Acute Renal Failure and Thiol-Disulfide Homeostasis

Otal, Yavuz; Demircan, Serkan; Şener, Alp; Alışık, Murat; Tanrıverdi, Fatih; Haydar, Fadime Güllü; Özhasenekler, Ayhan; Erel, Özcan

doi:10.4172/2161-0959.1000312

Cited by 15 publications

(14 citation statements)

References 21 publications

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“…More studies are needed for evaluating its role in early or advanced ccRCC. TDH status was used to evaluate the severity of multiple renal and inflammatory diseases (urolithiasis, obstructive uropathy, urinary tract infections, autosomal dominant polycystic disease, acute renal failure, chronic kidney disease, hemodialysis, peritoneal dialysis, renal transplantation) [ 29 , 30 , 31 , 32 , 34 , 35 , 63 , 64 , 65 ].…”

Section: Discussionmentioning

confidence: 99%

“…A dynamic thiol/disulfide equilibrium is pivotal in organizing antioxidant protection, xenobiotics detoxification, apoptosis, enzymatic regulation, transcription, cell division, cell growth, immune response, signal transduction, and cellular signal-transfer mechanisms [ 26 , 27 , 28 ]. The balance between the serum levels of thiol-proteins (albumin, cysteine, cysteinyl-glycine, glutathione, homocysteine, γ-glutamyl-cysteine-albumin) and the disulfides plays a protective role in cellular redox homeostasis [ 26 , 29 ]. In the literature, abnormal thiol/disulfide homeostasis was not evaluated in cancer patients, but it was associated with urolithiasis, hemodialysis, peritoneal dialysis, renal transplantation patients, acute renal failure, chronic kidney disease, obstructive uropathy, autosomal dominant polycystic kidney disease, urinary tract infections, and malignancy [ 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 ].…”

Section: Introductionmentioning

confidence: 99%

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Posttranslational Modifications Pattern in Clear Cell Renal Cell Carcinoma

et al. 2020

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Posttranslational modifications are dynamic enzymatic-mediated processes, regulated in time and space, associated with cancer development. We aimed to evaluate the significance of posttranslational modifications in the pathogenesis of clear cell renal cell carcinoma. The authors developed a prospective, observational study during a period of three years and included 55 patients with localized renal cell carcinoma and 30 heathy subjects. Glycosylation, nitration and carbonylation, thiol-disulfide homeostasis, methylation, phosphorylation and proteolytic cleavage were evaluated in the serum of the evaluated subjects in the present study. Our results showed some characteristics for early ccRCC: high production of cytokines, substrate hypersialylation, induced nitrosative and carbonylic stress, arginine hypermethylation, thiol/disulfide homeostasis (TDH) alteration, the regulatory role of soluble receptors (sRAGE—soluble receptor for advanced glycation end products, sIL-6R—soluble receptor for Interleukin 6) in RAGE and IL-6 signaling, the modulatory effect of TK1—thymidine kinase 1 and TuM2-PK—tumoral pyruvate-kinase 2 in controlling the level of phosphometabolites in neoplastic cells. These data could be the initial point for development of a panel of biomarkers such as total sialic acid, orosomucoids, nitrotyrosine, carbonylic metabolites, Asymmetric Dimethylarginines (ADMA), Symmetric Dimethylarginines (SDMA), and thiol-disulfide equilibrium for early diagnosis of ccRCC. Moreover, they could be considered a specific disease posttranslational modification signature which underlines the transition from early to advanced stages in this neoplasia, and of a therapeutic target in kidney oncogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Posttranslational Modifications Pattern in Clear Cell Renal Cell Carcinoma

et al. 2020

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“…The plasma thiol signaling network has been subject to investigation in several other diseases, including CVD, acute and chronic renal failure, diabetes mellitus, familial hypercholesterolemia, and rheumatoid arthritis (Banne et al, 2003; Giustarini et al, 2005; Wlodek et al, 2006; Kundi et al, 2015; Qian et al, 2015; Ates et al, 2016; Koning et al, 2016; Cortese-Krott et al, 2017; Otal et al, 2018; Simsek et al, 2018). In all these studies, significant disturbances of the plasma thiol/disulfide balance were reported, with increased oxidized thiol forms (disulfides) and decreased free thiols, as compared to healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Crohn’s Disease in Clinical Remission Is Marked by Systemic Oxidative Stress

