Objective: To explore the relationship between excitatory amino acids (EAAs) and acute in toxicated encephalopathy induced by 1,2-dichloroethane (1,2-DCE).
Methods: SD rats were randomly divided into 7 groups: 1 control group, 3 exposure (5.0, 10.0, 20.0 g/m(3)) groups and 3 duration (2, 4, 6 h after 10.0 g/m(3) exposure) groups. Rats were exposed to 1,2-DCE for 12 h by continual static inhalation. Water content of cerebral cortex and medulla was measured by wet-dry method; The contents of glutamate (Glu), aspartate (Asp), glycine (Gly) and gamma-aminobutyric acid (GABA) in brain tissues were determined by high performance liquid chromatography (HPLC).
Results: Water content of cerebral cortex in 3 exposure groups (76.10% +/- 1.41%, 76.45% +/- 0.75%, 79.95% +/- 1.45% respectively) were higher than that of control group (74.22% +/- 1.77%, P < 0.05, P < 0.01). That of medulla was increased significantly merely at 20.0 g/m(3) (71.77% +/- 3.07%, P < 0.05). Water content of cortex in 3 duration groups (79.36% +/- 2.10%, 79.48% +/- 1.21%, 80.64% +/- 1.93% respectively) were higher than that of 10.0 g/m(3) instant exposure group (P < 0.05). The content of Asp [(4.83 +/- 0.35) micro mol/g, (7.17 +/- 0.40) micro mol/g, (10.52 +/- 0.39) micro mol/g], Glu [(23.86 +/- 0.62) micro mol/g, (31.21 +/- 2.50) micro mol/g, (28.23 +/- 1.58) micro mol/g] and Gly [(5.59 +/- 1.01) micro mol/g, (6.06 +/- 0.83) micro mol/g, (7.26 +/- 1.34) micro mol/g] in exposure groups were higher than those of corresponding control groups [(3.72 +/- 0.48) micro mol/g, (21.09 +/- 1.20) micro mol/g, (3.83 +/- 0.44) micro mol/g, P < 0.05, P < 0.01]. Compared to 10.0 g/m(3) instant group, Asp content was increased at 2, 4, 6 h (P < 0.01), Glu content at 2, 4 h (P < 0.05), and peak value of Glu appeared at 4 h [(35.40 +/- 2.40) micro mol/g] while Gly content was significantly decreased (P < 0.01). GABA did not show evident changes in both exposure or duration groups (P > 0.05).
Conclusion: EAAs appears to be related with the development of acute intoxicated encephalopathy induced by 1,2-DCE, and its damage to neuron might be one of the mechanisms of brain edema.