Table 1.

Zinc exposure selectively increased DHAP and FBP levels, and this increase was reversed by addition of pyruvate or niacinamide

(Nanomoles/plate ± SEM)	Control	40 μm Zinc	Zinc + pyruvate	Zinc + niacinamide	Staurosporine
Glucose-6-phosphate	4.2  ± 0.6	7.6  ± 1.0	N.P.	N.P.	N.P.
Fructose-6-phosphate	1.6  ± 0.2	3.2  ± 0.4	N.P.	N.P.	N.P.
DHAP	5.2  ± 0.6	22.4  ± 0.8*	5.2  ± 0.6#	5.0  ± 0.6#	3.2  ± 2.2
Fructose bisphosphate	5.2  ± 0.8	51.4  ± 5.0*	5.0  ± 0.8#	11.2  ± 1.4#	5.8  ± 0.6
2-Phospho-glycerate	6.25  ±  0.5	11.7  ±  0.5*	N.P.	N.P.	N.P.
Phospho-enolpyruvate	5.75  ±  1.7	8.2  ± 4.7	N.P.	N.P.	N.P.
Pyruvate	14.2  ±  2.2	20  ± 4.5	N.P.	N.P.	N.P.

Near-pure cortical neuronal cultures were sham-washed or exposed to 40 μm Zn²⁺ in the presence or absence of 4 mm pyruvate or 1 mm niacinamide. The cells were then harvested and assayed for levels of the indicated glycolytic intermediates (results were pooled from three separate experiments; n = 5–8 cultures per condition). Exposure to 100 nm staurosporine for 4–6 hr, sufficient to trigger widespread apoptosis, did not mimic the ability of Zn²⁺ to elevate DHAP or FBP. N.P. indicates that the experiment was not performed. * signifies difference from sham-washed controls, and

signifies difference from Zn²⁺-treated cultures at p < 0.05 by one-way ANOVA, followed by a Bonferroni test.