study was to quantify its effects on iron overload and the resulting downstream toxic effects in cultured T51B rat liver epithelial cells. Methods: T51B cells were loaded with ferric ammonium citrate (FAC) with or without the iron delivery agent 8-hydroxyquinoline. Cytotoxicity was measured by methylthiazolyldiphenyl-tetrazolium bromide assay. Iron uptake and iron bioavailability were documented by chemical assay, quench of calcein fluorescence and ferritin induction. Reactive oxygen species (ROS) were measured by a fluorescence assay using 2,,7,-dichlorodihydrofluorescein diacetate. Oxidative stress signalling to jnk, c-jun and p38 was measured by a Western blot with phospho-specific antibodies. Results: Curcumin bound iron, but did not block iron uptake or bioavailability in T51B cells given FAC. However, it reduced cytotoxicity, blocked the generation of ROS and eliminated signalling to cellular stress pathways caused by iron. Inhibition was observed over a wide range of FAC concentrations (50,500 ,M), with an apparent IC50 in all cases between 5 and 10 ,M curcumin. In contrast, desferoxamine blocked both iron uptake and toxic effects of iron at concentrations that depended on the FAC concentration. The effects of curcumin also differed from those of ,-tocopherol, which did not bind iron and was less effective at blocking iron-stimulated ROS generation. Conclusions: Curcumin reduced iron-dependent oxidative stress and iron toxicity in T51B cells without blocking iron uptake. [source] A novel streptococcal integrative conjugative element involved in iron acquisitionMOLECULAR MICROBIOLOGY, Issue 5 2008Zoe Heather Summary In this study, we determined the function of a novel non-ribosomal peptide synthetase (NRPS) system carried by a streptococcal integrative conjugative element (ICE), ICESe2. The NRPS shares similarity with the yersiniabactin system found in the high-pathogenicity island of Yersinia sp. and is the first of its kind to be identified in streptococci. We named the NRPS product ,equibactin' and genes of this locus eqbA,N. ICESe2, although absolutely conserved in Streptococcus equi, the causative agent of equine strangles, was absent from all strains of the closely related opportunistic pathogen Streptococcus zooepidemicus. Binding of EqbA, a DtxR-like regulator, to the eqbB promoter was increased in the presence of cations. Deletion of eqbA resulted in a small-colony phenotype. Further deletion of the irp2 homologue eqbE, or the genes eqbH, eqbI and eqbJ encoding a putative ABC transporter, or addition of the iron chelator nitrilotriacetate, reversed this phenotype, implicating iron toxicity. Quantification of 55Fe accumulation and sensitivity to streptonigrin suggested that equibactin is secreted by S. equi and that the eqbH, eqbI and eqbJ genes are required for its associated iron import. In agreement with a structure-based model of equibactin synthesis, supplementation of chemically defined media with salicylate was required for equibactin production. [source] Distinct physiological responses of two rice cultivars subjected to iron toxicity under field conditionsANNALS OF APPLIED BIOLOGY, Issue 2 2009R.J. Stein Abstract Iron toxicity is recognised as the most widely distributed nutritional disorder in lowland and irrigated rice, derived from the excessive amounts of ferrous ions generated by the reduction of iron oxides in flooded soils. Rice cultivars with variable degrees of tolerance to iron toxicity have been developed, and cultural practices such as water management and fertilisation can be used to reduce its negative impact. However, because of the complex nature of iron toxicity, few physiological data concerning tolerance mechanisms to excess iron in field conditions are available. To analyse the physiological responses of rice to iron excess in field conditions, two rice cultivars with distinct tolerance to iron toxicity [BR-IRGA 409 (susceptible) and IRGA 420 (tolerant)] were grown in two areas, with a well-established history of iron toxicity (in Camaquć, RS, Brazil) and without iron toxicity (in Cachoeirinha, RS, Brazil). Plants from the susceptible cultivar grown in the iron-toxic site showed lower levels of chlorophylls and soluble proteins (together with higher carbonyl levels) indicating photooxidative and oxidative damage. The toxic effects observed were because of the accumulation of high levels of iron and not because of any indirectly induced shoot deficiency of other nutrients. Higher activities of antioxidative enzymes were also observed in leaves of plants from the susceptible cultivar only in the iron-toxic site, probably as a result of oxidative stress rather than because of specific involvement in a tolerance mechanism. There was no difference between cultivars in iron accumulation in the symplastic and apoplastic space of leaves, with both cultivars accumulating 85,90% of total leaf iron in the symplast. However, susceptible plants accumulated higher levels of iron in low-molecular-mass fractions than tolerant plants. The accumulation of iron in the low-molecular-mass fraction probably has a direct influence on iron toxicity, and the adaptive strategy of tolerant plants may rely on their capacity to buffer the iron amounts present in the low mass fraction, a new parameter to be considered when evaluating tolerance to iron excess in field-cultivated rice plants. [source] Effect of nitric oxide on iron-mediated cytotoxicity in primary cultured renal proximal tubulesCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2001Zhao-long Wu Abstract Nitric oxide (NO) has been proved to be a mediator of hypoxic injury in renal proximal tubules (PT), but its effect on iron-induced cytotoxicity has remained little known. In this study, we observed the relationship between NO production and lactate dehydrogenase (LDH) release in primary proximal tubular epithelia co-incubated with different doses of NTA-Fe and lipopolysaccharide (LPS) alone or in combination. NO production was monitored by NO2 concentration in supernatants based on the Griess reaction; while the semi-quantitative RT-PCR was applied to detect the inducible nitric oxide synthase (iNOS) mRNA level induced by NTA-Fe and LPS together. In addition, experimental groups were subjected to reactive oxygen species (ROS) scavengers to determine the impact of the interaction between NO and ROS on iron-mediated cytotoxicity. After a 12-h co-incubation, we found that NTA-Fe increased both LDH release and 2, production in a dose-dependent manner (P,<,0.001). The level of iNOS mRNA induced by LPS was enhanced by 500 ,m NTA-Fe (P,<,0.01), lower or higher concentrations had no effect. However, the supernatant 2, level in the same group did not change significantly (P,>,0.05) although tubular injury was aggravated (P,<,0.001). The addition of l -arginine increased LDH release from 25.05,±,8.36% in the iron group to 38.67,±,7.67% in iron plus LPS group (P,<,0.05); concomitantly, l -NAME mitigated iron toxicity in LPS-treated PT (P,<,0.05). Hydroxyl scavengers provided complete protection against iron-mediated cytotoxicity (P,<,0.001), but the decrease of 2, production was only significant in the LPS-treated group. In contrast, SOD was partially effective in the LPS group (P,<,0.05) whereas the 2, level in the supernatant was inversely raised (P,<,0.05). GSH had no effect on either iron toxicity or 2, production. Thus, we conclude that NO can exacerbate the cytotoxicity caused by NTA-Fe in cultured proximal tubular epithelia, but NO is not the only factor. NTA-Fe could enhance the upregulation of iNOS transcription induced by LPS in a specific concentration range, and its regulation of NO production might also involve a post-transcription mechanism. The hydroxyl group is the major mediator in our model and the pro-oxidant role of NO is probably due to its ability to promote the Fenton reaction and form both ONOO, and ,OH via its interaction with ROS. Copyright © 2001 John Wiley & Sons, Ltd. [source] | ||||||||||