scholarly journals Paraoxonase-1 Enzyme Activity and Oxidative Status in Pulmonary Hypertension Original Article

2020 ◽  
Vol 19 (4) ◽  
pp. 652-658
Author(s):  
Muhsin Kalyoncuoglu ◽  
Murat Baskurt ◽  
Aysem Kaya ◽  
Gunes M Dogan ◽  
Okay Abacl ◽  
...  

Objective: Oxidative stress has been considered to be one of the main causes for the development of pulmonary hypertension (PH) via leading alteration of pulmonary vasomotor tone induced by hypoxia. The aim of this study is to determine the serum paraoxonase-1 enzyme (PON-1) activity, arylesterase activity, the antioxidant-oxidant status in patients with PH and to compare with healthy controls. Material and Methods: Thirty five healthy ındividuals (mean age 45.7±5.9 years) as a control group and thirty eight patients (mean age 46.5±12.6 years) with a diagnosis of PH wereincluded in thestudy. Serum PON-1 and arylesterase activity, the total antioxidative capacity of plasma (TAC) and total oxidantstatus (TOS) were measured by using colorimetric methods. The Oxidative Stress Index (OSI) wascalculated as TOS/ TACX100. Results: Serum PON1 activity is significantly lower in PH patients when compared with healthy controls (p=0.001). The serum arylesterase activity and TAC, TOS and OSI status were similarin bothgroups. There is inverse correlation between serum PON1 activityand NYHA functionalcapacity (r:-0.649 p=0.001). Furthermore, PON1 activity of study patients are similarin the PH subgroups. Serum activity of PON1 wasfoundto bethe only independent parameter for the presence of PH in binary logistic regression analysis (OR 0.984, 95 % CI 0.977-0.992, p=0.001). Eight patients died follow up period (27.6±14.5 months) and none of theparametersincluding PON1 were associated with mortality. Conclusion: Serum PON1 activity of PH patients is lowerthanhealthypopulation, but does not predictmortality. Bangladesh Journal of Medical Science Vol.19(4) 2020 p.652-658

2017 ◽  
Vol 36 (3) ◽  
pp. 243-250 ◽  
Author(s):  
Mustafa Kaplan ◽  
Ihsan Ates ◽  
Mahmut Yüksel ◽  
Yasemin Ozderin Ozin ◽  
Muhammed Yener Akpinar ◽  
...  

SummaryBackground:The objective here is to examine the role of overall oxidative stress in the etiopathogenesis of gluten-sensitive enteropathy disease and its relationship with gluten free diet and autoantibodies.Methods:Eighty gluten-sensitive enteropathy patients and 80 control group participants were included in the study. As oxidative stress parameters, we researched total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), paraoxonase-1 and arylesterase parameters in the serum samples of gluten-sensitive enteropathy patients.Results:In comparison to the control group, gluten-sensitive enteropathy patients had lower TAS, paraoxonase-1 and arylesterase levels and gluten-sensitive enteropathy patients had considerable TOS and OSI levels. In contrast, patients who agreed to the gluten free eating routine had a higher OSI proportion and patients who did not conform to the gluten free eating regimen had a lower paraoxonase-1 level. An affirming reciprocation was de tected amidst TOS and OSI proportion and gluten-sensitive enteropathy autoantibodies and C-reactive protein levels and a negative correlation was found between arylesterase level and gluten-sensitive enteropathy autoantibodies.Conclusions:We observed oxidative stress levels to be higher in gluten-sensitive enteropathy patients contrasted with the control group. Oxidative stress level showed differences in gluten-sensitive enteropathy patients depending on gluten diet content and autoantibody positivity. In point of fact, C-reactive protein and gluten-sensitive enteropathy autoantibodies are identified with oxidative anxiety parameters resulting in the possibility that oxidative stress might be successful in the gluten-sensitive enteropathy pathogenesis.


2000 ◽  
Vol 98 (3) ◽  
pp. 355-363 ◽  
Author(s):  
Bharti MACKNESS ◽  
Paul N. DURRINGTON ◽  
Bashir ABUASHIA ◽  
Andrew J. M. BOULTON ◽  
Michael I. MACKNESS

