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Neuroscience. 2015 Aug 20;301:542-52. doi: 10.1016/j.neuroscience.2015.06.025. Epub 2015 Jun 23.

Sulforaphane rescues memory dysfunction and synaptic and mitochondrial alterations induced by brain iron accumulation.

Author information

1
Neurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil.
2
Laboratório de Biologia Genômica e Molecular, Faculty of Biosciences, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil; Programa de Pós-Graduação em Medicina e Ciências da Saúde, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil.
3
Laboratório de Biologia Genômica e Molecular, Faculty of Biosciences, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil; Programa de Pós-Graduação em Medicina e Ciências da Saúde, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil; National Institute for Translational Medicine (INCT-TM), 90035-003 Porto Alegre, RS, Brazil.
4
Neurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil; National Institute for Translational Medicine (INCT-TM), 90035-003 Porto Alegre, RS, Brazil.
5
Neurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil; National Institute for Translational Medicine (INCT-TM), 90035-003 Porto Alegre, RS, Brazil. Electronic address: nadja.schroder@pucrs.br.

Abstract

Iron overload contributes to the development of neurodegeneration and the exacerbation of normal apoptosis rates, largely due to its participation in the Fenton reaction and production of reactive oxygen species (ROS). Mitochondria constitute the major intracellular source of ROS and the main target of attack by free radicals. They are dynamic organelles that bind (fusion) and divide (fission) in response to environmental stimuli, developmental status, and energy needs of the cells. Sulforaphane (SFN) is a natural compound that displays antioxidant and anti-inflammatory activities. This study aims to investigate the effects of SFN on memory deficits and changes in markers of mitochondrial function, DNM1L and OPA1, and the synaptic marker, synaptophysin, induced by neonatal iron treatment. Male rats received vehicle or carbonyl iron (30mg/kg) from the 12th to the 14th postnatal day. In adulthood, they were treated with saline or SFN (0.5 or 5mg/kg) for 14days every other day. Memory deficits were assessed using the object recognition task. DNM1L, OPA1, and synaptophysin levels in the hippocampus were quantified by Western blotting. Results showed that SFN was able to reverse iron-induced decreases in mitochondrial fission protein, DNM1L, as well as synaptophysin levels in the hippocampus, leading to a recovery of recognition memory impairment induced by iron. These findings suggest that SFN may be further investigated as potential agent for the treatment of cognitive deficits associated with neurodegenerative disorders.

KEYWORDS:

iron; mitochondria; neurodegenerative disorders; recognition memory; sulforaphane; synapse

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