全氟辛烷磺酸盐的神经发育毒性研究
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摘要
PFOS是一种八碳全氟有机化合物,因其具有良好的理化特性,被广泛应用于工农业生产和日常用品制造。自从上个世纪50年代使用该化合物以来,环境中PFOS的浓度越来越高,使得人类及其它生物有更多的机会暴露PFOS。已在多种环境介质和野生动物及人体内检测到它的存在。由于该化合物具有难降解和易富集的特性,因此,它造成的环境污染范围及污染程度远远超出了人们的预想。2001年,它被列为美国环保局持久性环境污染物黑名单,要求进行严格管理。鉴于PFOS的全球分布,近年来,有关它的毒性已成为毒理学研究的热点。
科学研究表明,PFOS能引起实验动物体重减轻,肝肿大,脂质代谢和能量代谢障碍,激素代谢混乱,胚胎毒性和潜在的神经发育毒性。由于PFOS能通过胎盘屏障和血脑屏障,富集于胚胎和幼鼠脑组织,有关它的神经发育毒性备受关注。近年来的研究表明,产前和泌乳期PFOS暴露导致幼鼠运动功能和认知功能损伤,PFOS是一种潜在的神经发育毒物,但是它的毒作用机制还不清楚。本文拟采用产前PFOS暴露致幼鼠神经毒性及其可能毒作用机制研究,为评价该化合物的潜在健康影响提供实验和理论基础。
第一部分产前PFOS暴露对幼鼠海马基因表达谱的影响
目的：观察产前PFOS暴露致幼鼠海马组织基因表达谱的改变。方法：40只SD孕鼠随机分成对照组、0.1mg/kg-d PFOS组、0.6mg/kg-d PFOS组、2.0mg/kg-d PFOS组,从GD2天到GD21天,每天灌胃一次。分别在PND0天和PND21天分批处死幼鼠,收集血液,并迅速取出脑组织,冰上迅速分离海马和皮层。采用高效液相,串联质谱技术检测血液、皮层和海马中PFOS浓度；应用大鼠Agilent表达芯片筛选0.6mg/kg-dPFOS组幼鼠海马差异表达基因。结果：海马、皮层和血液中PFOS呈剂量依赖方式升高,PND0天幼鼠的PFOS浓度高于PND21天幼鼠。PFOS诱导的差异表达基因主要与细胞周期、细胞凋亡、LTP、钙离子信号途径、突触传递、神经退行性疾病、炎症等有关。结论：产前PFOS暴露改变了幼鼠海马组织钙离子信号途径、突触传递、神经退行性疾病、炎症等有关基因的表达。
第二部分产前PFOS暴露诱导幼鼠脑组织胶质样炎症反应
目的：观察产前PFOS暴露致子代海马和皮层的胶质样炎症反应。方法：40只SD孕鼠随机分成对照组、0.1mg/kg PFOS组、0.6mg/kg PFOS组、2.0mg/kg PFOS组,从GD2天到GD21天,每天灌胃一次。分别在PND0天和PND21天处死幼鼠,并迅速取出脑组织,冰上分离海马和皮层,或者4%的多聚甲醛固定。GFAP免疫组织化学检测星形胶质细胞增生；QPCR分析鼠海马和皮层GFAP, S100β, IL-1β, TNF-α, CREB, AP-1和NF-Kb mRNA含量；WB分析GFAP蛋白的含量。结果：产前PFOS暴露激活了幼鼠星形胶质细胞,诱导了海马和皮层中GFAP, S100β, IL-1β, TNF-α, CREB,AP-1和NF-Kb mRNA含量增加,同时也诱导21天龄幼鼠皮层和海马GFAP蛋白含量增加。结论：产前PFOS暴露导致星形胶质细胞激活,炎症因子表达增加,产生胶质样炎症反应,其机制可能与转录因子AP-1, CREB和NF-Kb表达升高有关。
第三部分产前PFOS暴露致幼鼠突触发生的影响
目的：观察产前PFOS暴露对子代神经元突触结构的影响。方法：40只SD孕鼠随机分成对照组、0.1mg/kg PFOS组、0.6mg/kg PFOS组、2.0mg/kg PFOS组,从GD2天到GD21天,每天灌胃一次。分别在PND0天和PND21天处死幼鼠,并迅速取出脑组织,冰上分离海马和皮层。QPCR检测Syp和Synl mRNA水平；WB检测Syp和Syn1蛋白含量；利用HE染色方法和电镜技术观察脑组织常规病理和超微结构改变。结果：PFOS暴露降低了突触小泡含量,增宽了突触间隙,并伴随突触标志物Syn1和Syp表达的改变。PND0天幼鼠和PND21天幼鼠海马组织Syp和Syn1含量呈现剂量依赖方式下降,而在皮层组织,PFOS抑制了Syn1表达,但是诱导了Syp含量呈现剂量依赖方式升高。同时,PFOS暴露减少了幼鼠海马神经突触小泡,导致活性区变窄。结论：PFOS诱导的神经发育毒性可能与改变突触小泡相关蛋白表达及突触超微结构有关。
Perfluorooctane sulfonate (PFOS), which is a kind of fluorine-saturated eight-carbon compounds belonged to the degradation product of many perfluorinated compounds, has been used in a variety of commercial and industrial applications. Since 1950s, concentration of PFOS in the environment increased gradually. PFOS is believed to be an emerging persistent organic pollutant because of its worldwide distribution, extreme stability and bioaccumulative nature. Recent years studies indicated that the scope and extent of environmental contamination caused by PFOS had gone beyond our anticipation. In 2001, it was classified as a kind of persistent organic pollutants by environmental protection agency of U.S and should be strictly administered. The study of toxicity about PFOS has been become one of the hotspots of toxicology research.
