RESUMEN
Abnormally high levels of iron are observed in the brain of patients suffering from neurodegenerative disorders. The mechanisms involved in iron accumulation in neurodegenerative disorders remain poorly understood. In the present study we investigated the effects of aging and neonatal iron overload on the mRNA expression of proteins critically involved in controlling iron homeostasis. Wistar rat pups received a single daily dose of vehicle or iron (10 mg/kg of b.w. of Fe(2+)), at postnatal days 12-14. The expression of Transferrin Receptor (TfR), H-Ferritin, and IRP2 were analyzed by a semi-quantitative reverse transcriptase polymerase chain reaction assay in cortex, hippocampus and striatum of rats sacrificed at three different ages (15-day-old; 90-day-old and 2-year old rats). Results indicate that TfR, H-ferritin, and IRP2 mRNA expression was differentially affected by aging and by neonatal iron treatment in all three brain regions. These findings might have implications for the understanding of iron homeostasis misregulation associated with neurodegenerative disorders.
Asunto(s)
Encéfalo/metabolismo , Homeostasis , Hierro/metabolismo , Proteínas del Tejido Nervioso/genética , ARN Mensajero/genética , Animales , Animales Recién Nacidos , Apoferritinas/genética , Secuencia de Bases , Cartilla de ADN , Femenino , Hierro/administración & dosificación , Proteína 2 Reguladora de Hierro/genética , Embarazo , Ratas , Ratas Wistar , Receptores de Transferrina/genética , Reacción en Cadena de la Polimerasa de Transcriptasa InversaRESUMEN
We have previously demonstrated that rats given iron neonatally presented memory deficits. The aim of the present study was to evaluate the effect of desferoxamine, a metal chelating agent, on memory deficits in an iron overload model in rats. Male rats received vehicle or iron orally at postnatal days 12-14 and desferoxamine (30 or 300 mg/kg) in the adulthood. After desferoxamine treatment, they were trained in a novel-object recognition task. Iron-treated rats showed recognition memory impairments when compared to controls. Iron-treated rats that received desferoxamine 300 mg/kg, showed normal recognition memory, suggesting that desferoxamine can reverse recognition memory deficits associated with iron accumulation. Further research is required to examine whether the findings from animal models of iron overload have implications for humans.