Developmental changes in transferrin and iron uptake by the brain in the rat

Taylor, Eve M.; Morgan, Evan H.

doi:10.1016/0165-3806(90)90103-6

Cited by 212 publications

(180 citation statements)

References 25 publications

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“…Adapted from Sun et al (1990). development, iron is used for mitochondriogenesis, neuronal maturation, synthesis of neurotransmitter, and myelination (Taylor and Morgan, 1990). Iron first appears in microglia within myelinogenic foci in white matter (Connor et al, 1995a).…”

Section: Ironmentioning

confidence: 99%

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

Chang

Claus

Vreman

et al. 2005

J Cereb Blood Flow Metab

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Intracranial bleeding is one of the most prominent aspects in the clinical diagnosis and prognosis of traumatic brain injury (TBI). Substantial amounts of blood products, such as heme, are released because of traumatic subarachnoid hemorrhages, intraparenchymal contusions, and hematomas. Despite this, surprisingly few studies have directly addressed the role of blood products, in particular heme, in the setting of TBI. Heme is degraded by heme oxygenase (HO) into three highly bioactive products: iron, bilirubin, and carbon monoxide. The HO isozymes, in particular HO-1 and HO-2, exhibit significantly different expression patterns and appear to have specific roles after injury. Developmentally, differences between the adult and immature brain have implications for endogenous protection from oxidative stress. The aim of this paper is to review recent advances in the understanding of heme regulation and metabolism after brain injury and its specific relevance to the developing brain. These findings suggest novel clinical therapeutic options for further translational study.

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Section: Ironmentioning

confidence: 99%

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

Chang

Claus

Vreman

et al. 2005

J Cereb Blood Flow Metab

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“…The amount of 131 I-albumin in the plasma and tissues was used to determine the plasma volume and the amount of plasma remaining in the tissue after perfusion. Tissue 59 Fe uptake was corrected for transferrin-bound iron by measuring the amount of 125 I-transferrin in the tissues (17).…”

Section: Methodsmentioning

confidence: 99%

Iron uptake from plasma transferrin by the duodenum is impaired in the Hfe knockout mouse

Trinder

Olynyk

Sly

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Hereditary hemochromatosis (HH) is a disorder of iron metabolism in which enhanced iron absorption of dietary iron causes increased iron accumulation in the liver, heart, and pancreas. Most individuals with HH are homozygous for a C282Y mutation in the HFE gene. The function of HFE protein is unknown, but it is hypothesized that it acts in association with ␤2-microglobulin and transferrin receptor 1 to regulate iron uptake from plasma transferrin by the duodenum, the proposed mechanism by which body iron levels are sensed. The aim of this study was to test this hypothesis by comparing clearance of transferrin-bound iron in Hfe knockout (KO) mice with that observed in C57BL͞6 control mice. The mice were fed either an iron-deficient, control, or iron-loaded diet for 6 weeks to alter body iron status. The mice then were injected i.v. with 59 Fe-transferrin, and blood samples were taken over 2 h to determine the plasma 59 Fe turnover. After 2 h, the mice were killed and the amount of radioactivity in the duodenum, liver, and kidney was measured. In both Hfe KO and C57BL͞6 mice, plasma iron turnover and iron uptake from plasma transferrin by the duodenum, liver, and kidney correlated positively with plasma iron concentration. However, duodenal iron uptake from plasma transferrin was decreased in the Hfe KO mice compared with the control mice. Despite this difference in duodenal uptake, the Hfe KO mice showed no decrease in iron uptake by the liver and kidney or alteration in the plasma iron turnover when compared with C57BL͞6 mice. These data support the hypothesis that HFE regulates duodenal uptake of transferrin-bound iron from plasma, and that this mechanism of sensing body iron status, as reflected in plasma iron levels, is impaired in HH.

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“…The critical period seems to have occurred during an intermediate period, instead of when the brain was least mature. Cerebral Fe uptake in rats peaks between birth and the 15 th postnatal day [27]. In this peak period, differentiation in the thresholds of regulatory mechanisms might be responsible for increased cerebral Fe uptake, which may explain why 10-12-day-old rats were most affected by the Fe-enriched diet.…”

Section: Fig 3 Evans Blue Staining Was Passed Over the Vascular Walmentioning

confidence: 99%

Investigation of iron’s neurotoxicity during cerebral maturation in the neonatal rat model of haemolysis

Akar¹,

Ünalp

Dınız³

et al. 2015

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Developmental changes in transferrin and iron uptake by the brain in the rat

Cited by 212 publications

References 25 publications

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

Iron uptake from plasma transferrin by the duodenum is impaired in the Hfe knockout mouse

Investigation of iron’s neurotoxicity during cerebral maturation in the neonatal rat model of haemolysis

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