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Considering the mutual relationship between redox disbalance and inflammation in Helicobacter pylori (HP) infection, we aimed to evaluate whether the polymorphisms in antioxidant glutathione transferases genes (GSTP1 rs1695, GSTP1rs1138272, GSTO1 rs4925 and GSTO2 rs156697) modify susceptibility to HP infection, as well as the severity of HP-associated gastric manifestation development. Therefore, GST gene polymorphisms were determined via the appropriate PCR in 101 HP-positive and 107 HP-negative patients. Our results show that carriers of the GSTP1*G/G variant genotype (rs1695) or at least one GSTP1*T variant allele (rs1138272) were more prone to the development of HP-positive gastritis compared with reference allele carriers (OR = 3.21, 95%CI = 1.15–8.91, p = 0.025 and OR = 2.31, 95%CI = 1.14–4.89, p = 0.021, respectively), which was confirmed by haplotype analysis. HP-positive carriers of the GSTO1*A variant allele showed increased risk of developing gastric atrophy and precancerous gastric lesions compared with the reference one (OR = 2.49, 95%CI:1.04–5.96, p = 0.04 and OR = 2.98, 95%CI = 1.21–7.34, p = 0.018, respectively). HP-positive carriers of the GSTO2*G variant allele were less prone to developing moderate/severe inflammatory infiltration (OR = 0.35, 95%CI = 1.04–5.96, p = 0.04), whereas the GSTP1*T variant allele was significantly associated with active inflammation (OR = 4.09, 95%CI = 1.04–5.96, p = 0.042). In conclusion, antioxidant GST genetic propensity seems to have an important impact on both acute and chronic forms of HP infection. [ABSTRACT FROM AUTHOR]

Introduction Heart failure (HF), as a chronic heart disease, is one of the leading causes of mortality worldwide. The metabolic requirements of the body are not satisfied because of the [...], Heart failure (HF) is one of the major cardiovascular causes of death worldwide. In this study, we explored the effects of folic acid (FA) on cardiometabolic, oxidative stress biomarker changes, and the activity of proliferation marker Ki67 in monocrotaline-induced HF. The research was conducted during a 4 week period using five experimental groups (eight animals per group): blank solution exposed controls (C1:1 mL/kg physiological saline, 1 day; C2:1 mL/kg physiological saline, 28 days), monocrotaline (MCT) induced HF (50 mg/kg MCT), FA (5 mg*[kg.sup.-1]*[day.sup.-1] FA), and MCT+FA (50 mg/kg MCT, 5 mg*[kg.sup.-1]*[day.sup.-1] FA). Superoxide dismutase and glutathione peroxidase activities together with total glutathione and parameters of oxidative damage of proteins were determined in cardiac tissue as well as cardiometabolic parameters in plasma or serum. The total glutathionylation was determined by Western blot and proliferation marker Ki67 was assessed by immunohistochemistry. The right ventricular (RV) wall hypertrophy and Ki67 positivity, accompanied by a significant increase of troponin T, has been shown in MCT-induced HF. The antioxidant effect of FA was reflected through superoxide dismutase activity, reduced Ki67 positivity in the RV wall, and a slightly decreased total glutathionylation level. Key words: heart failure, monocrotaline, oxidative stress, folic acid, Ki67, rat. L'insuffisance cardiaque (IC) est l'une des principales causes cardiovasculaires de deces a l'echelle mondiale. Cette etude portait sur les effets de l'acide folique (AF) sur les variations de marqueurs cardiometaboliques et du stress oxydatif, ainsi que sur l'activite du marqueur de proliferation Ki67 dans l'IC engendree par la monocrotaline (MCT). Nous avons mene l'etude pendant 4 semaines sur cinq groupes experimentaux de huit animaux chacun : temoins exposes a une solution a blanc (T1 : solution saline physiologique a 1 mL/kg sur 1 jour; T2 : salin physiologique a 1 mL/kg sur 28 jours), IC engendree par la MCT (a 50 mg/kg), AF (a 5 mg*[kg.sup.-1]*[jour.sup.-1]) et MCT+AF (a 50 mg/kg et a 5 mg*[kg.sup.-1]*[jour.sup.-1], respectivement). Nous avons mesure l'activite de la superoxyde dismutase et de la glutathion peroxydase de pair avec les taux de glutathion total et des parametres des dommages oxydatifs aux proteines dans le tissu cardiaque, ainsi que certains parametres cardiometaboliques dans le plasma ou le serum. Nous avons mesure la glutathionylation totale a l'aide de l'immunobuvardage de Western, et evalue les taux du marqueur de proliferation Ki67 a l'aide de l'immunohistochimie. Nous avons montre une hypertrophie de la paroi du ventricule droit (VD) et la presence du marqueur Ki67 (positivite), avec une augmentation notable des taux de troponine T dans l'IC engendree par la MCT. L'effet antioxydant de l'AF se manifestait par l'activite de la superoxyde dismutase, une diminution de la positivite au marqueur Ki67 dans la paroi du VD, ainsi que par une legere diminution du taux de glutathionylation totale. [Traduit par la Redaction] Mots-cles: insuffisance cardiaque, monocrotaline, stress oxydatif, acide folique, Ki67, rat.

