产前低水平暴露于一氧化碳会改变大鼠出生后海马一氧化氮合酶和血氧合酶活性的发育。

A. Vaccari, S. Ruiu, P. Saba, M. Fà, R. Cagiano, A. Coluccia, G. Mereu, L. Steardo, M. Tattoli, L. Trabace, V. Cuomo
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引用次数: 11

摘要

研究了产前CO暴露(妊娠0 ~ 20天150 ppm)对15、30、90 d大鼠海马神经元NO合成酶(nNOS)和血氧合酶(HO-2)异构体活性的影响。与HO-2不同,对照组海马nNOS活性从出生后15-90天开始增加。产前CO产生nNOS或HO-2的长期下降。结果表明,海马nNOS和HO-2活性的改变可能与大鼠产前暴露于CO水平导致的碳氧血红蛋白(HbCO)水平相当于人类吸烟者所观察到的认知缺陷和长期增强功能障碍有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Prenatal low-level exposure to CO alters postnatal development of hippocampal nitric oxide synthase and haem-oxygenase activities in rats.
The effects of prenatal CO exposure (150 ppm from days 0 to 20 of pregnancy) on the postnatal development of hippocampal neuronal NO synthase (nNOS) and haem-oxygenase (HO-2) isoform activities in 15-, 30- and 90-d-old rats were investigated. Unlike HO-2, hippocampal nNOS activity increased from postnatal days 15-90 in controls. Prenatal CO produced a long-lasting decrease in either nNOS or HO-2. The results suggest that the altered developmental profile of hippocampal nNOS and HO-2 activities could be involved in cognitive deficits and long-term potentiation dysfunction exhibited by rats prenatally exposed to CO levels resulting in carboxyhaemoglobin (HbCO) levels equivalent to those observed in human cigarette smokers.
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