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吸入甲醛对小鼠学习和记忆的影响。

Effect of inhaled formaldehyde on learning and memory of mice.

作者信息

Lu Z, Li C M, Qiao Y, Yan Y, Yang X

机构信息

College of Life Science, Central China Normal University, Wuhan, China.

出版信息

Indoor Air. 2008 Apr;18(2):77-83. doi: 10.1111/j.1600-0668.2008.00524.x.

DOI:10.1111/j.1600-0668.2008.00524.x
PMID:18333987
Abstract

UNLABELLED

In this study, we investigated the effect of inhaled formaldehyde on learning and memory capacity. After exposure to 0 (control), 1 and 3 mg/m(3) of gaseous formaldehyde respectively, the behavior of mice in a Morris water maze, the expression of NR1, NR2B mRNA and oxidative damage levels in mice brain were analyzed. The water maze performance, the activities of dismutase superoxide (SOD) and levels of glutathione (GSH) decreased significantly in 3 mg/m(3) group (P < 0.01, compared with control group); while malondialdehyde (MDA) contents and expression of NR1 and NR2B genes increased significantly after exposure to 3 mg/m(3) of gaseous formaldehyde (P < 0.05, <0.01, <0.01, compared with control group). These findings indicate that inhaled formaldehyde negatively affects learning and memory at 3 mg/m(3) of gaseous formaldehyde but not at lower levels. Oxidative stress-induced neuron damages in the brain may be the possible mechanism for these effects.

PRACTICAL IMPLICATIONS

This study indicates that inhaled formaldehyde starts to negatively affect learning and memory at a middle concentration of formaldehyde without interference of other indoor air pollutants. Oxidative damage, and the alteration of NMDA receptor expression, which were induced by formaldehyde inhalation, may be the possible mechanism for gaseous formaldehyde-induced neurotoxicity.

摘要

未标注

在本研究中,我们调查了吸入甲醛对学习和记忆能力的影响。分别将小鼠暴露于0(对照)、1和3 mg/m³的气态甲醛后,分析了小鼠在莫里斯水迷宫中的行为、小鼠脑中NR1、NR2B mRNA的表达以及氧化损伤水平。3 mg/m³组的水迷宫表现、超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)水平显著降低(与对照组相比,P < 0.01);而暴露于3 mg/m³气态甲醛后,丙二醛(MDA)含量以及NR1和NR2B基因的表达显著增加(与对照组相比,P < 0.05、<0.01、<0.01)。这些发现表明,吸入3 mg/m³气态甲醛会对学习和记忆产生负面影响,但较低水平则不会。大脑中氧化应激诱导的神经元损伤可能是这些影响的潜在机制。

实际意义

本研究表明,在没有其他室内空气污染物干扰的情况下,吸入中等浓度甲醛会开始对学习和记忆产生负面影响。吸入甲醛诱导的氧化损伤以及NMDA受体表达的改变可能是气态甲醛诱导神经毒性的潜在机制。

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