Myoglobin and cytochrome response during repair of iron deficiency in the rat.

Dallman, Peter R.; Schwartz, Herbert C.

doi:10.1172/jci105269

Cited by 65 publications

(35 citation statements)

References 17 publications

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“…The anemia in iron-depleted animals (IIB) treated with iron was repaired within 8-9 days, as in similar groups of animals reported previously [10]. The return to normal heart weight ratio is shown in table III.…”

Section: Rate Of Reversal After Institution Of a Complete Dietsupporting

confidence: 78%

“…Male rats of the Wistar strain were fed iron- [10] or copper-deficient diets [7] starting at 10 days of age (groups IIB and III, table I); iron-deficient group IIA was started on the diet at 36 days of age to provide a briefer period of depletion. All animals received the same diet based upon partially skimmed milk with a vitamin and mineral supplement containing no added iron or copper salts.…”

Section: Methodsmentioning

confidence: 99%

“…Other groups had free access to the diet. Groups IA and IB, which received the complete diet were also given copper (40 mg cupric sulfate/liter) and iron (250 mg ferrous ammonium citrate/liter) in their drinking water at levels previously found to be adequate [7,10]. In the deficient diets one or the other of the salts was omitted.…”

Section: Methodsmentioning

confidence: 99%

“…In the deficient diets one or the other of the salts was omitted. Essentially identical treatment for producing iron and copper deficiency had previously been shown to deplete liver hydrolyzable iron and copper, respectively, in addition to depressing hemoglobin and cytochrome concentrations [7,10]. Iron-deficient rats in group IIB were repleted by an initial intramuscular injection of 5 mg elemental iron as iron dextran [29], followed by iron supplementation in the drinking water as in the complete dietary regimen.…”

Section: Methodsmentioning

confidence: 99%

“…In mice, similar mor-phological changes are seen in hepatocytes after treatment with the copper-chelating agent cuprizone [23], and in response to a riboflavin-deficient diet [24]. Each of these deficiency states results in depletion of components of the electron-transport chain which are localized in the mitochondrial cristae [2,7,10]. This depletion appears to be the common feature in the production of the altered mitochondrial structure.…”

Section: Introductionmentioning

confidence: 98%

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Cardiac Hypertrophy in Rats with Iron and Copper Deficiency: Quantitative Contribution of Mitochondrial Enlargement

1970

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Section: Rate Of Reversal After Institution Of a Complete Dietsupporting

confidence: 78%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

See 3 more Smart Citations

Cardiac Hypertrophy in Rats with Iron and Copper Deficiency: Quantitative Contribution of Mitochondrial Enlargement

1970

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Pagophagia and Iron Lack

Coltman¹

1969

JAMA

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Iron overload and impaired iron handling contribute to the dystrophic pathology in models of Duchenne muscular dystrophy

Alves

Kysenius

Caldow

et al. 2022

J cachexia sarcopenia muscle

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Background Oxidative stress is implicated in the pathophysiology of Duchenne muscular dystrophy (DMD, caused by mutations in the dystrophin gene), which is the most common and severe of the muscular dystrophies. To our knowledge, the distribution of iron, an important modulator of oxidative stress, has not been assessed in DMD. We tested the hypotheses that iron accumulation occurs in mouse models of DMD and that modulation of iron through the diet or chelation could modify disease severity. Methods We assessed iron distribution and total elemental iron using LA-ICP-MS on skeletal muscle cross-sections of 8-week-old Bl10 control mice and dystrophic mdx mice (with moderate dystrophy) and dystrophin/utrophin-null mice (dko, with severe dystrophy). In addition, mdx mice (4 weeks) were treated with either an iron chelator (deferiprone 150 mg/kg/day) or iron-enriched feed (containing 1% added iron as carbonyl iron). Immunoblotting was used to determine the abundance of iron-and mitochondria-related proteins. (Immuno)histochemical and mRNA assessments of fibrosis and inflammation were also performed. ResultsWe observed a significant increase in total elemental iron in hindlimb muscles of dko mice (+50%, P < 0.05) and in the diaphragm of mdx mice (+80%, P < 0.05), with both tissues exhibiting severe pathology. Iron dyshomeostasis was further evidenced by an increase in the storage protein ferritin (dko: +39%, P < 0.05) and ferroportin compared with Bl10 control mice (mdx: +152% and dko: +175%, P < 0.05). Despite having features of iron overload, dystrophic muscles had lower protein expression of ALAS-1, the rate-limiting enzyme for haem synthesis (dko À44%, P < 0.05), and the haem-containing protein myoglobin (dko À54%, P < 0.05). Deferiprone treatment tended to decrease muscle iron levels in mdx mice (À30%, P < 0.1), which was associated with lower oxidative stress and fibrosis, but suppressed haem-containing proteins and mitochondrial content. Increasing iron via dietary intervention elevated total muscle iron (+25%, P < 0.05) but did not aggravate the pathology. Conclusions Muscles from dystrophic mice have increased iron levels and dysregulated iron-related proteins that are associated with dystrophic pathology. Muscle iron levels were manipulated by iron chelation and iron enriched feed. Iron chelation reduced fibrosis and reactive oxygen species (ROS) but also suppressed haem-containing proteins and mitochondrial activity. Conversely, iron supplementation increased ferritin and haem-containing proteins but did not alter ROS, fibrosis, or mitochondrial activity. Further studies are required to investigate the contribution of impaired ferritin breakdown in the dysregulation of iron homeostasis in DMD.

show abstract

Myoglobin and cytochrome response during repair of iron deficiency in the rat.

Cited by 65 publications

References 17 publications

Cardiac Hypertrophy in Rats with Iron and Copper Deficiency: Quantitative Contribution of Mitochondrial Enlargement

Cardiac Hypertrophy in Rats with Iron and Copper Deficiency: Quantitative Contribution of Mitochondrial Enlargement

Pagophagia and Iron Lack

Iron overload and impaired iron handling contribute to the dystrophic pathology in models of Duchenne muscular dystrophy

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