Acrylamide neurotoxicity on the cerebrum of weaning rats  

作　　者：Su-min Tian Yu-xin Ma Jing Shi Ting-ye Lou Shuai-shuai Liu Guo-ying Li 

机构地区：[1]School of Basic Medicine,Guangdong Pharmaceutical University [2]Xiqiao People’s Hospital [3]Clinical Laboratory of First Affiliated Hospital,Xinxiang Medical University [4]Guangzhou University of Chinese Medicine

出　　处：《Neural Regeneration Research》2015年第6期938-943,共6页中国神经再生研究（英文版）

基　　金：supported by the Medical Scientific Research Foundation of Guangdong Province in China,No.B2014202;the Natural Science Foundation of Guangdong Province in China,No.2014A030310455

摘　　要：The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group （5 mg/kg）. However, rats from the moderateand high-dose acrylamide groups （15 and 30 mg/kg） had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and ^-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohis- tochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group （5 mg/kg）. However, rats from the moderateand high-dose acrylamide groups （15 and 30 mg/kg） had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and ^-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohis- tochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

关 键 词：nerve regeneration γ-aminobutyric acid glial fibrillary acidic protein glutamic aciddecarboxylase NEUROTOXICITY WEANING organ index CEREBRUM cortex GLUTAMATE neural regeneration 

分 类 号：R114[医药卫生—卫生毒理学]