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The relationship between late-onset gestational diabetes mellitus [GDM] and oxidative stress is not well known, and the importance of the oxidant/antioxidant equilibrium in the clinical evolution and its complications require elucidation. The aim of the study was to evaluate the relationships between maternal levels of markers of oxidative stress in women with late-onset GDM that, potentially, may have considerable clinical implications in the pathogenesis and/or the evolution of GDM. Pregnant women ( n = 78; 53 with GDM, 25 controls), between the 24th and 29th week of gestation, were enrolled. Both groups were analysed for demographic data, perinatal and obstetrics outcomes together with the levels of the marker's oxidative stress and antioxidant status. Control versus patient results in the univariate analysis were the following: pre-gestational body mass index [BMI] 23.31 ± 4.2 vs. 27.13 ± 4.6 kg/m ( P = 0.001); weeks at delivery 39.2 ± 3.05 vs. 38.9 ± 1.8 ( P = 0.09); Caesarean delivery 12.5 vs. 43% ( P = 0.004); macrosomia 4 vs. 9.4% ( P = 0.6); lipoperoxides [LPO] 2.06 ± 1.00 vs. 3.14 ± 1.55 μmol/mg ( P = 0.001); catalase 3.23 ± 1.41 vs. 2.52 ± 1.3 nmol/min/ml ( P = 0.03); superoxide dismutase [SOD] 0.11 ± 0.04 vs. 0.08 ± 0.01 U/ml ( P = 0.0003); glutathione peroxidase [GPX] 0.03 ± 0.006 vs. 0.025 ± 0.006 nmol/min/ml ( P = 0.01); glutathione reductase [GSH] 0.004 ± 0.002 vs. 0.004 ± 0.004 nmol/min/ml ( P = 0.9)]; and glutathione transferase [GST] 0.0025 ± 0.0012 vs. 0.0027 ± 0.00017 nmol/min/ml ( P = 0.7). Multivariate analysis showed catalase might have a protective effect against GDM development and LPO seems to be a risk factor for the disease. These data suggest an increase in oxidative stress and a decrease in antioxidative defence in women with late-onset GDM and, as such, may have considerable clinical implications in the pathogenesis and/or the course of the pregnancy in these patients. [ABSTRACT FROM AUTHOR]

Antioxidant enzymes can modify cell response to nitrosative stress induced, for example, by nitric oxide or compounds decomposing with its formation. Therefore, we investigated the effects of S-nitrosoglutathione (GSNO) on cell survival, activity of antioxidant enzymes, and concentrations of reduced and oxidized glutathione in parental and isogenic strains defective in Cu,Zn- or Mn-superoxide dismutases (Cu,Zn-SOD and Mn-SOD, respectively), or in both of them. Stress was induced by incubation of the yeast with 1–20 mM GSNO. The strains used demonstrated different sensitivity to GSNO. A Cu,Zn-SOD-defective strain survived the stress better than the parental strain, while the double mutant was the most sensitive to GSNO. The ·NO-donor at low concentrations (1–5 mM) increased SOD activity, but its high concentrations (10 and 20 mM) decreased it. The activity of catalase in all strains was enhanced by GSNO. Inhibition of protein synthesis by cycloheximide did not prevent the activation of SOD, but it prevented the activation of catalase. These facts suggest that SOD was activated at a posttranslational level and catalase activity was enhanced via de novo synthesis. A GSNO-induced increase in oxidized glutathione level in the studied yeast strains might account for cell killing by GSNO due to the development of oxidative/nitrosative stress. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the oxidative DNA damage, antioxidant activity, and effects of antihypertensive drugs on oxidative stress in hypertensive patients with different stages of chronic kidney disease (CKD). Fifty-three non-dialyzed hypertensive CKD patients were included by the study. Serum and urinary 8-hydroxydeoxy guanosine (8-OHdG) levels (as a marker of oxidative DNA damage), serum superoxide dismutase (SOD), and glutathione peroxidase (G-Px) activities (as antioxidant enzymes) were measured. SOD activity was higher and G-Px activity was lower in the patient group as compared to control group. Serum and urinary 8-OHdG levels were found to be higher in the patients with proteinuria greater than 3 g/day than those in the patients with proteinuria less than 3 g/day. It has been determined that G-Px activity and urinary 8-OHdG level were lower in the patients treated with angiotensin-converting enzyme (ACE) inhibitor compared to patients treated with calcium channel blocker. The present data show oxidative DNA damage at a higher level in the patients with proteinuria greater than 3 g/day. In comparison to a calcium channel blocker, an ACE inhibitor seems much more protective against oxidative DNA damage in hypertensive patients with different stages of CKD. [ABSTRACT FROM AUTHOR]