Human serum paraoxonase 1 (PON1) is located on high-density lipoprotein and has been implicated in the detoxification of organophosphates, and possibly in the prevention of lipid peroxidation of low-density lipoprotein. PON1 has two genetic polymorphisms, both due to amino acid substitutions: one involving glutamine (Q genotype) and arginine (R genotype) at position 192, and the other involving leucine (L genotype) and methionine (M genotype) at position 55. We investigated the effects of these polymorphisms, and of a polymorphism of the PON2 gene at position 310 (Cys/Ser; C and S genotypes respectively), on serum PON1 activity and concentration, plasma lipids and lipoproteins and glycaemic control in 93 individuals with type II diabetes with no complications and in 101 individuals with type II diabetes with retinopathy. Serum PON1 activity in the group with no complications [median 164.1 nmol·min-1·ml-1 (range 8.0–467.8)] was significantly higher than in the group with retinopathy [113.4 nmol·min-1·ml-1 (3.0–414.6)] (P< 0.001), but the serum PON1 concentration was not different between the groups. The gene frequencies of the PON1-55 and PON1-192 polymorphisms and of the PON2-310 polymorphism were not different between the study populations. The PON1-55 and PON1-192 polymorphisms affected PON1 activity in the way described in a previous study of a control group and subjects with type II diabetes. The PON2-310 polymorphism also significantly affected serum PON1. PON1 activity was significantly higher in individuals with the PON2-310 CC genotype in both groups with type II diabetes, and the PON1 concentration was significantly higher in PON2-310 CC homozygotes with no complications than in the group with retinopathy. Neither the PON1-55 nor the PON1-192 polymorphism was correlated with the serum lipid or lipoprotein concentration in either group. In the group with retinopathy (but not the group with no complications), all three PON polymorphisms were correlated with glycaemic control, which was worse for the PON1-55 genotypes in the order MM > LM > LL (P = 0.0032), for the PON1-192 genotypes in the order RR > QR > QQ (P = 0.011) and for the PON2-310 genotypes in the order CC > CS > SS (P = 0.010). Low serum PON1 activity in retinopathy may be related to an increased tendency for lipid peroxidation. Our findings thus raise the possibility that, in retinopathy, the PON2 gene may influence PON1, and that an inter-relationship between the PON1 and PON2 genes may influence glycaemic control in subjects with type II diabetes complicated by retinopathy.


2014 ◽  
Vol 33 (11) ◽  
pp. 1134-1140 ◽  
Author(s):  
S Karadas ◽  
M Aslan ◽  
H Gonullu ◽  
C Kati ◽  
L Duran ◽  
...  

Background: Acetaminophen is at present one of the most commonly used analgesics and antipyretics. Recent evidence has suggested that oxidative stress is involved in the mechanism of acetaminophen intoxication. Paraoxonase-1 (PON1) plays an important role as an endogenous free-radical scavenging molecule. The aim of this study was to evaluate the influence of serum PON1 activity and oxidative stress in patients with acetaminophen intoxication. Methods: A total of 20 patients with acetaminophen intoxication and 25 healthy controls were enrolled. Serum total antioxidant capacity (TAC), lipid hydroperoxide (LOOH) levels, and paraoxonase and arylesterase activities were measured spectrophotometrically. Results: The serum TAC levels and the paraoxonase and arylesterase activities were significantly lower in patients with acetaminophen intoxication compared with controls (all, p < 0.001), while the serum LOOH levels were significantly higher ( p < 0.001). Conclusions: Our results suggest that decreased PON1 activity seems to be associated with increased oxidative stress in patients with acetaminophen intoxication. Measuring serum PON1 activity may be useful in assessing the development of toxicity risk in acetaminophen toxicity. It would be useful to recommend vitamins with antioxidant effects such as vitamins C and E along with medical treatments.


2016 ◽  
Vol 36 (7) ◽  
pp. 663-669
Author(s):  
S Karadas ◽  
M Aslan ◽  
MR Ceylan ◽  
M Sunnetcioglu ◽  
N Bozan ◽  
...  

Introduction: Anthrax is a bacterial disease caused by the aerobic sporeforming bacterium Bacillus anthracis. It has been suggested that oxidative stress plays an important role in the pathogenesis of B. anthracis. The aim of this study was to investigate serum paraoxonase 1 (PON1) activity, catalase activity, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) levels in patients with cutaneous anthrax. Materials and methods: Fifteen patients with cutaneous anthrax and 15 healthy controls were enrolled in this study. The serum MDA levels, SOD levels, paraoxonase, arylesterase, and catalase activities were measured using a spectrophotometer. Results: The serum SOD levels, paraoxonase, arylesterase, and catalase activities were significantly lower in patients with cutaneous anthrax than in controls (for all, p < 0.001), whereas MDA levels were significantly higher ( p < 0.001). No significant correlation was found between serum paraoxonase activity, arylesterase activity, SOD levels, and MDA levels (all, p > 0.05) in patients with cutaneous anthrax. Conclusions: The current study was the first to show decreased antioxidant levels and increased oxidant levels in patients with cutaneous anthrax. Therefore, decreased PON1 activity may play a role in the pathogenesis of cutaneous anthrax.


