Serum malondialdehyde levels, myeloperoxidase and catalase activities in patients with nephrotic syndrome

Beğenik, Hüseyin; Soyoral, Yasemin Usul; Erkoç, Reha; Emre, Habib; Taşkın, Abdullah; Taşdemir, Mehmet; Aslan, Mehmet

doi:10.1179/1351000213y.0000000048

Cited by 27 publications

(18 citation statements)

References 38 publications

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“…We also showed that 3‐AT significantly increased plasma MDA level (Fig. B ), which is consistent with higher plasma MDA in patients with lower catalase activity (Begenik et al., ). Notably, the inconsistency between lower myocardial and higher plasma MDA levels following 4‐MP, 3‐AT, or their combination (Fig.…”

Section: Discussionsupporting

confidence: 88%

Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats

Yao

Abdel‐Rahman

2017

Alcohol Clin Exp Res

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Background Ethanol-evoked oxidative stress, which contributes to myocardial dysfunction in proestrus rats, is mediated by increases in NADPH oxidase activity, malondialdehyde (MDA) and ERK1/2 phosphorylation. Whether these biochemical responses, which are triggered by alcohol-derived acetaldehyde in non-cardiac tissues, occur in proestrus rats’ hearts remains unknown. Therefore, we elucidated the roles of alcohol dehydrogenase (ADH), cytochrome P4502E1 (CYP2E1) and catalase, which catalyze alcohol oxidation to acetaldehyde, in these alcohol-evoked biochemical and hemodynamic responses in proestrus rats. Method Conscious proestrus rats prepared for measurements of left ventricular (LV) function and blood pressure (BP) received ethanol (1.5 g/kg, i.v infusion over 30 min) or saline 30 min after an ADH and CYP2E1 inhibitor, 4-MP (82 mg/kg, i.p), a catalase inhibitor, 3-AT (0.5 g/kg, i.v), their combination or vehicle. LV function and BP were monitored for additional 60 min after ethanol or saline infusion before collecting the hearts for ex vivo measurements of LV reactive oxygen species (ROS), NADPH oxidase activity, MDA, and ERK1/2 phosphorylation. Results Ethanol reduced LV function (dP/dtmax and LVDP) and BP, and increased cardiac NADPH oxidase activity, ROS and MDA levels, and ERK1/2 phosphorylation. Either inhibitor partially, and their combination significantly, attenuated these responses despite the substantially higher blood ethanol level, and the increased cardiac oxidative stress and reduced BP caused by 3-AT alone or with 4-MP. The inhibitors reduced cardiac MDA level and reversed ethanol effect on cardiac and plasma MDA. Conclusions Ethanol oxidative metabolism plays a pivotal role in the ethanol-evoked LV oxidative stress and dysfunction in proestrous rats. Notably, catalase inhibition (3-AT) caused cardiac oxidative stress and hypotension.

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Section: Discussionsupporting

confidence: 88%

Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats

Yao

Abdel‐Rahman

2017

Alcohol Clin Exp Res

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“…This is in agreement with published data showing improved endothelial function 24 hours after levosimendan treatment 18 , as leukocyte activation and especially MPO activity can significantly impair endothelial function 8 . Avgeropoulou and colleagues have found a decrease in MDA, a marker of oxidative stress, at day 5 after levosimendan treatment 26 , which supports our hypothesis of diminished PMN degranulation and MPO activity after levosimendan treatment, as MPO activity and MDA-levels usually correlate well 27 .…”

Section: Discussionsupporting

confidence: 86%

Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure

Adam

Meyer

Knors

et al. 2015

Sci Rep

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Treatment of decompensated heart failure often includes administration of levosimendan. Myeloperoxidase (MPO) is released during polymorphonuclear neutrophil (PMN) degranulation, and mediates dysregulation of vascular tone in heart failure. We evaluated the effects of levosimendan-treatment on MPO in patients with acute decompensation of chronic heart failure over a one week course. Plasma MPO levels were significantly decreased after levosimendan treatment (from 252.1 ± 31.1 pmol/l at baseline to 215.02 ± 27.96 pmol/l at 6 h, p < 0.05). Ex vivo incubation of whole blood with levosimendan decreased MPO release after PMN-stimulation (8.2 ± 1.4-fold increase at baseline vs. 6.0 ± 1.1-fold increase with levosimendan). MPO levels also significantly correlated with diastolic blood pressure over the time course. In a multivariate linear model, the main contributor to systolic, diastolic and mean blood pressure was level of PMN elastase. MPO contributed only in heparin-treated patients, suggesting a more significant role for endothelial-bound MPO than for circulating MPO or elastase with respect to blood pressure regulation. We here provide the first evidence that levosimendan treatment inhibits MPO release by PMNs in decompensated heart failure patients. This mechanism may regulate endothelial function and vascular tone in heart failure patients.

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“…An increased activity of NOX through increased expression of NOX gene in patients with INS would indicate higher cellular oxidative stress in PBL that may impair the structure and function of blood lymphocytes to compromise the immune system. Impairment of antioxidant enzymes such as catalase, myeloperoxidase, and SOD in plasma/serum of patients with INS has also been reported earlier (26). Increased levels of malondialdehyde, an index of lipid peroxidation, observed in our patients support earlier studies that suggest an increased cellular oxidative stress in NS.…”

Section: Discussionsupporting

confidence: 91%

NOX-mediated impairment of PDGF-induced DNA synthesis in peripheral blood lymphocytes of children with idiopathic nephrotic syndrome

Al‐Eisa

Dhaunsi

2017

Pediatr Res

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BackgroundCellular oxidative stress, inflammatory responses, and immunogenic events are involved in pathogenesis of idiopathic nephrotic syndrome (INS); however, the exact mechanism remains unknown. We examined NADPH oxidase (NOX) activity and platelet-derived growth factor (PDGF)-induced DNA synthesis in peripheral blood lymphocytes (PBL) of patients with INS.MethodsPBL from 15 patients with INS and 15 age- and gender-matched controls were isolated, and enzyme activities of NOX, catalase, and superoxide dismutase (SOD) were measured along with the assay of malondialdehyde levels and bromo-deoxyuridine incorporation. Protein expression of NOX-1 was measured using western blot analysis.ResultsPatients with INS had significantly (P<0.01) higher NOX activity and increased protein expression of NOX-1 in PBL as compared with controls. Catalase and SOD activities were markedly lower with lipid peroxide levels significantly (P<0.01) increased in patients with INS. Ex vivo DNA synthesis in PDGF-stimulated PBL was significantly (P<0.01) reduced in patients with INS; however, diphenyliodonium, an inhibitor of NOX, markedly corrected impairment in growth factor-induced BrdU incorporation.ConclusionsThese results show that NOX activation might have a role in regulation of lymphocytic activity in patients with INS through the impairment of PDGF mitogenic function and might contribute toward pathogenesis of nephrotic syndrome.

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Serum malondialdehyde levels, myeloperoxidase and catalase activities in patients with nephrotic syndrome

Cited by 27 publications

References 38 publications

Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats

Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats

Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure

NOX-mediated impairment of PDGF-induced DNA synthesis in peripheral blood lymphocytes of children with idiopathic nephrotic syndrome

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