Objective: To investigate the effect and mechanisms of dimethoate on the primary cultured cortical neuronal cell injury.
Methods: Cortical neuronal cells were isolated and cultured in serum free medium for 6 days in vitro, and 1, 5, 10, 50 and 100 micromol/L dimethoate were added to the medium and intracellular SOD, MDA and GSH. The content of excitatory amino acid was measured after 48 hours. Flow cytometry was used to detect the neuronal cell apoptosis.
Results: After 48 h, the activity of SOD and the content of GSH decreased [(1.04 +/- 0.02), (0.99 +/- 0.02), (0.96 +/- 0.02), (0.91 +/- 0.02) U/mg pro] [(219.35 +/- 6.79), (205.6 +/- 6.29), (194.06 +/- 2.63), (93.68 +/- 7.56) mg/g pro], and the content of MDA increased obviously with 5, 10, 50 and 100 micromol/L dimethoate [(21.22 +/- 0.29), (24.01 +/- 0.34), (27.15 +/- 1.02), (32.91 +/- 1.39) nmol/mg pro]; The content of Asp from 10 to 100 micromol/L dose group was higher than the control group and the content of Glu from 1 to 100 micromol/L dose group was higher than the control group. The apoptosis rate had great significance between 1 to 100 micromol/L dose groups and control group. When treated with dimethoate, MDA content in neuron was positively correlated with the content of EAAs with the increase of dimethoate. The correlative coefficient was 0.937 and 0.759 respectively (P < 0.01), while it was negatively correlated with the content of GSH. The correlative coefficient was -0.868 and -0.801 respectively (P < 0.01).
Conclusion: The oxidative damage and changes of excitatory amino acid content induced by Dimethoate contribute to the primary cultured rat cortical neuron apoptosis.