1 The cytotoxic effect of N-methyl-D-aspartate (NMDA) was studied in human CHP100 neuroblastoma cells. 2 Exposure for 50 min to NMDA (0.25-1.5 mM; n = 3-6 experiments per concentration) produced concentration-dependent cell death. The cell death produced by 1.0 mM NMDA was abolished by CGP37849 (0.1 mM) and was significantly reduced by removing glycine (0.2 mM) from the exposure solution. In addition, the NMDA lethal effect was evident when Ca2+ concentration in the exposure solution ranged from 0.8 to 1.8 mM. 3 NMDA (1.0 mM) treatment yielded a 170% increase in NO(2 -) production 1 min after exposure to the excitotoxin and this was accompanied by a significant increase in cGMP levels. 4 Superoxide dismutase (SOD; 100 U/ml) enhanced by 30% the cell death evoked by NMDA (0.5 mM). This effect was reversed by co-incubation with catalase (CAT; 100 U/ml), which per se did not significantly affect the lethality induced by NMDA. 5 In conclusion, the present data suggest that abnormal stimulation of the NMDA receptor complex leads to excessive production of NO which may be responsible for cGMP accumulation and human CHP100 neuroblastoma cell death.
|Number of pages||5|
|Publication status||Published - 1993|
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