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

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dc.contributor.authorAkar, Ebru
dc.contributor.authorUnalp, Aycan
dc.contributor.authorDiniz, Gulden
dc.contributor.authorOrtac, Ragip
dc.contributor.authorSenturk, Banu
dc.contributor.authorYilmaz, Osman
dc.contributor.authorKiray, Muge
dc.date.accessioned2024-02-23T14:40:56Z
dc.date.available2024-02-23T14:40:56Z
dc.date.issued2015
dc.departmentNEÜen_US
dc.description.abstractIntroduction: Haemolytic disease of newborns due to rhesus and ABO incompatibility is encountered frequently in neonatal clinics and may lead to severe haemolysis. In this study, it is suggested that important amounts of iron released with haemolysis may have a toxic effect on the brain parenchymal tissue, and the severity of the toxic effect can be correlated with the maturation of the brain barrier systems. To demonstrate the accumulation and the neurotoxic effects of free iron (Fe) in the brain an experimental haemolysis model with various maturation phases was performed. Material and methods: The study was composed of 48 Wistar rats with the following ages: five days old (Group A), 10 days old (Group 8), and 19 days old (Group C). Each group was divided into three experimental subgroups and three control groups. Experimental groups were treated with intraperitoneal 75 mg/kg/day phenyl hydrazine hydrochloride for haemolysis. Results: We demonstrated that the blood brain barrier (BBB) is permeable in five-day-old newborn rats and is mature in 10- and 19-day-old rats. Iron staining and neuronal damage were detected in group A and group 8 rats. No damage was detected in the brain tissue of group C animals. The presence of iron staining and neuronal damage in group B with mature BBB may suggest the existence of other incomplete barrier systems different from BBB that lead to iron accumulation in the brain. Conclusions: Blood brain barrier has a partial role in Fe transport, and the alternative barrier systems may also be involved. It could be supposed that after maturation of all barrier systems, excessive Fe penetration to the brain cannot occur Our findings showed that the toxic amounts of iron may penetrate into the brain parenchyma of newborns despite the BBB preservation and cause neuronal damage in newborns, but the mature brain is not affected by the same magnitude blood levels.en_US
dc.identifier.doi10.5114/fn.2015.54623
dc.identifier.endpage269en_US
dc.identifier.issn1641-4640
dc.identifier.issn1509-572X
dc.identifier.issue3en_US
dc.identifier.pmid26443317en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage262en_US
dc.identifier.urihttps://doi.org/10.5114/fn.2015.54623
dc.identifier.urihttps://hdl.handle.net/20.500.12452/16648
dc.identifier.volume53en_US
dc.identifier.wosWOS:000362463100009en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTermedia Publishing House Ltden_US
dc.relation.ispartofFolia Neuropathologicaen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectHaemolysisen_US
dc.subjectNeurotoxicen_US
dc.subjectFree Ironen_US
dc.subjectBrain Barrier Systemsen_US
dc.subjectNewbornen_US
dc.titleInvestigation of iron's neurotoxicity during cerebral maturation in the neonatal rat model of haemolysisen_US
dc.typeArticleen_US

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