2010 ◽  
Vol 57 (3) ◽  
Author(s):  
Marija Macan ◽  
Nada Vrkić ◽  
Ana Lucić Vrdoljak ◽  
Božica Radić ◽  
Vlasta Bradamante

We investigated the influence of high sucrose diet (HSD) after 3 or 5 weeks of administration on paraoxonase 1 (PON1) activity in plasma of normolipidemic rats and the relationship between serum PON1 activity, triacylglycerides (TGs), HDL and total cholesterol vs. the control group of rats fed normal, control diet (CD). Because the data about the influence of gemfibrozil (GEM) on PON1 activity are controversial, we also investigated its effects (administration in the 4th and 5th week in rats on HSD and CD) on plasma PON1 activity and lipid levels in normolipidemic rats, and in rats with hypertriglyceridemia caused by HSD. Our results obtained in rats on HSD show a significant increase of plasma TGs levels by 47% (P


2018 ◽  
Vol 8 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Hassan Ahmadvand ◽  
Esmaeel Babaeenezhad ◽  
Maryam Nasri ◽  
Leila Jafaripour ◽  
Reza Mohammadrezaei Khorramabadi

Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR significantly decreased the serum and renal levels of GSH, serum paraoxonase 1 (PON1) activity, and the serum and renal activities of catalase (CAT) and glutathione peroxidase (GPX). GSH administration could significantly improve the serum activities of AST, GGT, MPO, GPX and PON1 and serum levels of NO, renal MDA, GSH levels, and serum and also renal CAT activities. Conclusion: Our study indicated that GSH administration ameliorated RIR injury in rats by improving the activities of liver markers and antioxidant enzymes, the levels of MDA, NO, GSH and MPO activity.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Suzana Bojic ◽  
Jelena Kotur-Stevuljevic ◽  
Nevena Kalezic ◽  
Zorana Jelic-Ivanovic ◽  
Aleksandra Stefanovic ◽  
...  

Introduction. State of severe oxidative stress is encountered in sepsis. Paraoxonase 1 (PON1) protects against oxidative stress but also undergoes inactivation upon that condition. We investigated PON1 activity in surgical patients with sepsis in relation to oxidative stress status, inflammation, disease severity, and survival.Methods. Prospective observational study. Sixty-nine surgical patients with sepsis were compared to 69 age/sex matched healthy controls. PON1 paraoxonase and diazoxonase activities, selected biochemical, hematological and oxidative stress parameters were measured on admission to ICU and 24, 48, 72, and 96 hours later. Disease severity scores were calculated daily.Results. Septic patients had significantly lower PON1 activities compared to control group at all time points. PON1 activities had good capacity to differentiate septic patients from healthy controls. Low PON1 activities were associated with higher disease severity scores and higher risk of death. Correlation between PON1 activity and markers of inflammation failed to reach significance. Decrease in PON1 activity was correlated with an increase in reducing components in plasma.Conclusion. Our study demonstrated lower PON1 activity in surgical patients with sepsis compared to healthy controls. PON1 activity also reflected severity of the disease. Low PON1 activity was associated with higher mortality of surgical patients with sepsis.


2017 ◽  
Vol 15 (1) ◽  
pp. 57
Author(s):  
Natalia D Razgildina ◽  
Valentina V Miroshnikova ◽  
Aleksey V Fomichev ◽  
Ekaterina V Malisheva ◽  
Alexandra A Panteleeva ◽  
...  

Background. Liver enzyme paraoxonase 1 (PON1) plays an important role in protection the organism from toxic effects of organophosphorus compounds (OPs) via their hydrolysis whose rate and efficiency depend on PON1 serum level activity. PON1 activity is largely determined by the polymorphic variants of the PON1 gene. Effect of long-term work with exposure to the toxic OPs on the PON1 activity is almost unknown. The aim of the present work was to study the effect of long-term work with exposure to the toxic OPs on PON1 serum enzymatic activity depending on polymorphisms Q191R, L54M, C(-108)T PON1 gene. Materials and methods. PON1 serum enzymatic activity and PON1 polymorphisms were determined in men, who were categorized in 2 groups: workers of companies providing storage and disposal of the OPs (68) and control group (37). The PON1 191, PON1 55 and PON1 108 polymorphisms were studied by polymerase chain reaction/restriction fragment length polymorphism. PON1 serum enzymatic activity was measured by a spectrophotometric method using paraoxon. Results. PON1 activity in workers with exposure to the toxic OPs relative was increased compared to the control group (p = 0,027). Differences in serum PON1 activity was shown for the carriers of certain genotypes of the PON1 gene: PON1 serum activity was higher in workers compared to controls only for LL genotype (L54M polymorphism) and C allele (C(-108)T polymorphism) carriers (p < 0,001 and p = 0,002, correspondently). Conclusion. We suggest that the increase in serum PON1 activity in workers providing storage and disposal of OPs could be modulated with the polymorphic variants of the PON1 gene.


