Ferritin iron as substrate for synthesis of protoheme in intact rat liver mitochondria

Ulvik, Rune J.

doi:10.1016/0014-5793(81)81179-9

Cited by 9 publications

(4 citation statements)

References 30 publications

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“…A direct role for vitamin C in support of iron incorporation into protoporphyrin must also be considered. 18 The data also indicate that a high dose of ESA is associated with more hypochromic RBC ( Table 2). This is consistent with previous findings of increased hypochromic reticulocytes after EPO administration, 19 and may result from ESA stimulation of RBC production at a rate in excess of the rate of iron delivery to the bone marrow.…”

Section: Discussionmentioning

confidence: 85%

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Plasma vitamin C levels in ESRD patients and occurrence of hypochromic erythrocytes

Seibert

Richter²,

Kuhlmann

et al. 2016

Hemodialysis International

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Section: Discussionmentioning

confidence: 85%

“…An excess of this type of RBC is typically associated with impaired iron delivery to the bone marrow for erythropoiesis. A direct role for vitamin C in support of iron incorporation into protoporphyrin must also be considered …”

Section: Discussionmentioning

confidence: 99%

Plasma vitamin C levels in ESRD patients and occurrence of hypochromic erythrocytes

Seibert

Richter²,

Kuhlmann

et al. 2016

Hemodialysis International

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“…The MLIP is fueled from the CLIP as well as directly from the ELIP as explained above. Albeit the knowledge on iron shuttling across the outer mitochondrial membrane is still incomplete, the endosomal supply via a “kiss and run” mechanism could involve a distinct endosome-mitochondria interaction and the existence of specific mitochondrial ferritin binding sites has been proposed too [ 85 , 198 ]. In contrast, it has been demonstrated that the iron transfer across the inner mitochondrial membrane is mediated by the mitochondrial iron carrier mitoferrin 1,2 (Mfr1,2) [ 87 , 199 , 200 ], which may involve the regulation via Mfr protein stability as suggested by the interaction of Mfr1 with the mitochondrial inner membrane ATP-binding cassette transporter Abcb19 in erythroblasts [ 201 ].…”

Section: Cellular Iron Compartmentalizationmentioning

confidence: 99%

Oxidative Stress and the Homeodynamics of Iron Metabolism

2015

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Iron and oxygen share a delicate partnership since both are indispensable for survival, but if the partnership becomes inadequate, this may rapidly terminate life. Virtually all cell components are directly or indirectly affected by cellular iron metabolism, which represents a complex, redox-based machinery that is controlled by, and essential to, metabolic requirements. Under conditions of increased oxidative stress-i.e., enhanced formation of reactive oxygen species (ROS)-however, this machinery may turn into a potential threat, the continued requirement for iron promoting adverse reactions such as the iron/H2O2-based formation of hydroxyl radicals, which exacerbate the initial pro-oxidant condition. This review will discuss the multifaceted homeodynamics of cellular iron management under normal conditions as well as in the context of oxidative stress.Keywords: iron; oxidative stress; metabolism Systemic and Cellular Iron TransfersFerric iron or iron contained in heme is absorbed by intestinal enterocytes via heme carrier proteins (HCP1) [1], the divalent metal transporter DMT1 (SLC11A2) [2,3] or the integrin-mobilferrin pathway [4,5] (a review on intestinal iron absorption is given in [6,7]). The absorbed iron is then released from the enterocytes to the bloodstream as transferrin-bound iron (TBI) via ferroportin (see below). Under physiological conditions, the bulk of iron enters the cell bound as TBI via transferrin-receptor (TfR) mediated endocytosis followed by endosomal iron liberation. However, resorption of non-transferrin OPEN ACCESSBiomolecules 2015, 5 809 bound iron (NTBI) from the bloodstream may also occur either via DMT-1, the zinc transporter Zip14 (SLC39A14) [8,9] or specific citrate binding sites [10][11][12]. Notably, the serum content of labile NTBI is very low under normal conditions but may rise substantially in diseased states, such as thalassemia, where the high NTBI level-essentially caused by repeated blood transfusion-is considered to cause disease-related oxidative stress [13][14][15][16][17][18]. Similarly, serum ferritin which may serve as iron carrier too [19,20] and is also increased under certain pathological conditions, such as inflammation and cancer [21], can also be endocytosed [22][23][24][25] [34]. Finally, heme-bound iron will enter the cells via HCP1 [1] and tissue macrophages will also "ingest iron" upon phagocytosis of aged cells such as erythrocytes or via the haptoglobin/CD 163 or hemopexin/CD91 mediated uptake of hemoglobin or heme [35] and deliver the recycled iron back to the bloodstream, which is indispensable for the maintenance of systemic iron homeostasis [36].In contrast to several ways of cellular iron uptake, only two mechanisms of cellular iron release are known. Usually, iron release from a cell occurs via ferroportin (Fpn) [37][38][39][40][41] a membrane bound iron exporter, which is controlled by hepatocyte derived hepcidin [42,43], the hepcidin activity itself being regulated by the serine protease matriptase-2 [44,45]. The ferroportin-rel...

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“…In vitro and in vivo studies have described a ribo¯avin-dependent mechanism for iron mobilization in which ā avin mononucleotide (FMN)-dependent oxidoreductase catalyses the removal of iron from storage ferritin and makes it available for utilization in haem synthesis (Fig. 1) 94,95 . There is also an FMN-dependent oxidase instrumental in the conversion of vitamin B 6 to its active form, which ultimately stimulates globin production.…”

Section: Ribo¯avinmentioning

confidence: 99%

The role of vitamins in the prevention and control of anaemia

Fishman

Christian

West

2000

Public Health Nutr.

263

208

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Objective: While iron de®ciency is regarded as the major cause of nutritional anaemia, changes in vitamins A, B 12 , C and E, folic acid and ribo¯avin status have also been linked to its development and control. This paper provides a systematic review of vitamin supplementation trials relating to the control of nutritional anaemia. Methods: A MEDLINE search was used to ®nd reports of vitamin supplementation trials that reported changes in anaemia or iron status. Results: Vitamin A can improve haematological indicators and enhance the ef®cacy of iron supplementation. Both folate and vitamin B 12 can cure and prevent megaloblastic anaemia. Ribo¯avin enhances the haematological response to iron, and its de®ciency may account for a signi®cant proportion of anaemia in many populations. Vitamin C enhances the absorption of dietary iron, although population-based data showing its ef®cacy in reducing anaemia or iron de®ciency are lacking. Vitamin E supplementation given to preterm infants has not reduced the severity of the anaemia of prematurity. Vitamin B 6 effectively treats sideroblastic anaemia. Multivitamin supplementation may raise haemoglobin (Hb) concentration, but few studies have isolated the effect of multivitamins from iron on haematological status. Conclusions: In general, the public health impact of vitamin supplementation in controlling anaemia is not clear. Neither are the complex interactions involving multiple vitamins in haematopoiesis suf®ciently understood to explain the observed variability in haematological responses to vitamins by age, population, vitamin mixture and dosages. Further research is needed to understand the roles of individual and combined vitamin de®ciencies on anaemia to design appropriate micronutrient interventions to prevent anaemia.

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Ferritin iron as substrate for synthesis of protoheme in intact rat liver mitochondria

Cited by 9 publications

References 30 publications

Plasma vitamin C levels in ESRD patients and occurrence of hypochromic erythrocytes

Plasma vitamin C levels in ESRD patients and occurrence of hypochromic erythrocytes

Oxidative Stress and the Homeodynamics of Iron Metabolism

The role of vitamins in the prevention and control of anaemia

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