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Iron toxicity

Iron toxicity is a syndrome of disorders associated with large concentrations of Fe + in the soil solution. It is only found in flooded soils. A wide range of concentrations produce the symptoms, from 1000 to only 10mgL in soils with poor nutrient status—especially of P or K—or with respiration inhibitors such as H2S. There are large differences in tolerance between rice varieties. The effects include internal damage of tissues due to excessive uptake of Fe + impaired nutrient uptake, especially of P, K, Ca and Mg and increased diseases associated with imbalanced nutrition, such as brown leaf spot (caused by Helminthospo-rium oryzae), sheath blight (caused by Rhizoctonia solani) and blast (caused by Pyricularia oryzae). [Pg.214]

The circumstances of the toxicity are quite well established, though some of the details of the mechanisms involved are uncertain. Three main groups of Fe toxic soils are distinguished  [Pg.214]

Where Fe toxicity is associated with interflow the concentrations of dissolved Fe in the npwelling water have been fonnd to be too small to acconnt for the large concentrations of Fe + in the root zone, and most of the Fe + is apparently formed in situ. Therefore the interflow aggravates toxicity by some mechanism other than bringing in Fe +, possibly involving depletion of other nutrients and upsetting the plant s ability to exclude Fe (Section 6.5). [Pg.215]

It is often a symptom of imbalanced nutrition rather than high Fe + in the soil solution per se. Thus the soil solution Fe + concentrations at which it is reported vary from 10 to 1000mgL and it is more often associated with low levels of P, K, Ca and Mg and impaired ability of roots to exclude Fe +. [Pg.215]


There is a dark side to receptor-mediated endocyto-sis in that viruses which cause such diseases as hepatitis (affecting liver cells), poliomyelitis (affecting motor neurons), and AIDS (affecting T cells) initiate their damage by this mechanism. Iron toxicity also begins with excessive uptake due to endocytosis. [Pg.430]

Omara, F.O. and Blakley, B.R. (1993). Vitamin E is protective against iron toxicity and iron-induced hepatic vitamin E depletion in mice. J. Nutr. 123, 1649-1655. [Pg.245]

Wong, RW, Richa, DC, Hahn, P, Green, WR, and Dunaief, JL, 2007. Iron toxicity as a potential factor in AMD. Retina 27, 997-1003. [Pg.353]

Design concepts are now being applied more effectively to mineral supplements. For example, by controlling the redox potential of iron, toxic effects associated with excess Fe(II) during parental supplementation can be avoided. Peroxovanadate complexes can inhibit insulin-receptor-associated phosphotyrosine phosphatase and activate insulin receptor kinase, and both V(IV) and V(V) offer promise as potential insulin mimics. [Pg.185]

Acid sulfate soils are an especially difficult class of acid soil formed in former marine sediments that have been drained. The acidity is generated from the oxidation of pyrite in the soil resulting in acute aluminium toxicity, iron toxicity, and deficiencies of most nutrients, especially phosphate which becomes immobilized in ferric oxide. The development and management of acid sulfate soils are discussed in detail in Dost and van Breemen (1983) and Dent (1986). [Pg.213]

Razafinjara AL. 1999. Cation-anion balances and chemical changes in the rhizosphere of rice in an iron toxic soil. PhD thesis. University of the Philippines at Los Banos. [Pg.274]

Iron-gluconate complexes are sufficiently stable not to cause iron toxicity (in contrast to Fe aq, Fe aq, and complexes of low stability) and are safe and effective in hemodialysis. " There is information on iron transfer between gluconate and transferrin. Dithionite releases Fe + from gluconate. ... [Pg.491]

Unlabeled Uses Chronic iron toxicity, control of idiopathic methemoglobinemia, macular degeneration, prevention of common cold, urine acidifier... [Pg.91]

Chronic iron toxicity (iron overload), also known as hemochromatosis, results when excess iron is deposited in the heart, liver, pancreas, and other organs. It can lead to organ failure and death. It most commonly occurs in patients with inherited hemochromatosis, a disorder characterized by excessive iron absorption, and in patients who receive many red cell transfusions over a long period of time (eg, patients with thalassemia major). [Pg.734]

Exactly the opposite problem may occur for plants whose roots are growing in anaerobic media. In Hooded soils the roots may be exposed to high levels of irontll). posing potential problems of iron toxicity. Rice plants and water lilies with roots in anaerobic soils transport dioxygen (from the air or photosynthesis, or both) to the periphery of the roots where it oxidizes the iron(II) to irondll). In (his case the insolubility of Irondll) hydroxide is utilized to protect the plant from iron poisoning.113 A similar problem from too much iron occurs in parts of sub-Saharan Africa. [Pg.1004]

Eaton JW, Qian M (2002) Molecular bases of cellular iron toxicity. Free Radical Biol Med 32 833-840 Ebert G (1980) Biopolymere. Steinkopf, Darmstadt... [Pg.456]

Acute iron toxicity is seen almost exclusively in young children who have ingested a number of iron tablets. Although adults are able to tolerate large doses of oral iron without serious consequences, as... [Pg.743]

Link G, Saada A, Pinson A, et al. Mitochondrial respiratory enzymes are a major target of iron toxicity in rat heart cells. J Lab Clin Med 1998 131 466-474. [Pg.247]

Qll Iron preparations are a common cause of accidental poisoning in very young children, who may mistake iron tablets for sweets. How is acute iron toxicity treated ... [Pg.81]

A. Pietrangelo, Mechanism of Iron Toxicity, in Iron Chelation Therapy , 1st edn., ed. C. Hershko, Kluwer Academic/Plenum Publishers, New York, 2002, Vol. 509, p. 19. [Pg.2356]

Iron is an essential element for metabolic systems, but in iron-rich solutions toxicity can develop in both fish and biota. Iron toxicity has... [Pg.4729]


See other pages where Iron toxicity is mentioned: [Pg.384]    [Pg.369]    [Pg.136]    [Pg.205]    [Pg.708]    [Pg.272]    [Pg.202]    [Pg.214]    [Pg.215]    [Pg.421]    [Pg.123]    [Pg.734]    [Pg.734]    [Pg.734]    [Pg.709]    [Pg.1003]    [Pg.39]    [Pg.743]    [Pg.744]    [Pg.744]    [Pg.194]    [Pg.261]    [Pg.261]    [Pg.92]    [Pg.1957]    [Pg.1004]    [Pg.4741]    [Pg.578]    [Pg.619]   
See also in sourсe #XX -- [ Pg.194 ]

See also in sourсe #XX -- [ Pg.326 ]

See also in sourсe #XX -- [ Pg.131 ]

See also in sourсe #XX -- [ Pg.47 ]




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