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Sleep architecture alterations, among which sleep fragmentation is highly prevalent, represent risk factors for a variety of diseases, ranging from cardiovascular to brain disorders, including anxiety. What mediates anxiety occurrence upon sleep fragmentation is still a matter of debate. We hypothesized that the sleep fragmentation effects on anxiety are dependent on its duration and mediated by increased oxidative stress and alterations in the number of parvalbumin (PV+) interneurons in the hippocampus. Sleep was fragmented in rats by the treadmill method during a period of 14 days (SF group). Rats with undisturbed sleep in the treadmill (TC group) and those receiving equal amounts of treadmill belt motion (EC group) served as controls. To assess anxiety, we subjected rats to the open field, elevated plus maze, and light-dark tests on the 0, 7th, and 14th day. Upon the last test, brain structures were sampled for oxidative stress assessment and PV+ interneuron immunohistochemistry. The results of ethological tests of anxiety-linked behavior suggested duration-dependent anxiogenic potential of sleep fragmentation. Rats’ anxiety-linked behavior upon sleep fragmentation significantly correlated with oxidative stress. The rats with fragmented sleep (SF) showed significantly higher oxidative stress in the hippocampus, thalamus, and cortex, compared to controls (TC and EC), while the antioxidant enzymes’ activity was significantly decreased. No significant differences were observed in hippocampal PV+ interneurons among these groups. Our results showed that duration of sleep fragmentation is a significant determinant of anxiety-linked behavior, and these effects are mediated through oxidative distress in the brain. Herein, it is revealed that the sleep fragmentation-oxidative stress-anxiety axis contributes to our better understanding of pathophysiological processes, occurring due to disrupted sleep patterns.
Željko Grubač; Nikola Šutulović; Sonja Šuvakov; Djurdja Jerotić; Nela Puškaš; Djuro Macut; Aleksandra Rašić-Marković; Tatjana Simić; Olivera Stanojlović; Dragan Hrnčić. Anxiogenic Potential of Experimental Sleep Fragmentation Is Duration-Dependent and Mediated via Oxidative Stress State. Oxidative Medicine and Cellular Longevity 2021, 2021, 1 -14.
AMA StyleŽeljko Grubač, Nikola Šutulović, Sonja Šuvakov, Djurdja Jerotić, Nela Puškaš, Djuro Macut, Aleksandra Rašić-Marković, Tatjana Simić, Olivera Stanojlović, Dragan Hrnčić. Anxiogenic Potential of Experimental Sleep Fragmentation Is Duration-Dependent and Mediated via Oxidative Stress State. Oxidative Medicine and Cellular Longevity. 2021; 2021 ():1-14.
Chicago/Turabian StyleŽeljko Grubač; Nikola Šutulović; Sonja Šuvakov; Djurdja Jerotić; Nela Puškaš; Djuro Macut; Aleksandra Rašić-Marković; Tatjana Simić; Olivera Stanojlović; Dragan Hrnčić. 2021. "Anxiogenic Potential of Experimental Sleep Fragmentation Is Duration-Dependent and Mediated via Oxidative Stress State." Oxidative Medicine and Cellular Longevity 2021, no. : 1-14.
Background Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology. Methods We compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney). Findings We demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an "epigenetic clock"; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions. Interpretation Taken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia. Funding This work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics.
Sonja Suvakov; Ranine Ghamrawi; Hajrunisa Cubro; Haitao Tu; Wendy M. White; Yvonne S. Butler Tobah; Natasa M. Milic; Joseph P. Grande; Julie M. Cunningham; Fouad T. Chebib; Larissa G.P. Langhi Prata; Yi Zhu; Tamara Tchkonia; James L. Kirkland; Karl A. Nath; Aleksandar Milosavljevic; Vesna D. Garovic. Epigenetic and senescence markers indicate an accelerated ageing-like state in women with preeclamptic pregnancies. EBioMedicine 2021, 70, 1 .
