PDF(Pubmed)
Abstract：
UNASSIGNED: Nanotechnology has shown a remarkable progress nevertheless, there is a growing concern about probable neurotoxic and neurodegenerative effects due to NPs exposure. Various toxicological and epidemiological studies reported that the brain is a main target for ultrafine particles. Brain inflammation is considered as a possible mechanism that can participate to neurotoxic and neurodegenerative effects. Whether nanoparticles (NPs) may produce neurotoxicity and promote neurodegenerative is largely unstudied. The present study was done to investigate whether intranasal and intra-peritoneal exposure to cerium oxide nanoparticles (CeO2NPs, nanoceria (NC)) could cause neurotoxicity and neurodegenerative changes in the brain tissue through conducting some behavioral tests, biochemical evaluation, histopathological examinations of brain hippocampus and gene expressions.
UNASSIGNED: Fifteen mice were separated into 3 equal groups. In group (I) \"control group\", mice were received distilled water orally and kept as a control group. Mice in the group (II) \"NC I/P group\" were injected i.p with cerium oxide nanoparticles at a dose of 40 mg/kg b.wt, twice weekly for 3 weeks. In group (III) \"NC I/N group\" mice were received nanoceria intranasally (40 mg/kg b.wt), twice weekly for 3 weeks.
UNASSIGNED: Exposure to nanceria resulted in oxidative damage in brain tissue, a significant increase in malondialdehyde (MDA) and acetylcholinestrase (AchE) levels, significant decrease in reduced glutathione (GSH) concentration, upregulation in the apoptosis-related genes (c-Jun: c-Jun N-terminal kinases (JNKs), c-Fos: Fos protooncogene, AP-1 transcription factor subunit, c-Myc: c-myelocytomatosis oncogene product or MYC protooncogene, bHLH transcription factor), locomotor and cognitive impairment in mice but the effect was more obvious when nanoceria adminstred intraperitoneally.
UNASSIGNED: Nanoceria cause oxidative damage in brain tissue of mice when adminstred nanoceria intraperitoneally more than those received nanoceria intranasal.
UNASSIGNED: Fifteen mice were separated into 3 equal groups. In group (I) \"control group\", mice were received distilled water orally and kept as a control group. Mice in the group (II) \"NC I/P group\" were injected i.p with cerium oxide nanoparticles at a dose of 40 mg/kg b.wt, twice weekly for 3 weeks. In group (III) \"NC I/N group\" mice were received nanoceria intranasally (40 mg/kg b.wt), twice weekly for 3 weeks.
UNASSIGNED: Exposure to nanceria resulted in oxidative damage in brain tissue, a significant increase in malondialdehyde (MDA) and acetylcholinestrase (AchE) levels, significant decrease in reduced glutathione (GSH) concentration, upregulation in the apoptosis-related genes (c-Jun: c-Jun N-terminal kinases (JNKs), c-Fos: Fos protooncogene, AP-1 transcription factor subunit, c-Myc: c-myelocytomatosis oncogene product or MYC protooncogene, bHLH transcription factor), locomotor and cognitive impairment in mice but the effect was more obvious when nanoceria adminstred intraperitoneally.
UNASSIGNED: Nanoceria cause oxidative damage in brain tissue of mice when adminstred nanoceria intraperitoneally more than those received nanoceria intranasal.
摘要：
■纳米技术已经显示出显著的进步，人们越来越担心NPs暴露可能引起的神经毒性和神经退行性作用。各种毒理学和流行病学研究报道，大脑是超细颗粒的主要目标。脑炎症被认为是可能的机制，可以参与神经毒性和神经退行性作用。纳米颗粒（NPs）是否会产生神经毒性并促进神经退行性变，目前尚无研究。本研究是为了调查鼻内和腹膜内暴露于氧化铈纳米颗粒(CeO2NP，通过进行一些行为测试，纳米氧化铈（NC））可能会导致脑组织中的神经毒性和神经退行性变化，生化评价,脑海马和基因表达的组织病理学检查。
■将15只小鼠分成3个相等的组。在组（I）“控制组”中，小鼠口服蒸馏水作为对照组。组（II）“NCI/P组”中的小鼠以40mg/kgb.wt，每周两次，共3周。在组（III）中，“NCI/N组”小鼠鼻内接受纳米铈（40mg/kgb.wt），每周两次，共3周。
■暴露于nanceria导致脑组织氧化损伤，丙二醛（MDA）和乙酰胆碱酯酶（AchE）水平显着增加，还原型谷胱甘肽（GSH）浓度显着降低，凋亡相关基因的上调（c-Jun：c-JunN末端激酶（JNKs），c-Fos:Fos原癌基因,AP-1转录因子亚基,c-Myc：c-骨髓细胞瘤癌基因产物或MYC原癌基因，bHLH转录因子)，小鼠的运动能力和认知障碍，但腹膜内施用纳米铈后效果更明显。
■当腹膜内给予纳米二氧化铈比鼻内给予纳米二氧化铈时，纳米二氧化铈在小鼠脑组织中引起氧化损伤。
■将15只小鼠分成3个相等的组。在组（I）“控制组”中，小鼠口服蒸馏水作为对照组。组（II）“NCI/P组”中的小鼠以40mg/kgb.wt，每周两次，共3周。在组（III）中，“NCI/N组”小鼠鼻内接受纳米铈（40mg/kgb.wt），每周两次，共3周。
■暴露于nanceria导致脑组织氧化损伤，丙二醛（MDA）和乙酰胆碱酯酶（AchE）水平显着增加，还原型谷胱甘肽（GSH）浓度显着降低，凋亡相关基因的上调（c-Jun：c-JunN末端激酶（JNKs），c-Fos:Fos原癌基因,AP-1转录因子亚基,c-Myc：c-骨髓细胞瘤癌基因产物或MYC原癌基因，bHLH转录因子)，小鼠的运动能力和认知障碍，但腹膜内施用纳米铈后效果更明显。
■当腹膜内给予纳米二氧化铈比鼻内给予纳米二氧化铈时，纳米二氧化铈在小鼠脑组织中引起氧化损伤。