Scientific research have showed that PFOS can cause body weight of experimental animals lessen, liver hyperplasia, lipid metabolism and energy metabolism disorders, hormone metabolic disorders, embryonic toxicity and and potentially developmental neurotoxicity. Since PFOS can across the placental barrier and the blood brain barrier and can accumulate embryonic brain tissue, the developmental neurotoxicity has been attracted more attention. Recent studies show that prenatal and lactation exposure to PFOS exposure lead to the impairment of offspring movement function and cognitive function. Although PFOS is a potentially developmental nerve poison, its toxic effect mechanism is unclear. This study will explore that prenatal exposure to PFOS may cause offspring neurotoxicity and its mechanisms. It provides the experimental and theoretical basis for the evaluation of the potential health effects of PFOS.
PartⅠ:Gene expression profiling in the hippocampus of pups by prenatal exposure to PFOS
Objective:To study the changes of gene expression profile in the hippocampus of pups by prenatal exposure to PFOS. Method:Pregnant Sprague Dawley (SD) rats were administrated 0.1,0.6, and 2.0mg/kg bw/day by gavage from gestation day (GD) 2 to GD21. Control received 0.5% Tween-20 vehicle (4mg/kg bw/day). PFOS concentrations in hippocampus of offspring were observed on postnatal day (PND) 0 and PND21. Agilent expression microarray was used to evaluate the changes of gene expression profile in the hippocampus of pups by prenatal exposure to PFOS. Results:PFOS was increased in serum, hippocampus and cortex in dose-dependent manner, and gradually decreased depending on time. The concentrations of PFOS in tissue on PNDO were higher than on PND21. The differentially expressed genes were related to cell cycle, cell apoptosis, long-term potentiation, calcium ion signal pathways, synapse, neurodegenerative diseases, inflammation, etc. Conclusion:Prenatal exposure to PFOS altered the expression of genes that were related to cell cycle, cell apoptosis, long-term potentiation, calcium ion signaling pathways, synapse, and inflammation.