et al. 2019

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Introduction: Crohn’s disease (CD) is characterized by chronic and relapsing inflammation of the gastro-intestinal tract. It is assumed that oxidative stress contributes to CD pathogenesis, but systemic biomarkers for oxidative stress in CD are not yet identified. A reduction in free thiol groups in plasma proteins (“plasma free thiols”) reflects systemic oxidative stress since they are prime substrates for reactive oxygen species. Here, we determined the concentrations of plasma free thiols in CD patients and healthy controls and studied the putative correlation with disease parameters. Methods: Free thiols were quantified in plasma of patients with CD in clinical remission [according to the Harvey Bradshaw Index (HBI)] and healthy controls and adjusted for plasma albumin. Albumin-adjusted free thiol concentrations were analyzed for associations with clinical and biochemical disease markers. Results: Mean plasma free thiol concentrations were significantly lower in patients with CD ( n = 51) compared to healthy controls ( n = 27) (14.7 ± 2.4 vs. 17.9 ± 1.8 μmol/g albumin; P < 0.001). Patients with CD with above-average free thiols had significantly lower CRP levels (median 1.4 [interquartile range] [0.4; 2.6] vs. 3.6 [0.6; 7.0] mg/L; P < 0.05) and BMI (23.6 ± 4.8 vs. 27.1 ± 5.2 kg/m 2 ; P < 0.05). Patients with CD having solely colonic disease demonstrated markedly reduced plasma free thiol concentrations compared to patients with ileocolonic involvement (13.2 ± 1.8 vs. 15.2 ± 2.2 μmol/g; P < 0.05). Finally, plasma free thiol concentrations negatively correlated with biomarkers of inflammation, including hsCRP, SAA, IL-17A (all P < 0.05), and VEGF. Conclusion: Plasma free thiols are reduced in patients with CD in clinical remission compared to healthy controls. Thus, subclinical CD disease activity is reflected by systemic oxidative stress and plasma free thiols may be a relevant therapeutic target and biomarker to monitor disease activity in CD.

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“…[3,4] Since thiols have continuous interaction with almost all of the physiological oxidants, they are essential antioxidant buffers. [15,16] Thiol protein groups constitute a significant antioxidant group and are responsible for 52.9% of the total serum antioxidant capacity in healthy people. [17] A new and automated testing system was proposed by Erel and Neselioglu [5] to determine the dynamic thiol/disulphide homeostasis.…”

Section: Discussionmentioning

confidence: 99%

The thiol-disulphide homeostasis in patients with acute pancreatitis and its relation with other blood parameters

Haydar¹,

Otal²,

Şener³

et al. 2019

Ulus Travma Acil Cerrahi Derg

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BACKGROUND: Acute pancreatitis is a common disease seen in emergency departments because of abdominal pain. The present study aims to evaluate the relation between measurements of thiol-disulfide parameters in patients diagnosed with acute pancreatitis and other blood parameters. METHODS: A total of 56 (56%) patients, who were admitted to the emergency department, and 44 (44%) healthy volunteers participated in this study. A total of 100 samples were taken from the participants. Detailed blood samples were taken from the patients at the time of arrival at the hospital. The thiol-disulfide level in serum was examined using a brand new method that was developed by Erel and Neşelioğlu in the venous blood samples of the patients who were diagnosed with acute pancreatitis during the admission. The data were evaluated in the computer medium. RESULTS: Gallstones were defined as the etiology of AP in 41 patients (73.2%); in one patient, hypertriglyceridemia (1.7%); in four patients, alcohol use (7.1%), and idiopathic 10 patients (17.8%). While the blood thiol levels were low, the disulfide levels were high at a significant level. No statistically significant relations were detected between the amylase, lipase, neutrophil lymphocyte ratio (NLR), which are other blood parameters, and thiol-disulfide balance parameters. CONCLUSION: The disruption of the thiol-disulfide balance may play a role in the pathogenesis of acute pancreatitis. In acute pancreatitis, since the thiol level is decreased in the blood, administration of the complementary therapies for this thiol deficiency may contribute to the treatment of the disease.

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Acute Renal Failure and Thiol-Disulfide Homeostasis

Cited by 15 publications

References 21 publications

Posttranslational Modifications Pattern in Clear Cell Renal Cell Carcinoma

Posttranslational Modifications Pattern in Clear Cell Renal Cell Carcinoma

Crohn’s Disease in Clinical Remission Is Marked by Systemic Oxidative Stress

The thiol-disulphide homeostasis in patients with acute pancreatitis and its relation with other blood parameters

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