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孕期和哺乳期暴露于低水平氟化物的大鼠后代记忆的改变:涉及α7 烟碱型乙酰胆碱受体和氧化应激。

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.

机构信息

Toxicology Laboratory, INBIOSUR, Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur-CONICET, 8000 Bahía Blanca, Buenos Aires, Argentina.

Toxicology Laboratory, INBIOSUR, Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur-CONICET, 8000 Bahía Blanca, Buenos Aires, Argentina.

出版信息

Reprod Toxicol. 2018 Oct;81:108-114. doi: 10.1016/j.reprotox.2018.07.078. Epub 2018 Jul 29.

DOI:10.1016/j.reprotox.2018.07.078
PMID:30009953
Abstract

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.

摘要

日常氟化物(F)暴露主要取决于饮用水中该元素的摄入量。当在妊娠和哺乳期给予 F 时,它与后代的认知缺陷有关。然而,F 的神经毒性的机制仍不清楚。在本研究中,我们研究了在妊娠和哺乳期经口暴露于低水平 F 对成年雌性大鼠后代记忆的影响。我们还考虑了一种潜在的神经毒性机制。我们的结果表明,这种暴露降低了抑制回避任务中的下台阶潜伏期,并降低了海马体中α7 烟碱型乙酰胆碱受体(nAChR)的 mRNA 表达和过氧化氢酶活性。我们的数据表明,妊娠和哺乳期给予低浓度 F 会降低 90 日龄雌性后代的记忆力。这表明该机制可能与海马体中α7 nAChR 缺陷有关,这是由氧化应激引起的。

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