PartⅡ:The effect of inflammation-like glial response in offspring brain induced by prenatal PFOS exposure
Objective:To study the effect of inflammation-like glial response in offspring brain induced by prenatal PFOS exposure. Method:Pregnant Sprague Dawley (SD) rats were given 0.1,0.6, and 2.0mg/kg bw/day by gavage from gestation day (GD) 2 to GD21. Control received 0.5% Tween-20 vehicle (4ml/kg bw/day). Reactive astrocytes were detected by GFAP of immunohistochemical staining. QPCR was used to detect mRNA level of GFAP, S100β, IL-1β, TNF-α, CREB, AP-1and NF-κb in offspring hippocampus and cortex. The protein level of GFAP was detected by western blot. Results:In 2.0mg/kg-d PFOS group, the mRNA levels of GFAP, S100β, IL-1β,TNF-α, CREB, AP-1and NF-κb were significantly increased compared with control group either on PNDO or on PND21. Compared with control, the protein levels of GFAP were significantly increased in all treated groups either on PNDO or on PND21. Conclusion:PFOS can increase the expression of inflammatory factor and transcription factor as well as active astrocyte, and lead to the inflammation-like glial response in offspring brain.
PartⅢ:The effect of prenatal exposure to PFOS on synaptic ultra-structure of pups
Objective:To study the effect of prenatal exposure to PFOS on synaptic ultra-structure of pups. Method:Pregnant Sprague Dawley (SD) rats were adminstrated 0.1, 0.6, and 2.0mg/kg bw/day by gavage from gestation day (GD) 2 to GD21. Control received 0.5% Tween-20 vehicle (4mg/kg bw/day). QPCR was used to detect mRNA level of Synl and Syp in offspring hippocampus and cortex. The protein levels of Synl and Syp were detected by western blot. The synaptic ultra-structure of hippocampus was analyzed by electron microscope. Results:In 2.0mg/kg-d PFOS group, the expression of Synl and Syp in hippocampus were significant decreased compared with control group either on PNDO or on PND21. In cortex, the expression of Synl were significant decreased in PFOS-treated group, but the expression of Syp in cortex increased. In the hippocampus of PFOS exposed offspring, synaptic vesicles became decreased, active synaptic zone became shorter, and synaptic curvature became uneven.Conclusion:PFOS can change the expression of Syp and Synl as well as impair the synaptic ultra-structure, which may play an important role in the developmental neruotoxicity of PFOS.
科学研究表明,PFOS能引起实验动物体重减轻,肝肿大,脂质代谢和能量代谢障碍,激素代谢混乱,胚胎毒性和潜在的神经发育毒性。由于PFOS能通过胎盘屏障和血脑屏障,富集于胚胎和幼鼠脑组织,有关它的神经发育毒性备受关注。近年来的研究表明,产前和泌乳期PFOS暴露导致幼鼠运动功能和认知功能损伤,PFOS是一种潜在的神经发育毒物,但是它的毒作用机制还不清楚。本文拟采用产前PFOS暴露致幼鼠神经毒性及其可能毒作用机制研究,为评价该化合物的潜在健康影响提供实验和理论基础。
第一部分产前PFOS暴露对幼鼠海马基因表达谱的影响
目的：观察产前PFOS暴露致幼鼠海马组织基因表达谱的改变。方法：40只SD孕鼠随机分成对照组、0.1mg/kg-d PFOS组、0.6mg/kg-d PFOS组、2.0mg/kg-d PFOS组,从GD2天到GD21天,每天灌胃一次。分别在PND0天和PND21天分批处死幼鼠,收集血液,并迅速取出脑组织,冰上迅速分离海马和皮层。采用高效液相,串联质谱技术检测血液、皮层和海马中PFOS浓度；应用大鼠Agilent表达芯片筛选0.6mg/kg-dPFOS组幼鼠海马差异表达基因。结果：海马、皮层和血液中PFOS呈剂量依赖方式升高,PND0天幼鼠的PFOS浓度高于PND21天幼鼠。PFOS诱导的差异表达基因主要与细胞周期、细胞凋亡、LTP、钙离子信号途径、突触传递、神经退行性疾病、炎症等有关。结论：产前PFOS暴露改变了幼鼠海马组织钙离子信号途径、突触传递、神经退行性疾病、炎症等有关基因的表达。