AMA StyleSonja Suvakov, Ranine Ghamrawi, Hajrunisa Cubro, Haitao Tu, Wendy M. White, Yvonne S. Butler Tobah, Natasa M. Milic, Joseph P. Grande, Julie M. Cunningham, Fouad T. Chebib, Larissa G.P. Langhi Prata, Yi Zhu, Tamara Tchkonia, James L. Kirkland, Karl A. Nath, Aleksandar Milosavljevic, Vesna D. Garovic. Epigenetic and senescence markers indicate an accelerated ageing-like state in women with preeclamptic pregnancies. EBioMedicine. 2021; 70 ():1.
Chicago/Turabian StyleSonja Suvakov; Ranine Ghamrawi; Hajrunisa Cubro; Haitao Tu; Wendy M. White; Yvonne S. Butler Tobah; Natasa M. Milic; Joseph P. Grande; Julie M. Cunningham; Fouad T. Chebib; Larissa G.P. Langhi Prata; Yi Zhu; Tamara Tchkonia; James L. Kirkland; Karl A. Nath; Aleksandar Milosavljevic; Vesna D. Garovic. 2021. "Epigenetic and senescence markers indicate an accelerated ageing-like state in women with preeclamptic pregnancies." EBioMedicine 70, no. : 1.
Mechanisms of the brain-related comorbidities in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are still largely unknown, although CP/CPPS is one of the major urological problems in middle-aged men, while these neuropsychological incapacities considerably diminish life quality. The objectives of this study were to assess behavioral patterns in rats with CP/CPPS and to determine whether these patterns depend on alterations in the brain oxidative stress, corticosterone, and hippocampal parvalbumin-positive (PV+) interneurons. Adult male Wistar albino rats from CP/CPPS (intraprostatic injection of 3% λ-carrageenan, day 0) and sham (0.9% NaCl) groups were subjected to pain and anxiety-like behavior tests (days 2, 3, and 7). Afterwards, rats were sacrificed and biochemical and immunohistochemical analyses were performed. Scrotal allodynia and prostatitis were proven in CP/CPPS, but not in sham rats. Ethological tests (open field, elevated plus maze, and light/dark tests) revealed significantly increased anxiety-like behavior in rats with CP/CPPS comparing to their sham-operated mates starting from day 3, and there were significant intercorrelations among parameters of these tests. Increased oxidative stress in the hippocampus, thalamus, and cerebral cortex, as well as increased serum corticosterone levels and decreased number of hippocampal PV+ neurons, was shown in CP/CPPS rats, compared to sham rats. Increased anxiety-like behavior in CP/CPPS rats was significantly correlated with these brain biochemical and hippocampal immunohistochemical alterations. Therefore, the potential mechanisms of observed behavioral alterations in CP/CPPS rats could be the result of an interplay between increased brain oxidative stress, elevated serum corticosterone level, and loss of hippocampal PV+ interneurons.
Nikola Šutulović; Željko Grubač; Sonja Šuvakov; Djurdja Jerotić; Nela Puškaš; Djuro Macut; Aleksandra Rašić-Marković; Tatjana Simić; Olivera Stanojlović; Dragan Hrnčić. Experimental Chronic Prostatitis/Chronic Pelvic Pain Syndrome Increases Anxiety-Like Behavior: The Role of Brain Oxidative Stress, Serum Corticosterone, and Hippocampal Parvalbumin-Positive Interneurons. Oxidative Medicine and Cellular Longevity 2021, 2021, 1 -17.
AMA StyleNikola Šutulović, Željko Grubač, Sonja Šuvakov, Djurdja Jerotić, Nela Puškaš, Djuro Macut, Aleksandra Rašić-Marković, Tatjana Simić, Olivera Stanojlović, Dragan Hrnčić. Experimental Chronic Prostatitis/Chronic Pelvic Pain Syndrome Increases Anxiety-Like Behavior: The Role of Brain Oxidative Stress, Serum Corticosterone, and Hippocampal Parvalbumin-Positive Interneurons. Oxidative Medicine and Cellular Longevity. 2021; 2021 ():1-17.
