2015
DOI: 10.5114/fn.2015.54623
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Investigation of iron’s neurotoxicity during cerebral maturation in the neonatal rat model of haemolysis

Abstract: A b s t r a c t Introduction: Haemolytic disease of newborns due to rhesus and AB0 incompatibility is encountered frequently in neonatal clinics

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Cited by 6 publications
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“…Exposure to Fe is primarily through food consumption, although toxic levels of Fe accumulation are usually due to disrupted Fe homeostasis and metabolism in the brain 32 , 33 . Hemolysis, the breakdown of red blood cells, in the young brain with an immature blood-brain barrier (BBB) can also lead to aberrant Fe accumulation, which results in neuronal damages 34 . Fe accumulation can cause increased ROS levels, lipid peroxidation, protein oxidation, DNA damage, dopamine autoxidation, and mitochondrial fragmentation 35 38 .…”
Section: Essential Metalsmentioning
confidence: 99%
“…Exposure to Fe is primarily through food consumption, although toxic levels of Fe accumulation are usually due to disrupted Fe homeostasis and metabolism in the brain 32 , 33 . Hemolysis, the breakdown of red blood cells, in the young brain with an immature blood-brain barrier (BBB) can also lead to aberrant Fe accumulation, which results in neuronal damages 34 . Fe accumulation can cause increased ROS levels, lipid peroxidation, protein oxidation, DNA damage, dopamine autoxidation, and mitochondrial fragmentation 35 38 .…”
Section: Essential Metalsmentioning
confidence: 99%
“…. Iron (Fe): Excess Fe deposition in a developing brain due to haemolysis may lead to immature blood brain barrier formation and neuron damage or neurodegeneration with brain iron accumulation (NBIA)[22][23].5. Manganese (Mn):6.…”
mentioning
confidence: 99%