The association of lectin-like oxidized LDL receptor 1 (LOX-1) K167N and 3'UTR188CT polymorphisms with maternal plasma soluble LOX-1 levels and preeclampsia risk in Turkish population.

PURPOSE: To investigate the main effect of polymorphisms in genes involved in endothelial pathophysiological mechanisms, LOX-1 K167N and 3'UTR188CT single nucleotide polymorphisms (SNPs) in relation to preeclampsia (PE) risk and possible interactions between the gene polymorphisms and plasma oxLDL and soluble LOX-1 (sLOX-1) levels on PE in Turkish population. METHODS: LOX-1 K167N and 3'UTR188CT polymorphisms were studied in 113 pregnant women with preeclampsia and 96 healthy pregnant women by the PCR-RFLP techniques. sLOX-1 and oxLDL levels were determined by enzyme-linked immunosorbent assay (ELISA) in all study subjects. RESULTS: Patients having LOX-1 3'UTR188CT (OR 3.55, 95% CI 1.89-6.67, P = 0.001) or 3'UTR188CC (OR 3.04, 95% CI 1.25-7.38, P = 0.012) genotype had a significantly higher risk of PE than those with 3'UTR188TT genotype. Also, patients having K167N KK (OR 2.73, 95% CI 1.33-5.61, P = 0.005) genotype had a significantly higher risk of PE than those with K167N NN genotype. LOX-1 3'UTR188TT and LOX-1 K167N NN genotype carriers were associated with significantly increased serum sLOX-1 level (P = 0.001). We further investigated the potential combined effect of these polymorphic variants on risk of PE development. According to the combined genotype analysis of LOX-1 3'UTR188TT and K167N NN polymorphisms, sLOX-1 and oxLDL levels also showed significant differences between PE patients and controls with or without combined TT/NN genotype carriers. CONCLUSIONS: Our findings indicate that higher plasma sLOX-1 and oxLDL concentrations, and the LOX-1 3'UTR188C>T and LOX-1 K167N gene polymorphisms were significantly associated with risk of developing preeclampsia. Plasma sLOX-1 may be a potential therapeutic target in the treatment of preeclampsia.

Total antioxidant status and markers of oxidative stress in subjects with normal or impaired glucose regulation (IFG, IGT) in diabetic patients.

BACKGROUND: We investigated the ischemia-modified albumin (IMA), advanced oxidation protein products (AOPPs), prooxidants-antioxidants balance (PAB), and ferric reducing antioxidant power (FRAP) concentrations in patients with impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and diabetes mellitus (DM) and compared the results to those of normoglycemic individuals at baseline and 2 hours after glucose loading. METHODS: An oral glucose tolerance test was performed on age-matched subjects (n = 110) with a body mass index (BMI) < 27 kg/m(2). Subjects were categorized as normoglycemic (n = 35), IFG (n = 25), IGT (n = 30) and DM (n = 20) according to the WHO criteria. The IMA, AOPP, PAB, FRAP concentrations were determined by colorimetric methods. RESULTS: At baseline, the AOPP concentrations were significantly higher in subjects with IFG and DM compared to normoglycemic subjects (p < 0.01 for all cases). The IFG, IGT and DM patients had a significantly higher IMA at baseline when compared with the normoglycemic individuals (p < 0.001 for all cases). The IMA in IFG subjects was significantly elevated (p < 0.05), while in DM patients, the IMA was significantly decreased (p < 0.001) after glucose loading with respect to baseline concentrations. Following glucose loading, the PAB was significantly decreased from baseline concentrations in normoglycemic individuals (p < 0.001) and in the IFG (p < 0.001) and IGT (p < 0.001) patients. CONCLUSION: In subjects with impaired glucose metabolism, the hyperglycemia is associated with increased IMA, AOPP and PAB concentrations. Increased IMA in subjects with IFG and decreased FRAP concentrations in subjects with IGT after glucose loading suggests that an increase in glucose concentrations can lead to tissue damage by increasing oxidative stress.

Oxidative damage parameters in renal tissues of aged and young rats based on gender.

PURPOSE: Aging is characterized by a gradual functional decrease of all systems including the kidneys. Growing evidence links altered lipid protein redox-homeostasis with renal dysfunction. The effect of sexual dimorphism on the lipid protein redox-homeostasis mechanisms in the aging kidney is obscure. In the current study, we aimed to investigate redox homeostasis as it related to sexual dimorphism on protein oxidation and lipid peroxidation parameters, as protein carbonyl (PCO), total thiol (T-SH), advanced oxidation protein products (AOPP), malondialdehyde, glutathione (GSH), and superoxide dismutase (SOD) activity, as potential aging biomarkers, which may contribute to an analysis of the free radical theory of aging. MATERIALS AND METHODS: The study was carried out with 16 naturally aged rats (24 months old; eight males and eight females) and their corresponding young rat groups as controls (6 months old; eight males and eight females). All of the aforementioned parameters (PCO, T-SH, AOPP, MDA, GSH, SOD) were measured manually instead of automated devices or ELISA kits. RESULTS: PCO, AOPP, and malondialdehyde levels in aged rats were significantly higher in the older rat group than in the younger rat group, whereas SOD activities were significantly lower in old rats. T-SH levels were not significantly different in male groups; however, T-SH levels were lower in the aged female group than in the young female control group. In addition, GSH levels were significantly different between the aged rat group and the corresponding young control group for both genders. CONCLUSION: With respect to PCO and AOPP, impaired redox homeostasis is substantially more prominent in males than females. The decrease of G-SH levels in male groups could be attributed to stabilizing the redox status of protein thiol groups by the depletion of the GSH groups. Considering the results, the renal tissue proteins and lipids in different genders may have different susceptibilities to oxidative damage.

The role of pentraxin 3 as diagnostic value in classification of patients with heart failure.

OBJECTIVE: Pentraxin 3 (PTX3) is a new inflammatory marker that is the prototype of the long pentraxin group, while C-reactive protein (CRP) is the short pentraxin group. The aim of the present study was to investigate the clinical significance of plasma PTX3 and CRP levels in heart failure (HF). MATERIALS AND METHODS: The study included 22 male and 37 female patients with HF, and 23 healthy volunteers as the control group. Patients were divided into 4 groups (class I, II, III and IV) according to New York Heart Association functional class. RESULTS: Plasma PTX3 and CRP levels were significantly elevated in HF patients compared to healthy controls. Comparing PTX3 levels in patient groups, statistically significant difference was found between class-I and class-II, class-III and class-IV patients (p=0.009, p=0.001, p<0.001, respectively). There was a positive correlation between PTX3 and CRP levels (r=0.369, p=0.004). In receiver-operating characteristic (ROC) curves, area under the curve (AUC) values for PTX3 and CRP were 0.928 (p=0.001) and 0.834 (p=0.001), respectively. CONCLUSIONS: Plasma PTX3 levels are elevated in HF and might be used as diagnostic value in classification of patients with HF. It is still debated whether inflammation may be just a cause or a consequence of the disease. Therefore further work is needed to better understand in large populations of patients with HF.