Chicago/Turabian StyleNikola Šutulović; Željko Grubač; Sonja Šuvakov; Djurdja Jerotić; Nela Puškaš; Djuro Macut; Aleksandra Rašić-Marković; Tatjana Simić; Olivera Stanojlović; Dragan Hrnčić. 2021. "Experimental Chronic Prostatitis/Chronic Pelvic Pain Syndrome Increases Anxiety-Like Behavior: The Role of Brain Oxidative Stress, Serum Corticosterone, and Hippocampal Parvalbumin-Positive Interneurons." Oxidative Medicine and Cellular Longevity 2021, no. : 1-17.
Background: Increased oxidative stress is a hallmark of end-stage renal disease. Hemodialysis (HD) patients lacking glutathione transferase M1 (GSTM1) enzyme activity exhibit enhanced oxidative DNA damage and higher mortality rate than those with active GSTM1 enzyme. To our knowledge, this is the first study to use the vitamin E-bonded membranes (VEM) in patients with homozygous GSTM1 gene deletion, and we aimed to determine the effect of VEM on oxidative and inflammatory status in HD patients with homozygous GSTM1 gene deletion. Methods: GSTM1 genotypes were determined by polymerase chain reaction (PCR) in 170 chronic HD patients. Those with GSTM1-null genotype were randomized and 80 were included in the study. Forty of them were dialyzed for three months with VEM, while the other forty were dialyzed with high-flux same-surface polysulfone dialyzers. Markers of protein and lipid oxidative damage and inflammation (thiol groups, malondialdehyde (MDA), Interleukin-6 (IL-6)), together with plasma antioxidant activity (glutathione peroxidase (GPX), superoxide dismutase (SOD)) were determined. Results: Seventy-five patients finished the study. There were no differences at baseline in markers of protein and lipid oxidative damage, inflammation and plasma antioxidant activity. After three months of therapy, GPX, MDA, and thiol groups increased significantly in both groups, but without statistical significance between groups. SOD and C reactive protein (CRP) did not change significantly during the three-month period. IL-6 increased in the control group, and at the same time, decreased in the VEM group, but without statistical significance. Hemoglobin (Hb) value, red blood cells, erythropoiesis resistance index (ERI), serum ferritin and iron did not change significantly within or between groups. Regarding other laboratory parameters, proteins, albumins, triglycerides, serum phosphorus, serum bicarbonate and Kt/V showed significant improvements within groups but with no significant difference between groups. Conclusions: Our data shows that therapy with VEM over three months had no benefit over standard polysulfone membrane in decreasing by-products of oxidative stress and inflammation in dialysis patients lacking GSTM1 enzyme activity.
Petar Djuric; Sonja Suvakov; Tatjana Simic; Dragana Markovic; Djurdja Jerotic; Aleksandar Jankovic; Ana Bulatovic; Jelena Tosic Tosic Dragovic; Tatjana Damjanovic; Jelena Marinkovic; Radomir Naumovic; Nada Dimkovic. Vitamin E-Bonded Membranes Do Not Influence Markers of Oxidative Stress in Hemodialysis Patients with Homozygous Glutathione Transferase M1 Gene Deletion. Toxins 2020, 12, 352 .
AMA StylePetar Djuric, Sonja Suvakov, Tatjana Simic, Dragana Markovic, Djurdja Jerotic, Aleksandar Jankovic, Ana Bulatovic, Jelena Tosic Tosic Dragovic, Tatjana Damjanovic, Jelena Marinkovic, Radomir Naumovic, Nada Dimkovic. Vitamin E-Bonded Membranes Do Not Influence Markers of Oxidative Stress in Hemodialysis Patients with Homozygous Glutathione Transferase M1 Gene Deletion. Toxins. 2020; 12 (6):352.
