Recognition memory impairment and brain oxidative stress induced by
postnatal iron administration.
de Lima MN, Polydoro M, Laranja DC, Bonatto F, Bromberg E, Moreira JC,
Dal-Pizzol F, Schröder N
Eur J Neurosci. 2005 May ; 21(9): 2521-8

Iron accumulation in the brain has been implicated in the pathogenesis
of neurodegenerative disorders. It is known that iron catalyses the
formation of highly reactive hydroxyl radicals. Recent studies have
implicated oxidative damage in memory deficits in rats and humans. The
purpose of the present study was to investigate the long-term effects
of iron treatment in four different phases of the neonatal period on
recognition memory in rats. Additionally, parameters of oxidative
stress in cerebral regions related to memory formation were evaluated.
Male Wistar rats received vehicle or 10.0 mg/kg of Fe2+ orally at
postnatal days 5-7, 12-14, 19-21 or 30-32. Animals given iron at any
phase of the neonatal period showed impairments in long-term retention
of object recognition memory, although only the group given iron from
postnatal days 12-14 showed a complete memory blockade. Iron treatment
induced oxidative damage in the brain as assessed by the thiobarbituric
acid reactive species assay. Moreover, iron administration increased
superoxide production in submitochondrial particles, suggesting
impaired mitochondrial function; and there was an increase in
superoxide dismutase activity in brain regions susceptible to iron
administration. The results show that iron load in the early stages of
life induces cognitive impairment possibly by inducing oxidative damage
in the brain. These findings are consistent with the view that
oxidative stress may be related to the cognitive decline observed in
normal ageing.

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