FIG. 4.

Evidence that oxidation of sulfhydryl groups on cysteine residues may be involved in H₂O₂-induced glutamate receptor-independent neuronal injury. (a) Summary bar graph demonstrating the protective effect of thiol-reducing agent dithiothreitol (DTT) on H₂O₂-induced neuronal injury. Neurons were treated with 100 μM H₂O₂ in the presence of MK801, CNQX, and nimopidine for 1 h, either in the absence or presence of 1 or 2 mM DTT. Relative LDH release was measured 6 h after H₂O₂ exposure. One hour treatment with 100 μM H₂O₂ in the absence of DTT induced 0.39 ± 0.07of relative LDH release. However, in the presence of 1 or 2 mM DTT, relative LDH release by the same concentration of H₂O₂ was reduced to 0.30 ± 0.03 and 0.16 ± 0.01, respectively (n = 4 wells each, p < 0.05 between H₂O₂ alone and H₂O₂ with 2 mM DTT). *p < 0.05 compared with 100 μM H₂O₂ alone. (b) Summary data showing the relative LDH release induced by cysteine oxidizing agents 2,2′-dithiobis-5-nitropyridine (DTNP) in the presence of MK 801, CNQX, and nimodipine. LDH release was measured 6 h after 1 h exposure to 100 μM DTNP or vehicle control. Relative LDH release induced by DTNP was 0.39 ± 0.03 (n = 8 wells each, p < 0.01 compared with control group). Vehicle control for DTNP (3% acetone) did not induced significant increase in background LDH release (n = 4).