No abstract

PTX appears to have a protective effect against radiation damage. This protective effect is mediated in part by decreasing both inflammatory reactions and oxidative stress.

Oxidative DNA damage, caused by either endogenous or exogenous sources of reactive oxygen species (ROS), has been linked several diseases including Graves' disease (GD). 7,8-Dihydro-8-oxoguanine (8-oxoG) is a major lesion produced by ROS and is considered a key biomarker of oxidative DNA damage. In humans, 8-oxoG is mainly repaired by 8-oxoguanine DNA N-glycosylase-1 (hOGG1), which is an essential component of the base excision repair (BER) pathway. The functional studies showed that hOGG1 Ser326Cys polymorphism is associated with the reduced DNA repair activity and increased risk for some oxidative stress-related diseases. In this study, we firstly investigated hOGG1 Ser326Cys polymorphism in GD. According to our results, Cys/Cys genotype frequency in the GD patients (23.4%) was significantly higher than the controls (9.2%). Cys/Cys genotype had an 3.5-fold [95% CI (confidence interval): 2.10-6.01, p < 0.001] the Cys allele had 1.83-fold (95% CI: 1.43-2.34, p < 0.001) increase in the risk for developing GD. Our results suggest that Ser326Cys polymorphism of the hOGG1 gene is associated with GD risk.

In Turkish population, plasma HDL-C levels were found to be lower than in any other country and it is suggested that this is associated with genetic origin. The cholesteryl ester transfer protein (CETP) -629C > A polymorphism is associated with lower plasma CETP concentration, with increased HDL-C level. In the present study, the frequency of -629C > A polymorphism in patients with coronary artery disease (CAD) was investigated and the effect of genotype on HDL-C was evaluated in a Turkish population. For this aim CETP -629C > A polymorphism was studied in angiographically documented CAD patients and healthy controls. There was no statistical significance in the distribution of genotypes between patients and controls. Although A allele carriers with CAD had significantly lower HDL-C levels than controls, plasma lipid levels showed no difference according to the genotypes. Adjustment by a logistic regression model predicting CAD status through HDL-C and including some risk factors as covariate indicated that the HDL-C doesn't have a significant association with CAD risk in CA and AA genotype carriers. Smoking, gender and hypertension were the common predictors for the HDL-C levels in CA and AA carriers. Although HDL-C appeared to be the only significant predictor of CAD in our study groups, the contribution of CETP -629C > A polymorphism to the alterations in HDL-C level appears to be weak to mention a protective effect of this polymorphism for CAD. In conclusion, the findings of the present study indicate that the CETP -629C > A polymorphism is not among the determinants of the coronary artery disease in Turks.

Graves' disease (GD) is a multifactorial disease that develops as a result of complex interactions between genetic and environmental factors. The aim of our study is to determine the frequency of cytotoxic T-lymphocyte- associated antigen-4 (CTLA-4) A/G and TG C/T exon 33 SNPs (Tg E33SNP) in GD and to evaluate the relation between recurrence and these polymorphisms. A total of 187 subjects, including 97 previously treated GD patients and 90 age and gender matched control subjects were studied. We examined the relationship between the A/G and C/T polymorphism and various clinical and laboratory variables among patients with GD. TT genotype frequency in the GD patients was significantly higher than the controls. Number of recurrent patients was significantly higher in AG and GG carriers in comparison to AA carriers (57% and 45% vs 14%, p = 0.0001). CTLA-4 AG genotype had an eightfold (OR: 8.050; 95% CI: 2.87-22.5; p = 0.0001) and GG genotype had a sevenfold (OR: 7.025; 95% CI: 1.67-29.4; p = 0.007) increase in the risk of recurrence in the patients with GD. In conclusion, early interpretation for definitive treatment procedures (i.e., radioactive iodine or surgery) may be considered in the patients with G allele and E33SNP of Tg gene is conformed the susceptibility to GD in a Turkish population and having TT genotype increases the susceptibility to GD.

Oxidative stress has been implicated in etiopathogenesis of Graves' disease (GD). Increased lipid peroxidation and oxidative DNA damage have been found in GD patients. Oxidative DNA damage is mainly repaired by the base-excision repair (BER) pathway. Polymorphisms in DNA-repair genes have been associated with the increased risk of various diseases and could also be related to the etiology of GD. Therefore, we conducted a study including 197 patients with GD and age- and sex-matched 303 healthy subjects to examine the role of single-nucleotide polymorphisms of BER genes, APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) as a risk factor for GD. These polymorphisms were determined by quantitative real-time PCR and melting curve analysis using LightCycler. No significant association was observed between the variant alleles of APE/Ref-1 codon 148 [odds ratio (OR) = 0.89, 95% confidence interval (CI) = 0.69-1.17], XRCC1 codon 194 (OR = 1.24, 95% CI = 0.79-1.94), and XRCC1 codon 399 (OR = 1.12, 95% CI = 0.86-1.46) and GD. These preliminary results suggest that APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) polymorphisms are not significant risk factors for developing GD.

These results suggest that the grade of esophagitis is usually mild or moderate during childhood and factors apart from ROS, IL-8 and MCP-1 may be involved in the pathogenesis of reflux esophagitis in children.

Most of the studies concerning the effects of cyclosporin A (Cs A) on red blood cell (RBC) rheology were carried out in human transplant recipients who may still have residual insufficiency and concomitant administration of other immunosuppressive and antihypertensive drugs. The aim of this study is to evaluate the effects of Cs A on red cell rheology and membrane composition in nontransplant healthy rats. Female Wistar albino rats were divided into two groups of 10 animals each. Rats received 10 mg/kg Cs A, i.p. or saline for 4 weeks. Cs A administration significantly increased the RBC deformability, and plasma and blood viscosity (p < 0.001, p < 0.01 and p < 0.01, respectively). Cs A administration to the rats increased RBC membrane cholesterol (CHO) levels and the CHO/phospholipid (PL) ratio significantly (p < 0.01 and p < 0.05, respectively) but did not change RBC membrane proteins and membrane PL levels. These results suggest that Cs A changes the rheological functions of RBC and lipid content of RBC membrane in healthy rats and thereby it may play an important role in the regulation of microcirculation.