The effect of aminoguanidine (AG) on the malondialdehyde (MDA) concentration and activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-Px) in erythrocytes of rats with streptozotocin-induced diabetes was studied. Induction of diabetes resulted in an increase of MDA concentration and decreases of SOD and catalase activities after 6 and 12 weeks. GSH-Px activity increased after 6 weeks and returned to control values after 12 weeks. AG administration did not affect body weight, blood glucose level and HbA1c content in diabetic rats but led to a decrease of MDA concentration and SOD and catalase activities after 12 weeks of treatment, with no significant effect after 6 weeks. AG attenuated the GSH-Px increase after 6 weeks but augmented the activity of this enzyme after 12 weeks. These results confirm the presence of oxidative stress in streptozotocin-induced experimental diabetes and point to the beneficial antioxidant effect of AG.

These results confirm oxidative stress in erythrocytes of NIDDM patients with nephropathy. The intensity of oxidative stress appeared to be greater than in NIDDM patients without nephropathy.

These findings suggest that uraemia accelerates neutrophil apoptosis by increasing Fas/Apo-1, and that HD does not affect neutrophil apoptosis more than uraemia. In addition, HD produces only in a transient sequestration of potentially apoptotic neutrophils.

No abstract

These studies evaluated the nitric oxide (NO) release in peripheral blood during a four-hour hemodialysis (HD) with single-used cuprophane (CU), polysulfone (PS) and polyacrylonitrile (PAN) membranes in 10 chronic uremic patients. Continuous monitoring of blood NO concentrations was performed with a sterile NO sensor probe inserted vertically into the arterial blood line between the arteriovenous fistula and dialyzer. In the initial period of HD two peaks of blood NO concentrations were observed: the first occurred at the very start of HD and lasted approximately one minute, and the second peaked to a lesser extent at 20 to 26 minutes after the initiation of HD. The extent of NO release was dependent on the type of dialysis membrane used. Areas under curves for blood NO concentrations (in mumol x min) were as follows: CU, 450.8 +/- 163.3; PS, 247.3 +/- 150.6*; PAN, 200.4 +/- 91.0* (*P < 0.05 vs. CU). During the first hour of HD (N = 6) blood NO concentrations were significantly higher at the outlet of CU dialyzer than those found at the inlet. The areas under their curves (in mumol x min) were 169.1 +/- 1.9 and 107.5 +/- 1.6, respectively (P < 0.001). Areas under curves for blood NO concentrations measured for five minutes following a five-minute in vitro incubation of 5 ml heparinized uremic blood samples (N = 10) with dialysis membranes (50 cm2) were as follows (in nmol x min): CU, 2380 +/- 289*; PS, 1293 +/- 45*; PAN, 1117 +/- 37*; control, 502 +/- 56 (*P < 0.05 vs. control). The addition of sodium heparin to uremic blood platelet suspension induced an immediate rise in NO release in a dose-dependent manner, which proved to be a hyperbolic relationship. During HD with CU (N = 6), PS (N = 6) and PAN (N = 6) membranes blood plasma cGMP concentrations significantly increased, particularly at 20 and 60 minutes of the procedure. No significant differences in blood plasma cGMP levels were found between individual dialysis membranes, and no significant correlations were observed between blood plasma cGMP levels and blood NO concentrations. The results indicate that during HD NO is released in the peripheral blood due to blood-membrane and heparin-blood platelet interactions. The extent of intradialytic NO release is dependent on the type of dialysis membrane used (CU > PS approximately PAN).