Acute Iron Poisoning

Robotham, James L.; Lietman, Paul S.

doi:10.1001/archpedi.1980.02130210059016

Cited by 106 publications

(36 citation statements)

References 54 publications

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“…Although several of the findings in this patient suggest a functional iron deficiency in muscle mitochondria, other features, including lactic acidosis, are reminiscent of acute iron toxicity (60,61 ). In hepatocytes of rats given toxic doses of ferrous sulfate, the primary target of intracellular injury appears to be the mitochondria that show electron-dense deposits, presumed to be iron, in the intermembrane space and matrix; they also manifest decreased respiratory control (62).…”

mentioning

confidence: 94%

“…In hepatocytes of rats given toxic doses of ferrous sulfate, the primary target of intracellular injury appears to be the mitochondria that show electron-dense deposits, presumed to be iron, in the intermembrane space and matrix; they also manifest decreased respiratory control (62). It was proposed that excess ferric ions may shunt electrons away from the respiratory chain via the inner membrane ferric reductase which normally provides ferrous ions for the synthesis of heme (60,63). Reoxidization of ferrous to ferric ions by molecular oxygen would decrease respiratory chain activity and could precipitate a cellular energy crisis (64).…”

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confidence: 99%

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Mitochondrial myopathy with succinate dehydrogenase and aconitase deficiency. Abnormalities of several iron-sulfur proteins.

Hall¹,

Henriksson²,

Lewis³

et al. 1993

J. Clin. Invest.

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Recently, we described a patient with severe exercise intolerance and episodic myoglobinuria, associated with marked impairment of succinate oxidation and deficient activity of succinate dehydrogenase and aconitase in muscle mitochondria ( 1 ). We now report additional enzymatic and immunological characterization of mitochondria. In addition to severe deficiency of complex II, manifested by reduction of succinate dehydrogenase and succinate:coenzyme Q oxidoreductase activities to 12 and 22% of normal, respectively, complex III activity was reduced to 37% and rhodanese to 48% of normal. Furthermore, although complex I activity was not measured, immunoblot analysis of complex I showed deficiency of the 39-, 24-, 13-, and 9-kD peptides with lesser reductions of the 51-and 18-kD peptides. Immunoblots of complex III showed markedly reduced levels of the mature Rieske protein in mitochondria and elevated levels of its precursor in the cytosol, suggesting deficient uptake into mitochondria. Immunoreactive aconitase was also low. These data, together with the previous documentation of low amounts of the 30-kD iron-sulfur protein and the 13.5-kD subunit of complex II, compared to near normal levels of the 70-kD protein suggest a more generalized abnormality of the synthesis, import, processing, or assembly of a group of proteins containing iron-sulfur clusters. (J. Clin. Invest. 1993. 92:2660-2666.) Key words: myoglobinuria -electron transport * nicotinamide adenine dinucleotide (reduced form) dehydrogenase * ubiquinol-cytochrome c reductase * thiosulfate sulfurtransferase

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confidence: 94%

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confidence: 99%

Mitochondrial myopathy with succinate dehydrogenase and aconitase deficiency. Abnormalities of several iron-sulfur proteins.

Hall¹,

Henriksson²,

Lewis³

et al. 1993

J. Clin. Invest.

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“…The slow rate of solubilisation results in a more prolonged absorption which is responsible for low toxicity of carbonyl iron (Brittenham et al, 2001). Robotham and Lietman (1980) in their study involving adult human volunteers have demonstrated that the 10.000 mg dose of carbonyl iron (which is over half the lethal dose as ferrous sulphate) when given to four volunteers developed no evidence of toxicity. Studies by Gorduek et al (1986) have shown that patient with mild IDA, can correct anemia and rebuild iron stores with short course of carbonyl iron.…”

Section: Discussionmentioning

confidence: 99%

Comparative study of serum ferritin levels after oral supplementation with ferrous sulphate and carbonyl iron in mild iron deficiency anemia in pregnancy

Chandrika¹,

Vasudha²

2010

International Journal of Biological and Chemical Sciences

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Iron supplementation is almost universally recommended during pregnancy to correct or prevent iron deficiency. Iron status can be assessed prepartum by estimating blood hemoglobin concentration, serum iron, serum total iron binding capacity (TIBC) and serum ferritin. This study attempts to know the therapeutic efficacy of the drugs, ferrous sulphate and carbonyl iron, in improving the iron stores to meet the increased demand during pregnancy. A comparative study was done in two groups of 36 pregnant women each. One group was supplemented with ferrous sulphate and the other group with carbonyl iron. The biochemical parameters assessing iron status, serum ferritin, serum iron and serum TIBC along with hemoglobin concentration were estimated before and after supplementation in both groups. Though not statistically significant, an increase was seen in the mean levels of serum ferritin in pregnant women who were supplemented with carbonyl iron compared to those who were supplemented with ferrous sulphate. Therefore, carbonyl iron can be preferred over ferrous sulphate in treating iron deficiency anemia in pregnancy, with added advantages of lesser side effects and shorter duration of therapy, which has been established in earlier studies.

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“…The current drug of choice for acute iron poisoning is deferoxamine (Desferal). Deferoxamine (DFO)' is a potent hydroxamate-type iron chelator isolated from Streptomyces pilosus, and is administered both intravenously and by gavage after acute iron poisoning (3). Historically, DFO represented a tremendous improvement over previous therapies for iron poisoning; the mortality associated with iron poisoning dropped from almost 50% to -1% with the introduction of DFO treatment (4).…”

Section: Introductionmentioning

confidence: 99%

Acute iron poisoning. Rescue with macromolecular chelators.

Mahoney¹,

Hallaway²,

Hedlund³

et al. 1989

J. Clin. Invest.

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Acute iron intoxication is a frequent, sometimes life-threatening, form of poisoning. Present therapy, in severe cases, includes oral and intravenous administration of the potent iron chelator, deferoxamine. Unfortunately, high dose intravenous deferoxamine causes acute hypotension additive with that engendered by the iron poisoning itself. To obviate this problem, we have covalently attached deferoxamine to high molecular weight carbohydrates such as dextran and hydroxyethyl starch. These macromolecular forms of deferoxamine do not cause detectable decreases in blood pressure of experimental animals, even when administered intravenously in very large doses, and persist in circulation much longer than the free drug. These novel iron-chelating substances, but not deferoxamine itself, will prevent mortality from otherwise lethal doses of iron administered to mice either orally or intraperitoneally. Further reflecting this enhanced therapeutic efficacy, the high molecular weight iron chelators also abrogate iron-mediated hepatotoxicity, suppressing the release of alanine aminotransferase. We conclude that high molecular weight derivatives of deferoxamine hold promise for the effective therapy of acute iron intoxication and may also be useful in other clinical circumstances in which control of free, reactive iron is therapeutically desirable.

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Acute Iron Poisoning

Cited by 106 publications

References 54 publications

Mitochondrial myopathy with succinate dehydrogenase and aconitase deficiency. Abnormalities of several iron-sulfur proteins.

Mitochondrial myopathy with succinate dehydrogenase and aconitase deficiency. Abnormalities of several iron-sulfur proteins.

Comparative study of serum ferritin levels after oral supplementation with ferrous sulphate and carbonyl iron in mild iron deficiency anemia in pregnancy

Acute iron poisoning. Rescue with macromolecular chelators.

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