The effects of iron deficiency on the respiratory function and cytochrome content of rat heart mitochondria.

Blayney, Lynda Mary; Bailey-Wood, R.; Jacobs, Alan R.; Henderson, A R; Muir, John

doi:10.1161/01.res.39.5.744

Cited by 73 publications

(48 citation statements)

References 25 publications

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“…The experimental animals showed a gradual drop of haemoglobin from the onset of bleeding, confirming the pattern previously observed in rats (Blayney et al, 1976) and mice (Hamilton, 1978). The hamster model developed by Rennie, MacDonald & Douglas (1982), however, had a different haematological pattern.…”

Section: Resultssupporting

confidence: 86%

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Experimental iron deficiency in Syrian hamsters (Mesocricetus auratus)

1983

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SummaryAn animal model was developed in which the effect of iron deficiency on the oral muCOsa could be studied. Iron deficiency was induced by feeding hamsters a low-iron powdered diet together with withdrawal of 0'5 ml of blood weekly, for a period of 9 weeks. At the end of this period the mean haematological values for control animals were, Hb 15'9 S/dl, plasma iron 40'3 pmol/l, TIBe 90'5 pmol/l and transferrin saturation 44'5%, compared with 7'4, 7'2, 111'4 and 6'5 respectively for experimental animals. These results were reproducible in successiv"e groups of animals and indicate that this is a useful model for the study of iron deficiency anaemia.

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Section: Resultssupporting

confidence: 86%

“…Animal models, using rats, have been employed and biochemical studies of changes in heart (Blayney et al, 1976), brain (Mackler et al, 1978) and striated muscle (Finch et al, 1976) reported. However, little information is available on the oral mucosa, which usually shows marked atrophy under such conditions.…”

Section: Discussionmentioning

confidence: 99%

Experimental iron deficiency in Syrian hamsters (Mesocricetus auratus)

1983

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“…By these mechanisms, this protein regulates plasma iron concentration according to the need of the body (Knutson 2010, Anderson et al 2007, Ganz and Nemeth 2012, and this could explain why serum iron concentration was kept similar to the control group levels. Our data on Hb content in this condition is also consistent with those of Blayney et al (1976) study, in which no significant difference in Hb concentration was observed in rats receiving oral iron supplementation. Interestingly, the rats subjected to iron supplementation and iron restriction showed a significant increase in red blood cell quantity, but a reduction of their mean corpuscular volume, which could explain why the hematocrit remained similar to the control group.…”

Section: Discussionsupporting

confidence: 92%

Iron restriction increases myoglobin gene and protein expression in Soleus muscle of rats

Souza

Brunetto

Nunes

2016

An. Acad. Bras. Ciênc.

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Iron is an important trace element for proper cell functioning. It is present in cytochromes, hemoglobin and myoglobin (Mb), where it binds to oxygen. It is also an electron acceptor in the respiratory chain. Mb is an 18 kDa heme-protein, highly expressed in skeletal muscle and heart. The expression of several genes involved in the metabolism of iron is post-transcriptionally regulated by this element. Iron was shown to interfere with the polyadenylation step, modifying their poly (A) tail length and, as a consequence, their stability and translation rate. The aim of this study was to investigate whether iron supplementation or long and short-term restriction affects Mb gene and protein expression, as well as Mb mRNA poly(A) tail length, in cardiac and skeletal muscles of rats. Long-term iron restriction caused an increase in Mb gene and protein expression in Soleus muscle. No changes were observed in extensor digitorum longus muscle and heart. Short-term iron supplementation after iron deprivation did not alter Mb gene expression and mRNA poly(A) tail length in all tissues studied. These results indicate that Mb gene and protein expression is upregulated in response to iron deprivation, an effect that is tissue-specific and seems to occur at transcriptional level.

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“…Two studies fed iron-deficient diets to rats and examined cardiac muscle. 15,16 Rats receiving iron-deficient diet were anemic. Cardiac muscle examined by transmission electron microscopy showed mitochondrial swelling and abnormal sarcomere structure.…”

Section: Experimental Evidence With Iron and Muscle Functionmentioning

confidence: 99%

“…15 In another study, iron deficiency was associated with impairment of myocardial mitochondrial electron transport in rat heart. 16 …”

Section: Experimental Evidence With Iron and Muscle Functionmentioning

confidence: 99%

Iron Deficiency and Heart Disease: Ironclad Evidence?

Carson

Adamson

2010

Hematology

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Patients with heart failure have elevated levels of circulating inflammatory cytokines and commonly have iron deficiency anemia or anemia of chronic inflammation. Clinical trials in patients with congestive heart failure and iron deficiency have demonstrated that intravenous iron treatment appears to improve subjective and objective outcomes. Most patients in these trials were not anemic or only had mild anemia, and hemoglobin concentration rose only slightly after treatment with iron. Experimental evidence demonstrates that iron is a cofactor for muscle function, which could explain the improvement in clinical outcomes. Many questions remain to be answered to understand the role of iron therapy in patients with congestive heart failure.In a landmark randomized clinical trial, Anker and colleagues 1 found that intravenous iron improved symptoms and physical function in patients with chronic heart failure and anemia. This trial potentially has broad implications for the hematologist, cardiologist, and internist. In this paper, we review the essential background information on anemia and heart failure, including the frequency, causes, and consequences of anemia in heart failure. We summarize the results of this trial in detail and describe the strengths and weaknesses. We then describe potential pathophysiological explanation(s) for the results. We finish with a description of the many uncertainties and questions that this trial raises. Prevalence and Consequences of Anemia in Heart FailureThe prevalence of anemia varies by age and gender. In an analysis of a representative population of community-dwelling persons from the US (NHANES-III [Third National Health and Nutrition Examination Survey]), the prevalence of anemia in patients 65 years and older was 10.6% and rises to over 20% in 85-year-old individuals. 2 However, in patients with congestive heart failure, the prevalence may be much higher. In a large cohort of patients with congestive heart failure, 37.2% were anemic. 3 In contrast, the prevalence of anemia was 17% in a population-based cohort of patients with new-onset congestive heart failure (mean age 78) from Canada. 4 The patient with heart failure who has anemia has an increased risk of death. In a systematic review of 153,180 patients with heart failure, 48% of anemic patients died within 6 months, compared with 29.5% of nonanemic patients (adjusted hazard ratio 1.46; 95% CI 1.26 -1.69). 3 This experience is similar to the Canadian cohort in which the risk of death was 1.34 times higher in anemic than in nonanemic patients with heart failure. 4 It is unknown if the increased risk of death is from anemia or is just a marker for underlying severity of disease.

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The effects of iron deficiency on the respiratory function and cytochrome content of rat heart mitochondria.

Cited by 73 publications

References 25 publications

Experimental iron deficiency in Syrian hamsters (Mesocricetus auratus)

Experimental iron deficiency in Syrian hamsters (Mesocricetus auratus)

Iron restriction increases myoglobin gene and protein expression in Soleus muscle of rats

Iron Deficiency and Heart Disease: Ironclad Evidence?

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