Hemolytic drugs aniline and dapsone induce iron release in erythrocytes and increase the free iron pool in spleen and liver.

@article{Ciccoli1999HemolyticDA,
  title={Hemolytic drugs aniline and dapsone induce iron release in erythrocytes and increase the free iron pool in spleen and liver.},
  author={Lucia Ciccoli and Marco Ferrali and Viviana Rossi and Cinzia Signorini and Carlo Alessandrini and Mario Comporti},
  journal={Toxicology letters},
  year={1999},
  volume={110 1-2},
  pages={
          57-66
        }
}
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Primaquine-Induced Hemolytic Anemia: Formation of Free Radicals in Rat Erythrocytes Exposed to 6-Methoxy-8-hydroxylaminoquinoline
TLDR
The hypothesis that oxygen-derived and possibly other free radicals are involved in the mechanism underlying MAQ-NOH-induced hemolytic anemia is supported.
Iron release, superoxide production and binding of autologous IgG to band 3 dimers in newborn and adult erythrocytes exposed to hypoxia and hypoxia-reoxygenation.
Protection of erythrocytes against oxidative damage and autologous immunoglobulin G (IgG) binding by iron chelator fluor-benzoil-pyridoxal hydrazone.
Up-regulation of heme oxygenase-1 in rat spleen after aniline exposure.
Iron Release in Erythrocytes and Plasma Non Protein-bound Iron in Hypoxic and Non Hypoxic Newborns
TLDR
When term plus preterm newborns were divided in two groups, normoxic and hypoxic, according to cord blood pH, it was found that both iron release and NBPI were markedly higher in the hypoxic newborns compared to normoxic ones.
Iron release, oxidative stress and erythrocyte ageing.
High-dose clastogenic activity of aniline in the rat bone marrow and its relationship to the carcinogenicity in the spleen of rats
  • E. Bomhard
  • Biology, Medicine
    Archives of Toxicology
  • 2003
TLDR
Several lines of evidences are presented against a causal relationship between the clastogenic activity in male PVG rats at 400 and 500 mg/kg and the carcinogenicity in the spleen of Fischer 344 rats starting at 30  mg/kg in males.
Blood cell oxidative stress precedes hemolysis in whole blood-liver slice co-cultures of rat, dog, and human tissues.
Genotoxic Activities of Aniline and its Metabolites and Their Relationship to the Carcinogenicity of Aniline in the Spleen of Rats
TLDR
It is concluded that there is no relationship between the damage to the chromosomes at high, toxic doses of aniline and its major metabolites p-aminophenol/p-hydroxyacetanilide and theAniline-induced spleen tumors in the rat.
Methemoglobin—It's not just blue: A concise review
  • J. Umbreit
  • Biology, Medicine
    American journal of hematology
  • 2007
TLDR
Hemoglobin has functions besides carrying oxygen to the tissues, and regulates vascular tone and inflammation via a redox couple with methemoglobin, paralleled by the well‐described role in the oxidation of various drugs resulting in methemoglobinemia.
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References

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Role of dapsone hydroxylamine in dapsone-induced hemolytic anemia.
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  • Biology, Medicine
    The Journal of pharmacology and experimental therapeutics
  • 1988
TLDR
Data indicate that the hydroxylamine metabolites of dapsone are direct acting hemolytic agents that are formed from daps one in sufficient amounts to account for their being the sole mediators of dapone-induced hemolysis and anemia in the rat.
Dapsone-induced hemolytic anemia: effect of dapsone hydroxylamine on sulfhydryl status, membrane skeletal proteins and morphology of human and rat erythrocytes.
TLDR
Although the morphology of human red cells was altered, the incidence and degree of change were considerably less than those of rat red cells, suggesting that human cells are probably less sensitive than rat cells to dapsone hydroxylamine-induced oxidative damage.
Iron release, lipid peroxidation, and morphological alterations of erythrocytes exposed to acrolein and phenylhydrazine.
TLDR
Morphological studies carried out with scanning electron microscopy showed a number of alterations in the shape of the incubated erythrocytes, including echinocyte transformation and the appearance of codocyte, stomatocyte, and cnizocyte like forms, which were more prominent with increasing lipid peroxidation and hemolysis.
Dapsone-induced hemolytic anemia: effect of N-hydroxy dapsone on the sulfhydryl status and membrane proteins of rat erythrocytes.
Iron release and membrane damage in erythrocytes exposed to oxidizing agents, phenylhydrazine, divicine and isouramil.
TLDR
Mouse erythrocytes were incubated with oxidizing agents and a rapid release of iron in a desferrioxamine-chelatable form was seen, suggesting a role for GSH in preventing iron release when oxidative stress is imposed by the oxidants.
Release of free, redox-active iron in the liver and DNA oxidative damage following phenylhydrazine intoxication.
Role of aniline metabolites in aniline-induced hemolytic anemia.
TLDR
Phenylhydroxylamine is suggested to be the active metabolite that mediates aniline-induced hemolytic anemia and the area under the blood time course curve for phenylhydroxlamine plus nitrosobenzene was equivalent in rats administered equitoxic doses of anilines or phenyl Hydroxylamines, indicating that sufficient phenylHydroxylaminate is formed in vivo during anilin clearance to account for anilina's toxicity.
Allyl alcohol-induced hemolysis and its relation to iron release and lipid peroxidation.
Iron release and erythrocyte damage in allyl alcohol intoxication in mice.
Dapsone-induced hemolytic anemia.
TLDR
In studies on rat red cells, it is established that the N-hydroxy metabolites of dapsone, DDS- NOH and MADDS-NOH, are direct-acting hemolytic agents, and that the action of these toxic metabolites in the red cell induces premature sequestration by the spleen.
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