第二部分产前PFOS暴露诱导幼鼠脑组织胶质样炎症反应
目的：观察产前PFOS暴露致子代海马和皮层的胶质样炎症反应。方法：40只SD孕鼠随机分成对照组、0.1mg/kg PFOS组、0.6mg/kg PFOS组、2.0mg/kg PFOS组,从GD2天到GD21天,每天灌胃一次。分别在PND0天和PND21天处死幼鼠,并迅速取出脑组织,冰上分离海马和皮层,或者4%的多聚甲醛固定。GFAP免疫组织化学检测星形胶质细胞增生；QPCR分析鼠海马和皮层GFAP, S100β, IL-1β, TNF-α, CREB, AP-1和NF-Kb mRNA含量；WB分析GFAP蛋白的含量。结果：产前PFOS暴露激活了幼鼠星形胶质细胞,诱导了海马和皮层中GFAP, S100β, IL-1β, TNF-α, CREB,AP-1和NF-Kb mRNA含量增加,同时也诱导21天龄幼鼠皮层和海马GFAP蛋白含量增加。结论：产前PFOS暴露导致星形胶质细胞激活,炎症因子表达增加,产生胶质样炎症反应,其机制可能与转录因子AP-1, CREB和NF-Kb表达升高有关。
第三部分产前PFOS暴露致幼鼠突触发生的影响
目的：观察产前PFOS暴露对子代神经元突触结构的影响。方法：40只SD孕鼠随机分成对照组、0.1mg/kg PFOS组、0.6mg/kg PFOS组、2.0mg/kg PFOS组,从GD2天到GD21天,每天灌胃一次。分别在PND0天和PND21天处死幼鼠,并迅速取出脑组织,冰上分离海马和皮层。QPCR检测Syp和Synl mRNA水平；WB检测Syp和Syn1蛋白含量；利用HE染色方法和电镜技术观察脑组织常规病理和超微结构改变。结果：PFOS暴露降低了突触小泡含量,增宽了突触间隙,并伴随突触标志物Syn1和Syp表达的改变。PND0天幼鼠和PND21天幼鼠海马组织Syp和Syn1含量呈现剂量依赖方式下降,而在皮层组织,PFOS抑制了Syn1表达,但是诱导了Syp含量呈现剂量依赖方式升高。同时,PFOS暴露减少了幼鼠海马神经突触小泡,导致活性区变窄。结论：PFOS诱导的神经发育毒性可能与改变突触小泡相关蛋白表达及突触超微结构有关。
Perfluorooctane sulfonate (PFOS), which is a kind of fluorine-saturated eight-carbon compounds belonged to the degradation product of many perfluorinated compounds, has been used in a variety of commercial and industrial applications. Since 1950s, concentration of PFOS in the environment increased gradually. PFOS is believed to be an emerging persistent organic pollutant because of its worldwide distribution, extreme stability and bioaccumulative nature. Recent years studies indicated that the scope and extent of environmental contamination caused by PFOS had gone beyond our anticipation. In 2001, it was classified as a kind of persistent organic pollutants by environmental protection agency of U.S and should be strictly administered. The study of toxicity about PFOS has been become one of the hotspots of toxicology research.
Scientific research have showed that PFOS can cause body weight of experimental animals lessen, liver hyperplasia, lipid metabolism and energy metabolism disorders, hormone metabolic disorders, embryonic toxicity and and potentially developmental neurotoxicity. Since PFOS can across the placental barrier and the blood brain barrier and can accumulate embryonic brain tissue, the developmental neurotoxicity has been attracted more attention. Recent studies show that prenatal and lactation exposure to PFOS exposure lead to the impairment of offspring movement function and cognitive function. Although PFOS is a potentially developmental nerve poison, its toxic effect mechanism is unclear. This study will explore that prenatal exposure to PFOS may cause offspring neurotoxicity and its mechanisms. It provides the experimental and theoretical basis for the evaluation of the potential health effects of PFOS.
