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发育过程中接触香烟烟雾II:成年子代的海马蛋白质组和代谢组图谱

Developmental cigarette smoke exposure II: Hippocampus proteome and metabolome profiles in adult offspring.

作者信息

Neal Rachel E, Jagadapillai Rekha, Chen Jing, Webb Cindy, Stocke Kendall, Greene Robert M, Pisano M Michele

机构信息

Department of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY, USA; Birth Defects Center, University of Louisville, Louisville, KY, USA.

Department of Molecular, Cellular, and Craniofacial Biology, ULSD, University of Louisville, Louisville, KY, USA.

出版信息

Reprod Toxicol. 2016 Oct;65:436-447. doi: 10.1016/j.reprotox.2016.05.007. Epub 2016 May 18.

DOI:10.1016/j.reprotox.2016.05.007
PMID:27208486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5091087/
Abstract

Exposure to cigarette smoke during development is linked to neurodevelopmental delays and cognitive impairment including impulsivity, attention deficit disorder, and lower IQ. Utilizing a murine experimental model of "active" inhalation exposure to cigarette smoke spanning the entirety of gestation and through human third trimester equivalent hippocampal development [gestation day 1 (GD1) through postnatal day 21 (PD21)], we examined hippocampus proteome and metabolome alterations present at a time during which developmental cigarette smoke exposure (CSE)-induced behavioral and cognitive impairments are evident in adult animals from this model system. At six month of age, carbohydrate metabolism and lipid content in the hippocampus of adult offspring remained impacted by prior exposure to cigarette smoke during the critical period of hippocampal ontogenesis indicating limited glycolysis. These findings indicate developmental CSE-induced systemic glucose availability may limit both organism growth and developmental trajectory, including the capacity for learning and memory.

摘要

发育过程中接触香烟烟雾与神经发育延迟和认知障碍有关,包括冲动、注意力缺陷障碍和智商降低。利用一种小鼠实验模型,即从妊娠全程直至相当于人类妊娠晚期海马体发育阶段(妊娠第1天(GD1)至出生后第21天(PD21))“主动”吸入香烟烟雾,我们研究了在该模型系统中成年动物出现发育性香烟烟雾暴露(CSE)诱导的行为和认知障碍时海马体蛋白质组和代谢组的变化。在6个月大时,成年后代海马体中的碳水化合物代谢和脂质含量在海马体发生的关键时期仍受先前接触香烟烟雾的影响,表明糖酵解受限。这些发现表明,发育性CSE诱导的全身葡萄糖可用性可能会限制生物体的生长和发育轨迹,包括学习和记忆能力。

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