Fig. 1. Release of lactate dehydrogenase (LDH) from neurons–glia after exposure to iron. Primary neuronal–glial cultures (13–16 days in culture) were exposed to iron (0–300 μm FeCl2:FeSO4, 1:1) or to the neuronal excitotoxin, N -methyl-d-aspartate (NMDA; 100 μm) for 30 min in a balanced salt solution. LDH release was measured 24 h later. Values are mean ± SD of 10 observations from two to three different cell preparations expressed in units of enzymatic activity (nanomoles lactate oxidized to pyruvate per minute at room temperature). All values were significantly different from each other (P < 0.001), except there was no difference between Fe 100 and NMDA 100. Control = no iron–no NMDA; Fe 100 = 100 μm FeCl2:FeSO4; Fe 300 = 300 μm FeCl2:FeSO4; NMDA 100 = 100 μm NMDA.

Fig. 1. Release of lactate dehydrogenase (LDH) from neurons–glia after exposure to iron. Primary neuronal–glial cultures (13–16 days in culture) were exposed to iron (0–300 μm FeCl2:FeSO4, 1:1) or to the neuronal excitotoxin, N -methyl-d-aspartate (NMDA; 100 μm) for 30 min in a balanced salt solution. LDH release was measured 24 h later. Values are mean ± SD of 10 observations from two to three different cell preparations expressed in units of enzymatic activity (nanomoles lactate oxidized to pyruvate per minute at room temperature). All values were significantly different from each other (P < 0.001), except there was no difference between Fe 100 and NMDA 100. Control = no iron–no NMDA; Fe 100 = 100 μm FeCl2:FeSO4; Fe 300 = 300 μm FeCl2:FeSO4; NMDA 100 = 100 μm NMDA.

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