Acrylamide-induced Subacute Neurotoxic Effects on the Cerebral Cortex and Cerebellum at the Synapse Level in Rats.

Bin Zhang; Hua Shao; Xiu Hui Wang; Xiao Chen; Zhong Sheng LI; Peng Cao; Dan Zhu; Yi Guang Yang; Jing Wei Xiao; Bin LI

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Acrylamide-induced Subacute Neurotoxic Effects on the Cerebral Cortex and Cerebellum at the Synapse Level in Rats.

Author: Bin ZHANG ¹ ; Hua SHAO ² ; Xiu Hui WANG ¹ ; Xiao CHEN ¹ ; Zhong Sheng LI ¹ ; Peng CAO ¹ ; Dan ZHU ¹ ; Yi Guang YANG ¹ ; Jing Wei XIAO ¹ ; Bin LI ¹
Author Information

1. 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.
2. Shandong Academy of Occupational Health and Occupational Medicine, Jinan 250012, Shandong, China.
Publication Type:Journal Article
Keywords: Acrylamide (ACR); Neurotoxicity; P-Synapsin I; Synapsin I; Synaptic vesicles
MeSH: Acrylamide; toxicity; Animals; Cerebellum; cytology; drug effects; Cerebral Cortex; cytology; drug effects; Drug Administration Schedule; Gait; Gene Expression Regulation; drug effects; Male; Neurons; drug effects; Neurotoxicity Syndromes; pathology; Rats; Rats, Sprague-Dawley; Synapses; drug effects; Synapsins; genetics; metabolism; Synaptic Vesicles; drug effects; physiology; Weight Loss; drug effects
From: Biomedical and Environmental Sciences 2017;30(6):432-443
CountryChina
Language:English
Abstract:
OBJECTIVETo investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats.
METHODSThirty-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.
RESULTSThe 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.
CONCLUSIONSubacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.