The tumor microenvironment is affected by reactive oxygen species and has been suggested to have an important role in ovarian cancer (OC) tumorigenesis. The role of glutathione transferases (GSTs) in the maintenance of redox balance is considered as an important contributing factor in cancer, including OC. Furthermore, GSTs are mostly encoded by highly polymorphic genes, which further highlights their potential role in OC, known to originate from accumulated genetic changes. Since the potential relevance of genetic variations in omega-class GSTs (GSTO1 and GSTO2), with somewhat different activities such as thioltransferase and dehydroascorbate reductase activity, has not been clarified as yet in terms of susceptibility to OC, we aimed to investigate whether the presence of different GSTO1 and GSTO2 genetic variants, individually or combined, might represent determinants of risk for OC development. Genotyping was performed in 110 OC patients and 129 matched controls using a PCR-based assay for genotyping single nucleotide polymorphisms. The results of our study show that homozygous carriers of the GSTO2 variant G allele are at an increased risk of OC development in comparison to the carriers of the referent genotype (OR1 = 2.16, 95% CI: 0.88–5.26, p = 0.08; OR2 = 2.49, 95% CI: 0.93–6.61, p = 0.06). Furthermore, individuals with GST omega haplotype H2, meaning the concomitant presence of the GSTO1*A and GSTO2*G alleles, are more susceptible to OC development, while carriers of the H4 (*A*A) haplotype exhibited lower risk of OC when crude and adjusted haplotype analysis was performed (OR1 = 0.29; 95% CI: 0.12–0.70; p = 0.007 and OR2 = 0.27; 95% CI: 0.11–0.67; p = 0.0054). Overall, our results suggest that GSTO locus variants may confer OC risk. [ABSTRACT FROM AUTHOR]

Introduction: Overall survival of patients with end-stage renal disease (ESRD) remains poor. Oxidative stress is one of the major risk factors associated with mortality in this patient group. As glutathione S-transferases (GST) are well-established antioxidants, we hypothesized that a model including GST gene polymorphisms, oxidative damage byproducts and cell adhesion markers has a prognostic role in ESRD patient survival.Methods: A prospective study of 199 patients with ESRD on haemodialysis was conducted. GST genotype, oxidative stress byproducts and cell adhesion molecules were measured in plasma. Multivariate Cox regression and Kaplan-Meier survival analyses were performed to test the predictive ability of these parameters in the 8-year follow-up period.Results: GSTM1-null genotype was associated with significantly shorter overall (HR 1.6, p = 0.018) and cardiovascular-specific (HR 2.1, p = 0.010) survival. Oxidative stress byproducts (advanced oxidation protein products [AOPP], prooxidant-antioxidant balance [PAB], malondialdehyde [MDA]) and cell adhesion molecules (soluble vascular cell adhesion molecule-1 [sVCAM-1] and soluble intercellular adhesion molecule-1 [sICAM-1]) demonstrated a significant predictive role in terms of overall and cardiovascular survival. When 6 biomarkers (GSTM1 genotype, high AOPP/PAB/MDA/-sVCAM-1/sICAM-1) were combined into a scoring model, a significantly shorter overall and cardiovascular survival was observed for patients with the highest score (p < 0.001).Conclusion: We identified a novel panel of biomarkers that can be utilized in predicting survival in ESRD patients. This biomarker signature could enable better monitoring of patients and stratification into appropriate treatment groups. [ABSTRACT FROM AUTHOR]