Chicago/Turabian StylePetar Djuric; Sonja Suvakov; Tatjana Simic; Dragana Markovic; Djurdja Jerotic; Aleksandar Jankovic; Ana Bulatovic; Jelena Tosic Tosic Dragovic; Tatjana Damjanovic; Jelena Marinkovic; Radomir Naumovic; Nada Dimkovic. 2020. "Vitamin E-Bonded Membranes Do Not Influence Markers of Oxidative Stress in Hemodialysis Patients with Homozygous Glutathione Transferase M1 Gene Deletion." Toxins 12, no. 6: 352.
Background and Objectives: One of the most frequent genetic alterations reported to date in prostate cancer (PC) is aberrant methylation of glutathione transferase P1 (GSTP1). Taking into consideration the involvement of oxidative stress in PC pathogenesis and recent advances in scientific understanding of the role of GSTP1*Ala114Val rs1138272 polymorphism in carcinogenesis, we hypothesized that this single-nucleotide polymorphism (SNP) influences the risk of PC independently of, or in combination with, other GST polymorphisms, including GSTP1*IIe105Val rs1695 or GSTM1 and GSTT1 deletion polymorphisms. Materials and Methods: Genotyping was performed in 237 PC cases and in 236 age-matched controls by multiplex polymerase chain reaction (PCR) for deletion of GST polymorphisms and by quantitative PCR for SNPs. Results: We found that carriers of either GSTP1*Val (rs1138272) or GSTP1*Val (rs1695) variant alleles had a PC risk compared to individuals with both referent alleles (OR = 4.93, 95%CI: 2.89–8.40, p < 0.001 and OR = 1.8, 95%CI: 1.19–2.73, p = 0.006, respectively). Additionally, in a haplotype analysis we found that individuals with GSTP1*C haplotype, represented by both variant alleles (GSTP1*Val rs1695 + GSTP1*Val rs1138272), had a 5.46 times higher risk of PC development compared to individuals with the most frequent haplotype (95%CI = 2.56–11.65, p < 0.001), suggesting a potential role of those variants in PC susceptibility. A regression analysis on the number of risk-associated alleles per individual (GSTM1*active, GSTT1*null, GSTP1*Val rs1695 and GSTP1*Val rs1138272) showed a significant increase in the risk of developing PC, from 3.65-fold in carriers of two risk alleles (95%CI = 1.55–8.61, p = 0.003) to an approximately 12-fold increase in carriers of all four risk alleles (95%CI = 3.05–44.93, p < 0.001). Conclusion: Prostate cancer may be influenced by multiple glutathione transferase (GST) polymorphic genes, especially GSTP1, highlighting the role of gene–gene interactions in human susceptibility to this cancer.
Veljko Santric; Milica Djokic; Sonja Suvakov; Marija Pljesa-Ercegovac; Marina Nikitovic; Tanja Radic; Miodrag Acimovic; Vesna Stankovic; Uros Bumbasirevic; Bogomir Milojevic; Uros Babic; Zoran Dzamic; Tatjana Simic; Dejan Dragicevic; Ana Savic-Radojevic. GSTP1 rs1138272 Polymorphism Affects Prostate Cancer Risk. Medicina 2020, 56, 128 .
AMA StyleVeljko Santric, Milica Djokic, Sonja Suvakov, Marija Pljesa-Ercegovac, Marina Nikitovic, Tanja Radic, Miodrag Acimovic, Vesna Stankovic, Uros Bumbasirevic, Bogomir Milojevic, Uros Babic, Zoran Dzamic, Tatjana Simic, Dejan Dragicevic, Ana Savic-Radojevic. GSTP1 rs1138272 Polymorphism Affects Prostate Cancer Risk. Medicina. 2020; 56 (3):128.
