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镉对仔鼠关键脑区酶活性的发育神经毒性

Developmental neurotoxicity of cadmium on enzyme activities of crucial offspring rat brain regions.

作者信息

Stolakis Vasileios, Tsakiris Stylianos, Kalafatakis Konstantinos, Zarros Apostolos, Skandali Nikolina, Gkanti Vasiliki, Kyriakaki Argyro, Liapi Charis

机构信息

Laboratory of Pharmacology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

出版信息

Biometals. 2013 Dec;26(6):1013-21. doi: 10.1007/s10534-013-9678-3. Epub 2013 Sep 25.

Abstract

Cadmium (Cd) is an environmental contaminant known to exert significant neurotoxic effects on both humans and experimental animals. The aim of this study was to shed more light on the effects of gestational (in utero) and lactational maternal exposure to Cd (50 ppm of Cd as Cd-chloride in the drinking water) on crucial brain enzyme activities in important rat offspring brain regions (frontal cortex, hippocampus, hypothalamus, pons and cerebellum). Our study provides a brain region-specific view of the changes in the activities of three crucial brain enzymes as a result of the developmental neurotoxicity of Cd. Maternal exposure to Cd during both gestation and lactation results into significant changes in the activities of acetylcholinesterase and Na(+),K(+)-ATPase in the frontal cortex and the cerebellum of the offspring rats, as well as in a significant increase in the hippocampal Mg(2+)-ATPase activity. These brain-region-specific findings underline the need for further research in the field of Cd-induced developmental neurotoxicity. Deeper understanding of the mechanisms underlying the neurodevelopmental deficits taking place due to in utero and early age exposure to Cd could shed more light on the causes of its well-established cognitive implications.

摘要

镉(Cd)是一种环境污染物,已知会对人类和实验动物产生显著的神经毒性作用。本研究的目的是进一步阐明孕期(子宫内)和哺乳期母体接触镉(饮用水中含50 ppm氯化镉形式的镉)对重要大鼠后代脑区(额叶皮质、海马体、下丘脑、脑桥和小脑)关键脑酶活性的影响。我们的研究提供了因镉的发育神经毒性导致三种关键脑酶活性变化的脑区特异性观点。孕期和哺乳期母体接触镉会导致后代大鼠额叶皮质和小脑乙酰胆碱酯酶以及Na(+)、K(+)-ATP酶活性发生显著变化,同时海马体Mg(2+)-ATP酶活性显著增加。这些脑区特异性发现强调了在镉诱导的发育神经毒性领域进一步研究的必要性。深入了解由于子宫内和幼年接触镉导致神经发育缺陷的潜在机制,可能会更清楚地揭示其已明确的认知影响的原因。

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