Zhang Bin, Shao Hua, Wang Xiu Hui, Chen Xiao, Li Zhong Sheng, Cao Peng, Zhu Dan, Yang Yi Guang, Xiao Jing Wei, Li Bin
Department of Toxicology, Key Lab of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.
Shandong Academy of Occupational Health and Occupational Medicine, Jinan 250012, Shandong, China.
Biomed Environ Sci. 2017 Jun;30(6):432-443. doi: 10.3967/bes2017.057.
To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats.
Thirty-six Sprague Dawley (SD) rats were randomized into three groups, (1) a 30 mg/kg ACR-treated group, (2) a 50 mg/kg ACR-treated group, and (3) a normal saline (NS)-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated.
The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals (P < 0.05). Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group (P < 0.05). Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance (AZD) and the nearest neighbor distance (NND) of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool (RRP) was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups.
Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.
研究丙烯酰胺（ACR）对大鼠中枢神经系统（CNS）突触水平的亚急性神经毒性作用。
将36只Sprague Dawley（SD）大鼠随机分为三组，（1）30mg/kg ACR处理组，（2）50mg/kg ACR处理组，（3）生理盐水（NS）处理对照组。每天记录体重和神经学变化。试验结束时，采集大脑皮质和小脑组织，用光学显微镜和电子显微镜观察。此外，研究大脑皮质和小脑中突触素I和磷酸化突触素I的表达。
与未处理的个体相比，50mg/kg ACR处理的大鼠体重显著降低（P<0.05）。与NS对照组相比，暴露于ACR的大鼠步态评分显著增加（P<0.05）。组织学检查表明，50mg/kg ACR处理组存在神经元结构损伤。30mg/kg和50mg/kg ACR处理组的大脑皮质和小脑中突触小泡的活性区距离（AZD）和最近邻距离（NND）均增加。突触小泡在易释放池（RRP）中的分布比例降低。此外，30mg/kg和50mg/kg ACR处理组的大脑皮质和小脑中突触素I和磷酸化突触素I的表达水平均降低。
亚急性ACR暴露导致大鼠CNS神经病变。突触蛋白和小泡的功能损伤可能是ACR神经毒性的一种机制。