Chicago/Turabian StyleVeljko Santric; Milica Djokic; Sonja Suvakov; Marija Pljesa-Ercegovac; Marina Nikitovic; Tanja Radic; Miodrag Acimovic; Vesna Stankovic; Uros Bumbasirevic; Bogomir Milojevic; Uros Babic; Zoran Dzamic; Tatjana Simic; Dejan Dragicevic; Ana Savic-Radojevic. 2020. "GSTP1 rs1138272 Polymorphism Affects Prostate Cancer Risk." Medicina 56, no. 3: 128.
ObjectivesPreeclampsia is a cardiovascular pregnancy complication which occurs in 5-10% of pregnancies that can lead to a number of pregnancy complications including maternal and foetal death. Long-term, preeclampsia is associated with up to 8-fold increased risk of cardiovascular disease (CVD) for both mothers and their offspring. The lack of mechanistic data in relation to the causes or consequences of preeclampsia has prevented the development of effective therapeutic or monitoring strategies.Study designThis study investigates common underlying mechanisms of preeclampsia and CVD, specifically hypertension and heart failure with preserved ejection fraction (HFpEF) using “in silico” approach of publicly available datasets. Integrated techniques were designed to mine data repositories and identify relevant biomarkers associated with these three conditions.Main outcomes measuresThe knowledge base tools were employed that enabled the analysis of these biomarkers to discover potential molecular and biological links between these three conditions.ResultsOur bioinformatics “in silico” analyses of the publically available datasets identified 76 common biomarkers between preeclampsia, hypertension and HFpEF. These biomarkers were representative of 29 pathways commonly enriched across the three conditions which were largely related to inflammation, metabolism, angiogenesis, remodelling, haemostasis, apoptosis, endoplasmic reticulum (ER) stress signalling and the renin-angiotensin-aldosterone (RAAS) system.ConclusionsThis bioinformatics approach which uses the wealth of scientific data available in public repositories can be helpful to gain a deeper understanding of the overlapping pathogenic mechanisms of associated diseases, which could be explored as biomarkers or targets to prevent long-term cardiovascular complications such as hypertension and HFpEF following preeclampsia.HighlightsWomen with preeclampsia have increased risk of cardiovascular disease later in life but the mechanism is poorly understood.“In silico” analyses of publically available datasets provided overlapping biomarkers and pathogenic pathways between preeclampsia, hypertension and heart failure with preserved ejection fraction (HFpEF).These data could be utilised in the future studies that may lead to the development of better risk stratification strategies or preventative treatments for women post preeclampsia.
Sonja Suvakov; Emma Bonner; Valentina Nikolic; Djurdja Jerotic; Tatjana P Simic; Vesna D Garovic; Guillermo Lopez-Campos; Lana McClements. Overlapping Pathogenic Signalling Pathways and Biomarkers in Preeclampsia and Cardiovascular Disease. 2020, 1 .
AMA StyleSonja Suvakov, Emma Bonner, Valentina Nikolic, Djurdja Jerotic, Tatjana P Simic, Vesna D Garovic, Guillermo Lopez-Campos, Lana McClements. Overlapping Pathogenic Signalling Pathways and Biomarkers in Preeclampsia and Cardiovascular Disease. . 2020; ():1.
Chicago/Turabian StyleSonja Suvakov; Emma Bonner; Valentina Nikolic; Djurdja Jerotic; Tatjana P Simic; Vesna D Garovic; Guillermo Lopez-Campos; Lana McClements. 2020. "Overlapping Pathogenic Signalling Pathways and Biomarkers in Preeclampsia and Cardiovascular Disease." , no. : 1.
