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Alterations in the memory of rat offspring exposed to low levels of fluoride during gestation and lactation: Involvement of the α7 nicotinic receptor and oxidative stress

•Exposure to low levels of Fluoride (F) during pregnancy and lactation were studied.•Low F concentrations produced dysfunction in the central nervous system.•Female adult offspring exposed to low F concentrations showed memory impairment.•Exposure to F reduced expression of α7 nAChR subunit mRNA in...

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Published in:Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2018-10, Vol.81, p.108-114
Main Authors: Bartos, Mariana, Gumilar, Fernanda, Gallegos, Cristina E., Bras, Cristina, Dominguez, Sergio, Mónaco, Nina, Esandi, María del Carmen, Bouzat, Cecilia, Cancela, Liliana M., Minetti, Alejandra
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Language:English
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Summary:•Exposure to low levels of Fluoride (F) during pregnancy and lactation were studied.•Low F concentrations produced dysfunction in the central nervous system.•Female adult offspring exposed to low F concentrations showed memory impairment.•Exposure to F reduced expression of α7 nAChR subunit mRNA in hippocampus.•Low F concentrations induced oxidative stress in hippocampus. Daily exposure to fluoride (F) depends mainly on the intake of this element with drinking water. When administered during gestation and lactation, F has been associated with cognitive deficits in the offspring. However, the mechanisms underlying the neurotoxicity of F remain obscure. In the current study, we investigated the effects of oral exposure to low levels of F during the gestational and lactation periods, on the memory of adult female rat offspring. We also considered a possible underlying neurotoxic mechanism. Our results showed that this exposure reduced step-down latency in the inhibitory avoidance task, and decreased both mRNA expression of the α7 nicotinic receptor (nAChR) and catalase activity in hippocampus. Our data indicates that low F concentrations administrated during gestation and lactation decrease the memory of 90-day-old female offspring. This suggests that the mechanism might be connected with an α7 nAChR deficit in the hippocampus, induced by oxidative stress.
ISSN:0890-6238
1873-1708
DOI:10.1016/j.reprotox.2018.07.078