2017 ◽  
Vol 16 (10) ◽  
pp. 2515-2520 ◽  
Author(s):  
Hongguo Yang ◽  
Yanyan Zhao ◽  
Yunbo Ma ◽  
Qiang Wen ◽  
Minghui Zhang

Purpose: To investigate the effect of moxifloxacin on paraoxonase-1 (PON1)  activity, and serum oxidative stress in patients with multiple drug-resistant tuberculosis (MDR-TB).Methods: A total ofof 130 MDR-TB patients who were treated with moxifloxacin from October 2014 to October 2010 in Eastern Medical District of Linyi People's Hospital of Shandong Province, China were randomly divided into an observation group (65 cases, moxifloxacin group) and control group (65 cases, non-moxifloxacin group). Total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), PON1 levels and treatment efficacy for groups were determined.Results: Compared with pre-treatment levels, TOS (23.3 ± 4.7 vs 13.9 ± 3.3 umol H2O2 Eq/L, t = 13.20, p = 0.00) and OSI (17.4 ± 4.8 vs 5.7 ± 1.4 U, t = 18.87, p = 0.00) of the observation group significantly decreased, while TAS (1.4 ± 0.5 vs 3.5 ± 0.7 umol Trolox Eq/L, t = 19.68, p = 0.00) and PON1 (15.5 ± 6.9 vs 31.1 ± 8.3 U/L, t = 11.65, p = 0.00) significantly increased. TOS (23.3 ± 4.7 vs 13.9 ± 3.3 umol H2O2 Eq/L, t = 7.73, p < 0.05) and OSI (16.9 ± 5.5 vs 7.4 ± 3.2U, t = 12.04, p = 0.05) reduced significantly in the control group. Moxifloxacin correlated positively with △TAS (r = 0.697, p = 0. 04) and △PON1 (r = 0.785, p = 0.01), but correlation with △TOS (r = -0.625, p = 0.01) was negative. Efficacy was significantly higher in the observation group than that in the control group (81.54 % vs 56.92 %, p =0.00).Conclusion: Oxidative stress injury in MDR-TB patients may be effectively managed by combination of moxifloxacin with anti-TB treatmentKeywords: Multiple drug-resistant TB, Moxifloxacin, Paraoxonase, Oxidative stress


2011 ◽  
Vol 29 (2) ◽  
pp. 175-180 ◽  
Author(s):  
Ercan Varol ◽  
Atilla Icli ◽  
Fatih Aksoy ◽  
Hasan Aydin Bas ◽  
Recep Sutcu ◽  
...  

The objective of the present study was to determine the plasma total oxidative status (TOS) and total antioxidant capacity (TAC) in patients with endemic fluorosis. A total of 79 (35 males and 44 females; mean age 44.0 ± 11.9 years) patients with endemic fluorosis and 55 (23 males and 32 females; mean age 48.3 ± 8.5 years) age-, sex- and body mass index-matched healthy controls were included in this study. The urine fluoride levels and plasma TOS and TAC levels were measured. The urine fluoride levels of fluorosis patients were significantly higher than control subjects as expected (1.91 ± 0.15 vs. 0.49 ± 0.13 mg/L, respectively; p < 0.001). TOS was significantly higher in fluorosis group than in control group (17.55 ± 3.82 vs. 15.06 ± 4.31 μmol H2O2 Eq/L, respectively; p = 0.001). TAC was significantly lower in fluorosis group than in control group (1.60 ± 0.36 vs. 1.82 ± 0.51 mmol Trolox Eq/L, respectively; p = 0.004). Oxidative stress index (OSI) was significantly higher in fluorosis group than in control group (11.5 ± 3.8 vs. 8.8 ± 3.7, respectively; p < 0.001). Correlation analysis in all the groups indicated that TAC was negatively correlated with urine fluoride ( r = −0.25, p = 0.003), TOS was positively correlated with urine fluoride ( r = 0.34, p < 0.001) and OSI was positively correlated with urine fluoride ( r = 0.36, p < 0.001). The results of our study demonstrate that oxidative stress plays an important role in the pathogenesis of the endemic fluorosis.


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