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铅暴露对小鼠嗅球中一氧化氮相关基因表达的影响。

Effects of lead exposure on nitric oxide-associated gene expression in the olfactory bulb of mice.

机构信息

Department of Public Health, Keimyung University, 1000 Shindang-dong, Daegu 704-701, Republic of Korea.

出版信息

Biol Trace Elem Res. 2011 Sep;142(3):683-92. doi: 10.1007/s12011-010-8791-1. Epub 2010 Aug 3.

DOI:10.1007/s12011-010-8791-1
PMID:20680508
Abstract

Lead (Pb) is known to have toxic effects on the brain; however, data regarding its specific toxic effects on the olfactory bulb are lacking. Therefore, we investigated the relationship between acute Pb exposure and alterations in gene expression associated with the nitric oxide signaling pathway in the olfactory bulb of mice. After administration of Pb (intraperitoneal injections of 1 or 10 mg/kg Pb(CH(3)CO(2))(2) · 3H(2)O once per day for 4 days), body weight, motor activity, and gene expression in the olfactory bulb of mice were examined. High doses of Pb resulted in significant decreases in body weight, but motor coordination was not significantly altered until 11 days after the end of Pb treatment. The expression patterns of dimethylarginine dimethylaminohydrolase 1 (Ddah1), superoxide dismutase 1 (Sod1), and superoxide dismutase (Ccs) were increased, whereas expression of the Stratifin (Sfn) gene was significantly decreased following treatment with 10 mg/kg Pb. The expression patterns of nitric oxide synthases at the mRNA and protein levels, however, were not significantly altered by treatment with 10 mg/kg Pb. These findings indicate that Pb-induced neurotoxicity may be modulated in part by the expression of Ddah1, Sod1, Ccs, and Sfn in the olfactory bulb.

摘要

铅(Pb)已知对大脑有毒性作用;然而,关于其对嗅球的特定毒性作用的数据尚缺乏。因此,我们研究了急性 Pb 暴露与嗅球中一氧化氮信号通路相关的基因表达改变之间的关系。在给予 Pb 后(腹腔注射 1 或 10 mg/kg Pb(CH(3)CO(2))(2)·3H(2)O,每天一次,共 4 天),检查了小鼠的体重、运动活动和嗅球中的基因表达。高剂量 Pb 导致体重显著下降,但运动协调在 Pb 处理结束后 11 天才明显改变。二甲基精氨酸二甲氨基水解酶 1(Ddah1)、超氧化物歧化酶 1(Sod1)和超氧化物歧化酶(Ccs)的表达模式增加,而 Stratifin(Sfn)基因的表达在 10 mg/kg Pb 处理后显著降低。然而,10 mg/kg Pb 处理并未显著改变一氧化氮合酶的 mRNA 和蛋白质水平的表达模式。这些发现表明,Pb 诱导的神经毒性可能部分通过嗅球中 Ddah1、Sod1、Ccs 和 Sfn 的表达来调节。

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