Association of plasma proteins at multiple stages of glycation and antioxidant status with erythrocyte oxidative stress in patients with type 2 diabetes.

This study examines the individual stages of plasma protein glycation, antioxidant status and their association with erythrocyte oxidative stress in patients with type 2 diabetes mellitus (T2DM). Study was carried out on blood from 70 patients with T2DM and 40 healthy age- and gender-matched volunteers. Biomarkers of plasma protein glycation (fructosamine, protein carbonyls, advanced glycation end products [AGEs], amyloid), antioxidant status (thiols, total antioxidant capacity and erythrocyte oxidative parameters), osmotic fragility, lipid peroxidation (LPO), reduced glutathione (GSH) and catalase were determined. Plasma glycation markers were higher in T2DM patients than in healthy volunteers: fructosamine 578 vs. 525 micromol/mL; carbonyl 21.23 vs. 18.84 nmol/mg protein (P < or = 0.01); AGEs 213.94 vs. 178.27 AU/mg protein (P < or = 0. 05); and amyloid 0.53 vs. 0.40 A530 nm (P < 0.01). Plasma antioxidant status was significantly reduced in patients with diabetes compared to the healthy volunteers, with lower plasma protein thiols (1.16 vs. 1.36 nmol/mg protein; P < 0.01) and total antioxidant capacity (26 vs. 34 micromol; P < 0.01). Erythrocytes from the patient group were found to show greater oxidative damage, with elevated numbers of fragile cells and increased LPO, and reduced GSH level. Among the glycation markers, positive correlations were evident between fructosamine and amyloid (r = 0.350, P < 0.001) and AGEs and amyloid (r = 0.070). Plasma glycation markers showed negative correlation with plasma antioxidant status while positive correlation was demonstrated between erythrocytes fragility and AGEs and amyloid. Erythrocyte LPO levels correlated positively with amyloid. These data suggest that increased levels of multiple plasma protein glycation products in T2DM patients play a key role in reduced plasma antioxidant status and amplified erythrocyte oxidative damage.

Changes in zinc uptake in response to ascorbic acid and folic acid in rat liver slices under normal and oxidative stress conditions.

Zinc plays a dual role, as an integral part of metabolic machinery and in defense against reactive oxygen species. Hepatocytes are important sites for zinc metabolism for synthesis of zinc metalloproteins and maintaining its homeostasis. However, the factors influencing post absorptive zinc metabolism under normal and oxidative stress (OS) conditions are not well understood. Using rat liver slices, we conducted a series of four in vitro zinc uptake experiments to study influence of ascorbic acid and folic acid in normal and oxidative stress conditions with Zn concentrations representing deficient to excess states (7.7-30.7 millimole/L). Zinc uptakes under OS at these four zinc levels were lower than the normal conditions. Folic acid showed significant inhibitory effect on zinc uptake under both normal and OS conditions in a dose response manner. Nevertheless, dose response of ascorbic acid at four zinc levels indicated its marked enhancing effect under OS condition. Differences in zinc uptake trend lines between the normal and OS conditions for interaction of both the vitamins narrowed down as the zinc levels increased. Our results suggest that folic acid causes inhibitory effect, while ascorbic acid may be protective in OS with reference to zinc uptake.