PartⅠ:Gene expression profiling in the hippocampus of pups by prenatal exposure to PFOS
Objective:To study the changes of gene expression profile in the hippocampus of pups by prenatal exposure to PFOS. Method:Pregnant Sprague Dawley (SD) rats were administrated 0.1,0.6, and 2.0mg/kg bw/day by gavage from gestation day (GD) 2 to GD21. Control received 0.5% Tween-20 vehicle (4mg/kg bw/day). PFOS concentrations in hippocampus of offspring were observed on postnatal day (PND) 0 and PND21. Agilent expression microarray was used to evaluate the changes of gene expression profile in the hippocampus of pups by prenatal exposure to PFOS. Results:PFOS was increased in serum, hippocampus and cortex in dose-dependent manner, and gradually decreased depending on time. The concentrations of PFOS in tissue on PNDO were higher than on PND21. The differentially expressed genes were related to cell cycle, cell apoptosis, long-term potentiation, calcium ion signal pathways, synapse, neurodegenerative diseases, inflammation, etc. Conclusion:Prenatal exposure to PFOS altered the expression of genes that were related to cell cycle, cell apoptosis, long-term potentiation, calcium ion signaling pathways, synapse, and inflammation.
PartⅡ:The effect of inflammation-like glial response in offspring brain induced by prenatal PFOS exposure
Objective:To study the effect of inflammation-like glial response in offspring brain induced by prenatal PFOS exposure. Method:Pregnant Sprague Dawley (SD) rats were given 0.1,0.6, and 2.0mg/kg bw/day by gavage from gestation day (GD) 2 to GD21. Control received 0.5% Tween-20 vehicle (4ml/kg bw/day). Reactive astrocytes were detected by GFAP of immunohistochemical staining. QPCR was used to detect mRNA level of GFAP, S100β, IL-1β, TNF-α, CREB, AP-1and NF-κb in offspring hippocampus and cortex. The protein level of GFAP was detected by western blot. Results:In 2.0mg/kg-d PFOS group, the mRNA levels of GFAP, S100β, IL-1β,TNF-α, CREB, AP-1and NF-κb were significantly increased compared with control group either on PNDO or on PND21. Compared with control, the protein levels of GFAP were significantly increased in all treated groups either on PNDO or on PND21. Conclusion:PFOS can increase the expression of inflammatory factor and transcription factor as well as active astrocyte, and lead to the inflammation-like glial response in offspring brain.
PartⅢ:The effect of prenatal exposure to PFOS on synaptic ultra-structure of pups
Objective:To study the effect of prenatal exposure to PFOS on synaptic ultra-structure of pups. Method:Pregnant Sprague Dawley (SD) rats were adminstrated 0.1, 0.6, and 2.0mg/kg bw/day by gavage from gestation day (GD) 2 to GD21. Control received 0.5% Tween-20 vehicle (4mg/kg bw/day). QPCR was used to detect mRNA level of Synl and Syp in offspring hippocampus and cortex. The protein levels of Synl and Syp were detected by western blot. The synaptic ultra-structure of hippocampus was analyzed by electron microscope. Results:In 2.0mg/kg-d PFOS group, the expression of Synl and Syp in hippocampus were significant decreased compared with control group either on PNDO or on PND21. In cortex, the expression of Synl were significant decreased in PFOS-treated group, but the expression of Syp in cortex increased. In the hippocampus of PFOS exposed offspring, synaptic vesicles became decreased, active synaptic zone became shorter, and synaptic curvature became uneven.Conclusion:PFOS can change the expression of Syp and Synl as well as impair the synaptic ultra-structure, which may play an important role in the developmental neruotoxicity of PFOS.
引文
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