Background and Objectives: Experimental data show that superoxide dismutase 2 (SOD2) is involved in ochratoxin (OTA)-induced nephrotoxicity, whereas clinical data indicate the role of SOD2 rs4880 or glutathione peroxidase 1 (GPX1) rs1050450 polymorphisms in end-stage renal disease and urothelial carcinoma risk, known to be the major complications of Balkan endemic nephropathy (BEN). Therefore, we hypothesized that SOD2 and GPX1 gene polymorphisms would influence the risk of BEN and its associated tumors. Materials and Methods: The study was conducted in 207 BEN patients and 86 controls from endemic areas. Results: Individuals with both copies of variant SOD2 allele, known for lower mitochondrial antioxidant protection, are at a significantly higher BEN risk (OR = 2.6, p = 0.021). No association was observed between GPX1 gene polymorphism and BEN risk. Combining SOD2 and GPX1 genotypes did not alter the risk of BEN development. Regarding the risk of urothelial tumors in BEN patients, none of the polymorphisms studied was significantly associated with the risk of these tumors. Conclusions: Polymorphism in SOD2 rs4880 gene affects the risk of BEN development. Hence, SOD2 genotyping could, together with a panel of other enzymes, be used as a biomarker of susceptibility in BEN areas.
Biljana Dragicevic; Sonja Suvakov; Djurdja Jerotic; Zorica Reljic; Ljubica Djukanovic; Ivanka Zelen; Marija Pljesa-Ercegovac; Ana Savic-Radojevic; Tatjana Simic; Dejan Dragicevic; Marija Matic. Association of SOD2 (rs4880) and GPX1 (rs1050450) Gene Polymorphisms with Risk of Balkan Endemic Nephropathy and its Related Tumors. Medicina 2019, 55, 435 .
AMA StyleBiljana Dragicevic, Sonja Suvakov, Djurdja Jerotic, Zorica Reljic, Ljubica Djukanovic, Ivanka Zelen, Marija Pljesa-Ercegovac, Ana Savic-Radojevic, Tatjana Simic, Dejan Dragicevic, Marija Matic. Association of SOD2 (rs4880) and GPX1 (rs1050450) Gene Polymorphisms with Risk of Balkan Endemic Nephropathy and its Related Tumors. Medicina. 2019; 55 (8):435.
Chicago/Turabian StyleBiljana Dragicevic; Sonja Suvakov; Djurdja Jerotic; Zorica Reljic; Ljubica Djukanovic; Ivanka Zelen; Marija Pljesa-Ercegovac; Ana Savic-Radojevic; Tatjana Simic; Dejan Dragicevic; Marija Matic. 2019. "Association of SOD2 (rs4880) and GPX1 (rs1050450) Gene Polymorphisms with Risk of Balkan Endemic Nephropathy and its Related Tumors." Medicina 55, no. 8: 435.
The oxidative stress response via Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) interlinks inflammation- and metabolism-related pathways in chronic kidney disease. We assessed the association between polymorphisms in Nrf2, superoxide dismutase (SOD2), glutathione peroxidase (GPX1), and the risk of end-stage renal disease (ESRD). The modifying effect of these polymorphisms on both oxidative phenotype and ESRD prognosis, both independently and/or in combination with the glutathione S-transferase M1 (GSTM1) deletion polymorphism, was further analyzed. Polymorphisms in Nrf2 (rs6721961), SOD2 (rs4880), GPX1 (rs1050450), and GSTM1 were determined by PCR in 256 ESRD patients undergoing hemodialysis and 374 controls. Byproducts of oxidative stress were analyzed spectrophotometically or by ELISA. Time-to-event modeling was performed to evaluate overall survival and cardiovascular survival. The SOD2 Val/Val genotype increased ESRD risk (OR = 2.01, p = 0.002), which was even higher in combination with the GPX1 Leu/Leu genotype (OR = 3.27, p = 0.019). Polymorphism in SOD2 also showed an effect on oxidative phenotypes. Overall survival in ESRD patients was dependent on a combination of the Nrf2 (C/C) and GPX1 (Leu/Leu) genotypes in addition to a patients’ age and GSTM1 polymorphism. Similarly, the GPX1 (Leu/Leu) genotype contributed to longer cardiovascular survival. Conclusions: Our results show that SOD2, GPX1, and Nrf2 polymorphisms are associated with ESRD development and can predict survival.
