We evaluated the ability of zinc to modulate the superoxide anion released by isolated, phorbol myristate acetate (PMA)-stimulated polymorphonuclear leukocytes (PMNs). In the presence of zinc at physiological level (20 micromol/l), PMNs released 20% less superoxide anions than untreated cells, whereas at higher zinc concentration (200 micromol/l), a 40%-increase in superoxide anion production was detected. The direction (suppression or stimulation) of superoxide anion generation was dependent upon extracellular zinc level and did not discriminate type 1 and 2 diabetic subjects from normal controls. The mechanism(s) of dose-dependent pro- and antioxidative effects of zinc on isolated PMNs in vitro as well as the implication of this finding for the modulatory effect of Zn on PMN-superoxide anion production in vivo need further investigation.

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The aims of this study were to determine whether in vitro nonenzymatic glycation of proteins by sialic acid (sialylation) induces the generation of fluorescence, and whether the presence of this keto sugar may affect the generation of fluorescence induced by other sugars. Incubation of bovine serum albumin (BSA; 1.5 mM) with sugars (50 mM in 0.2 M phosphate buffer, pH 7.4, at 37 degrees C) resulted in a time-dependent increase of formaldehyde release (moles/moles of protein). On the 17th day of incubation, the value was 0.53 +/- 0.06, 0.78 +/- 0.15 and 1.23 +/- 0.18 for sialic acid, fructose and glucose respectively, compared with 0.37 +/- 0.05 for BSA. The fluorescence intensity (arbitrary units/mg protein) was higher after 17 days of incubation with fructose (16.9 +/- 1.8) than with glucose (12.7 +/- 1.3), while no significant increase was noted with sialic acid compared with BSA (3.8 +/- 0.4). Fluorescence intensity increase by incubation with glucose (50 mM) was significantly reduced by sialic acid (20 mM) after both 10 (P < 0.001) and 14 (P < 0.001) days of incubation, while inhibition was weaker after 14 (P < 0.05) than after 10 (P < 0.001) days when fructose (50 mM) was used as the glycating agent. This indicates that sialic acid can be potentially used to limit the damage from adverse glycation-induced processes.

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