摘要
为探讨PFOS胚胎期及哺乳期暴露对动物子代学习记忆能力影响的分子机理,采用微小RNA(miRNA)芯片技术检测PFOS胚胎期及哺乳期暴露对出生第1和7天大鼠脑组织miRNA表达的影响,分析突触可塑性相关miRNA表达的差异变化。结果显示,经PFOS暴露后出生第1和7天的大鼠脑组织中分别有24和17个miRNA发生显著性差异表达(p<0.05),其中与突触传递和神经递质转运等相关的miRNA的差异表达最为显著,主要包括miR-466b、miR-672、miR-297、miR-674-3p和miR-207。差异表达miRNA的路径分析显示出生后1和7d的大鼠的长时程增强效应(LTP)均受PFOS显著影响(p<0.05),这说明PFOS胚胎期及哺乳期暴露可能通过影响LTP的形成、发展和维持过程对大鼠子代大脑学习记忆能力造成威胁,并且miR-466b、miR-672、miR-297、miR-674-3p和miR-207可能参与了其中的调控过程。
To explore the molecular mechanism underlying the toxic effect of PFOS prenatal and neonatal ex- posure on the study and memory ability of offspring, miRNA arrays were used to profde the expression of brain miRNAs in neonatal rats on postnatal day （PND） 1 and 7 with prenatal and neonatal exposure of PFOS. The results showed that twenty-four brain miRNAs on PND 1 and seventeen on PND 7 rats were significantly changed after PFOS exposure （p 〈 0.05）. miR-466b, miR-672, miR-297, miR-674-3p and miR-207, which partici- pate in neurotransmitter transport and synaptic transmission, showed the highest differential expression. The analysis of pathways associated with differentially expressed miRNAs indicated that long-term potentiation （LTP） in rat pups on PND 1 and 7 rats were significantly affected by PFOS exposure （p 〈 0.05）. It is demon- strated that prenatal and neonatal exposure of PFOS could threaten the study and memory ability of rat off- spring through the effect of the formation, maturation and maintenance of LTP. Moreover, miR-466b, miR-672, miR-297, miR-674-3p and miR-207 might be involved in the above process.
出处
《生态毒理学报》
CAS
CSCD
北大核心
2012年第5期491-500,共10页
Asian Journal of Ecotoxicology
基金
国家自然科学基金项目(21177020
20837004)