Djurdja Jerotic; Marija Matic; Sonja Suvakov; Katarina Vucicevic; Tatjana Damjanovic; Ana Savic-Radojevic; Marija Pljesa-Ercegovac; Vesna Coric; Aleksandra Stefanovic; Jasmina Ivanisevic; Zorana Jelic-Ivanovic; Lana McClements; Nada Dimkovic; Tatjana Simic. Association of Nrf2, SOD2 and GPX1 Polymorphisms with Biomarkers of Oxidative Distress and Survival in End-Stage Renal Disease Patients. Toxins 2019, 11, 431 .
AMA StyleDjurdja Jerotic, Marija Matic, Sonja Suvakov, Katarina Vucicevic, Tatjana Damjanovic, Ana Savic-Radojevic, Marija Pljesa-Ercegovac, Vesna Coric, Aleksandra Stefanovic, Jasmina Ivanisevic, Zorana Jelic-Ivanovic, Lana McClements, Nada Dimkovic, Tatjana Simic. Association of Nrf2, SOD2 and GPX1 Polymorphisms with Biomarkers of Oxidative Distress and Survival in End-Stage Renal Disease Patients. Toxins. 2019; 11 (7):431.
Chicago/Turabian StyleDjurdja Jerotic; Marija Matic; Sonja Suvakov; Katarina Vucicevic; Tatjana Damjanovic; Ana Savic-Radojevic; Marija Pljesa-Ercegovac; Vesna Coric; Aleksandra Stefanovic; Jasmina Ivanisevic; Zorana Jelic-Ivanovic; Lana McClements; Nada Dimkovic; Tatjana Simic. 2019. "Association of Nrf2, SOD2 and GPX1 Polymorphisms with Biomarkers of Oxidative Distress and Survival in End-Stage Renal Disease Patients." Toxins 11, no. 7: 431.
Newly discovered glutathione transferase omega 1 (GSTO1-1) plays an important role in the glutathionylation cycle, a significant mechanism of protein function regulation. GSTO1-1 expression pattern has not been studied in transitional cell carcinoma (TCC), as yet. A total of 56 TCC tumor and corresponding non-tumor specimens were investigated. Glutathione content and thioltransferase activity were measured spectrophotometrically. Protein-glutathione mixed disulfides were measured fluorimetrically. GSTO1-1 expression was determined by immunoblot and qPCR. Immunoprecipitation with GSTO1-1 antibody was followed by immunoblot using anti-GSTO1, GSTP1, c-Jun, JNK, Akt, phospho-Akt, and ASK1 antibody, while for the total S-glutathionylation levels non-reducing electrophoresis was performed. The contents of reduced glutathione and thioltransferase activity were significantly increased in tumor compared to non-tumor tissue. The increased GSTO1 expression in tumor tissue showed clear correlation with grade and stage. However, decreased total protein glutathionylation level in tumor compared to non-tumor samples was found. Immunoprecipitation has shown an association of GSTO1-1 with GSTP1, Akt, phospho-Akt, and ASK1 proteins. GSTO1 deglutathionylase activity suggests its potential important role in redox perturbations present in TCC. Increased GSTO1-1 expression might contribute to TCC development and/or progression supporting the notion that GSTO1-1 may be a promising novel cancer target.
Tatjana Djukic; Tatjana Simic; Marija Pljesa-Ercegovac; Marija Matic; Sonja Suvakov; Vesna Coric; Dejan Dragicevic; Ana Savic-Radojevic. Upregulated glutathione transferase omega-1 correlates with progression of urinary bladder carcinoma. Redox Report 2017, 22, 486 -492.
AMA StyleTatjana Djukic, Tatjana Simic, Marija Pljesa-Ercegovac, Marija Matic, Sonja Suvakov, Vesna Coric, Dejan Dragicevic, Ana Savic-Radojevic. Upregulated glutathione transferase omega-1 correlates with progression of urinary bladder carcinoma. Redox Report. 2017; 22 (6):486-492.
