Niu Qiao, Guo Xiao-li
Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan 030001, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2007 Feb;25(2):65-8.
To study the role of N-methyl-D-aspartate receptor 1 in acute intoxicated encephalopathy induced by 1,2- dichloroethane(1,2-DCE).
Forty-two Sprague-Dawley rats, which had been randomly divided into 1 control, 3 exposure and 3 after-exposure observation groups were exposed to 1,2-DCE for 12 hr by continual static inhalation except control group. Dosage of exposure groups was 5.0, 10.0, 20.0 g/m(3) on sequence. That of after-exposure observation groups was 10.0 g/m(3). Rats of after-exposure observation groups were observed continually for 2,4,6 hr after exposure. The expression of N-methyl-D-aspartate receptor-1 (NMDAR1) was detected by immunohistochemical method.
NMDAR1 stained neurons were mainly distributed at cerebral cortex and hippocampus. Compared with that of control group, the percentages of positive cells of NMDAR1 increased evidently at 10.0, 20.0 g/m(3) groups (P < 0.05). They were (18.33 +/- 1.86)%, (64.17 +/- 2.86)% at cerebral cortex, (15.5 +/- 1.87)%, (47.83 +/- 2.16)% at hippocampus. The percentages were also elevated obviously in 2, 4, 6 h after-exposure observation groups. They were (39.07 +/- 3.01)% (70.17 +/- 2.93)% (39.83 +/- 2.32)% at cerebral cortex, (16.30 +/- 1.03)% (19.80 +/- 1.17)% (16.50 +/- 1.05)% at hippocampus; Compared with that of 10.0 g/m(3) group, the percentages increased significantly only in 4 hr group at hippocampus.
The overactivation of NMDAR1 is the main route by which excitatory amino acids chose to join the development of acute intoxicated encephalopathy induced by 1,2-DCE.
