孕期和哺乳期胆碱缺乏对仔鼠脑抗氧化状态、乙酰胆碱酯酶、（钠，钾）-ATP酶和镁离子-ATP酶活性的影响
Effects of gestational and lactational choline deprivation on brain antioxidant status, acetylcholinesterase, (Na(+),K(+))- and Mg(2+)-ATPase activities in offspring rats.
作者信息
Liapi Charis, Feskou Irini, Zarros Apostolos, Galanopoulou Panagiota, Tsakiris Stylianos
机构信息
Department of Experimental Pharmacology, Medical School, University of Athens, Athens, Greece.
出版信息
Clin Chem Lab Med. 2007;45(5):651-6. doi: 10.1515/CCLM.2007.118.
BACKGROUND
Choline plays an important role in brain development. Choline-deficient diet (CDD) is known to produce (among other effects) a decrease in acetylcholine in rat brains. The aim of our study was to investigate how CDD administration during gestation and lactation could affect total antioxidant status (TAS) and activities of acetylcholinesterase (AChE), (Na(+),K(+))- and Mg(2+)-ATPase in the brains of both male and female newborn and suckling (21-day-old) rats.
METHODS
Three different experiments were performed. Whole brains were obtained from: (a) newborn rats following gestational CDD (experiment I); (b) 21-day-old rats following gestational but not lactational CDD (experiment II); and (c) 21-day-old rats following gestational and lactational CDD (experiment III). Enzyme activities and TAS were measured spectrophotometrically.
RESULTS
In choline-deprived (CD) newborn rats, TAS and AChE and Na(+),K(+)-ATPase activities were significantly reduced by 23%, 24% and 50%, respectively, in the brains of both sexes. Gestational CDD caused only a decrease in TAS (-27%, p<0.001) in suckling rat brains in both sexes. No changes were observed for the other enzyme activities. Moreover, gestational and lactational CDD also led only to a decrease in TAS (-24%, p<0.001) in the suckling rat brains of both sexes. Mg(2+)-ATPase activities showed no changes after any of the experimental procedures.
CONCLUSIONS
Our data suggest that the lower enzyme activities in newborn CD brains were restored to normal after 21 days of either normal or CDD lactation, possibly due to novel synaptogenesis, endogenous neuroregulation, and/or to other substances acquired by lactation. The increase in homocysteine concentration due to choline deficiency reported in the literature may be the cause of the low antioxidant capacity observed in offspring rat brains. Brain Na(+),K(+)-ATPase inhibition (induced by CDD) could result in modulations of neural excitability, metabolic energy production and neurotransmission.
背景
胆碱在大脑发育中起着重要作用。已知胆碱缺乏饮食（CDD）会（除其他影响外）导致大鼠大脑中乙酰胆碱减少。我们研究的目的是调查在妊娠和哺乳期给予CDD如何影响雄性和雌性新生及哺乳（21日龄）大鼠大脑中的总抗氧化状态（TAS）以及乙酰胆碱酯酶（AChE）、（Na⁺，K⁺）-ATP酶和Mg²⁺-ATP酶的活性。
方法
进行了三项不同的实验。全脑取自：（a）妊娠CDD后的新生大鼠（实验I）；（b）妊娠但非哺乳期CDD后的21日龄大鼠（实验II）；以及（c）妊娠和哺乳期CDD后的21日龄大鼠（实验III）。酶活性和TAS通过分光光度法测量。
结果
在胆碱缺乏（CD）的新生大鼠中，两性大脑中的TAS、AChE和Na⁺，K⁺-ATP酶活性分别显著降低23%、24%和50%。妊娠CDD仅导致两性哺乳大鼠大脑中的TAS降低（-27%，p<0.001）。其他酶活性未观察到变化。此外，妊娠和哺乳期CDD也仅导致两性哺乳大鼠大脑中的TAS降低（-24%，p<0.001）。任何实验程序后Mg²⁺-ATP酶活性均无变化。
结论
我们的数据表明，新生CD大脑中较低的酶活性在正常或CDD哺乳期21天后恢复正常，这可能是由于新的突触形成、内源性神经调节和/或通过哺乳获得的其他物质。文献中报道的由于胆碱缺乏导致的同型半胱氨酸浓度升高可能是后代大鼠大脑中观察到的低抗氧化能力的原因。大脑Na⁺，K⁺-ATP酶抑制（由CDD诱导）可能导致神经兴奋性、代谢能量产生和神经传递的调节。
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