Chicago/Turabian StyleTatjana Djukic; Tatjana Simic; Marija Pljesa-Ercegovac; Marija Matic; Sonja Suvakov; Vesna Coric; Dejan Dragicevic; Ana Savic-Radojevic. 2017. "Upregulated glutathione transferase omega-1 correlates with progression of urinary bladder carcinoma." Redox Report 22, no. 6: 486-492.
Chronic kidney disease is described as a progressive and irreversible deterioration in kidney function. When there is less than 10% of nephron function pertained, patients face end-stage renal disease, where renal replacement therapy is needed. Data show that the most common method used to treat advanced and permanent kidney failure is hemodialysis. . Increased oxidative stress is a hallmark of end-stage renal disease (ESRD). Glutathione S-transferases (GST) are involved in the detoxification of xenobiotics and protection of oxidative damage. The role of genetic polymorphism of antioxidant enzymes GSTA1, GSTM1, GSTP1 and GSTT1 in susceptibility towards end-stage renal disease development has become prominent recently. Furthermore, GST gene polymorphism may modulate the degree of oxidative stress byproducts in end-stage renal disease patients and, therefore, influence their overall and cause-specific cardiovascular mortality.
Sonja Suvakov; Tatjana Simic; Tatjana Damjanovic; Šuvakov Sonja; Simić Tatjana. Glutathione transferase gene polymorphism in end stage renal disease. Medicinski podmladak 2016, 67, 36 -41.
AMA StyleSonja Suvakov, Tatjana Simic, Tatjana Damjanovic, Šuvakov Sonja, Simić Tatjana. Glutathione transferase gene polymorphism in end stage renal disease. Medicinski podmladak. 2016; 67 (3):36-41.
Chicago/Turabian StyleSonja Suvakov; Tatjana Simic; Tatjana Damjanovic; Šuvakov Sonja; Simić Tatjana. 2016. "Glutathione transferase gene polymorphism in end stage renal disease." Medicinski podmladak 67, no. 3: 36-41.
The presence of glutathione transferase (GST) M1 null genotype (GSTM1-null) in end-stage renal disease (ESRD) patients is associated with lower overall survival rate in comparison to those with GSTM1-active variants. We examined association between GSTM1 and GSTT1 deletion polymorphisms as well as SNPs in GSTA1/rs3957357 and GSTP1/rs1695 genes with overall and cause-specific cardiovascular mortality in ESRD patients.
Sonja Suvakov; Tatjana Damjanovic; Tatjana Pekmezovic; Jovana Jakovljevic; Ana Savic-Radojevic; Marija Pljesa-Ercegovac; Slavica Radovanovic; Dragan V Simic; Steva Pljesa; Milos Zarkovic; Jasmina Mimic-Oka; Nada Dimkovic; Tatjana Simic. Associations of GSTM1*0 and GSTA1*Agenotypes with the risk of cardiovascular death among hemodialyses patients. BMC Nephrology 2014, 15, 12 -12.
AMA StyleSonja Suvakov, Tatjana Damjanovic, Tatjana Pekmezovic, Jovana Jakovljevic, Ana Savic-Radojevic, Marija Pljesa-Ercegovac, Slavica Radovanovic, Dragan V Simic, Steva Pljesa, Milos Zarkovic, Jasmina Mimic-Oka, Nada Dimkovic, Tatjana Simic. Associations of GSTM1*0 and GSTA1*Agenotypes with the risk of cardiovascular death among hemodialyses patients. BMC Nephrology. 2014; 15 (1):12-12.
Chicago/Turabian StyleSonja Suvakov; Tatjana Damjanovic; Tatjana Pekmezovic; Jovana Jakovljevic; Ana Savic-Radojevic; Marija Pljesa-Ercegovac; Slavica Radovanovic; Dragan V Simic; Steva Pljesa; Milos Zarkovic; Jasmina Mimic-Oka; Nada Dimkovic; Tatjana Simic. 2014. "Associations of GSTM1*0 and GSTA1*Agenotypes with the risk of cardiovascular death among hemodialyses patients." BMC Nephrology 15, no. 1: 12-12.