Plasma Advanced Oxidation Protein Products Levels Research Articles

Trace Elements Status and Their Associations With Related Antioxidant Enzyme Activities in Patients Receiving Peritoneal Dialysis and Hemodialysis

It remains ambiguous as to whether the status of trace elements would affect their related enzyme activities toward defending a possible higher oxidative stress in patients receiving peritoneal dialysis (PD) or hemodialysis (HD) treatment. We investigated copper (Cu), zinc (Zn), and selenium (Se) status in patients receiving PD or HD treatments and further determined the association of these trace elements with their related antioxidant capacities in those patients. Sixty PD and 80 HD patients before and after HD treatment had their blood drawn. Demographic, clinical, and 24-hour diet recall data were recorded and collected. Plasma trace elements, oxidative stress indicators, and antioxidant enzyme activities were measured. Patients receiving PD or HD treatments experienced similar Zn and Cu intakes. PD and HD patients displayed adequate mean plasma Cu, Zn, and Se levels. Patients receiving PD treatment showed significantly higher levels of Cu, Zn, advanced oxidation protein products (AOPPs), and superoxide dismutase (SOD) activity, but had significantly lower levels of Se and total antioxidant capacity when compared to levels in the HD patients at the pre-HD session. The levels of 3 trace elements and AOPP increased significantly, while the levels of glutathione (GSH), oxidized glutathione (GSSG), GPx, and SOD activities decreased significantly after receiving HD treatment than did the levels in the pre-HD session. Plasma Cu, Se, and Zn levels had a different correlation with plasma AOPP level, GPx, and SOD activities during PD, pre- or post-HD sessions. Plasma Cu, Zn, and Se levels did not have any association with their associated enzyme activities in patients with PD, while plasma Cu and Zn levels may have influenced SOD activity in HD patients. An adequate Cu, Zn, and Se status is required in order to help their associated enzyme activity cope with increased oxidative stress during PD or HD sessions.

Upregulation of exofacial peroxiredoxin-thioredoxin system of lymphocytes and monocytes in preeclampsia.

An imbalanced redox homeostasis resulting in oxidative stress is present in preeclampsia. Peroxiredoxin-1 (PRDX1) and thioredoxin-1 (TRX1) regulatory enzymes are also contributing to the redox homeostasis, but were not investigated so far in preeclampsia. Thus, we have aimed to characterize PRDX1, TRX1 and oxidative stress biomarkers in blood samples of pregnant women with preeclampsia. Twelve patients with preeclampsia (PE) were enrolled into the study. Seven third trimester healthy pregnant women (HP) were accepted as control group. Peripheral venous blood samples of healthy and preeclamptic pregnant women were analyzed. Plasma level of advanced oxidation protein products (AOPP) was determined by spectrophotometry. The exofacial PRDX1 and TRX1 expression of lymphocytes and monocytes was detected by flow cytometry. The plasma AOPP level was significantly higher in preeclampsia compared to the healthy pregnant group. Significantly higher percentage of PRDX1 and TRX1 expressing lymphocytes and monocytes were detected in the blood samples of preeclamptic women compared to healthy pregnant controls. The ratio of circulating PRDX1 and TRX1 expressing lymphocytes and monocytes showed a significant inverse correlation with the birth weight of newborns. We have revealed that the level of advanced oxidation protein products is increased and the exofacial peroxiredoxin-1 and thioredoxin-1 system in lymphocytes and monocytes is upregulated in preeclampsia. In addition, the ratio of peroxiredoxin-1 and thioredoxin-1 positive circulating lymphocytes and monocytes correlates inversely with the neonatal birth weight, which finding indicates that pregnancies complicated by intrauterine growth restriction are accompanied by a higher level of oxidative stress.

Advanced Oxidation Protein Products Induce G1/G0-Phase Arrest in Ovarian Granulosa Cells via the ROS-JNK/p38 MAPK-p21 Pathway in Premature Ovarian Insufficiency.

The mechanism underlying the role of oxidative stress and advanced oxidation protein products (AOPPs) in the aetiology of premature ovarian insufficiency (POI) is poorly understood. Here, we investigated the plasma AOPP level in POI patients and the effects of AOPPs on granulosa cells both in vitro and in vivo. KGN cells were treated with different AOPP doses, and cell cycle distribution, intracellular reactive oxygen species (ROS), and protein expression levels were measured. Sprague–Dawley (SD) rats were treated daily with PBS, rat serum albumin, AOPP, or AOPP+ N-acetylcysteine (NAC) for 12 weeks to explore the effect of AOPPs on ovarian function. Plasma AOPP concentrations were significantly higher in both POI and biochemical POI patients than in controls and negatively correlated with anti-Müllerian hormone and the antral follicle count. KGN cells treated with AOPP exhibited G1/G0-phase arrest. AOPP induced G1/G0-phase arrest in KGN cells by activating the ROS-c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK)-p21 pathway. Pretreatment with NAC, SP600125, SB203580, and si-p21 blocked AOPP-induced G1/G0-phase arrest. In SD rats, AOPP treatment increased the proportion of atretic follicles, and NAC attenuated the adverse effects of AOPPs in the ovary. In conclusion, we provide mechanistic evidence that AOPPs may induce cell cycle arrest in granulosa cells via the ROS-JNK/p38 MAPK-p21 pathway and thus may be a novel biomarker of POI.

Bradykinin and oxidative stress in patients with hereditary angioedema due to C1 inhibitor deficiency.

Hereditary angioedema (HAE) is a rare autosomal dominant disease caused by genetic dysfunction of C1 inhibitor (C1-INH) due to mutations in the SERPING1 gene. The disorder is mediated mainly by bradykinin. The clinical course of the disease is varied and not related to genetic changes. We aimed to evaluate redox homeostasis of peripheral blood mononuclear cells (PBMCs) in patients with HAE due to C1-INH deficiency (C1 INH HAE) by measuring the levels of reactive oxygen species (ROS) of PBMCs as well as plasma advanced glycation end products (AGEs) and advanced oxidation protein products (AOPPs). We also aimed to assess the effect of bradykinin on ROS levels. We enrolled 30 adults with C1-INH-HAE and 15 healthy individuals. The levels of ROS were measured by flow cytometry, while the plasma levels of AGEs and AOPPs were determined spectrophotometrically by enzyme‑ linked immunosorbent assays. Basal and hydrogen peroxide (H2O2)-induced ROS levels were higher in patients with HAE when compared with controls (P = 0.002 and P = 0.001, respectively), indicating abnormalities in redox homeostasis. Plasma AOPP and AGE levels were similar in both groups. Bradykinin reduced basal and H2O2-induced ROS generation in PBMCs only in patients with HAE (P = 0.03). The higher basal and H2O2-induced ROS levels in patients with C1 INH HAE indicate redox imbalance. However, by reducing basal and H2O2-induced ROS levels, bradykinin shows antioxidant action in this disorder.

Advanced oxidation protein products in nondiabetic end stage renal disease patients on maintenance haemodialysis

In chronic kidney disease (CKD), the impairment of the excretory function leads to elevation in the blood concentrations of urea, creatinine, and various protein metabolic products. Advanced oxidation protein products (AOPP), along with protein carbonyls, protein-bound di-tyrosines and S-thiolated proteins, are considered biomarkers of oxidative stress in end-stage renal disease (ESRD) patients on maintenance haemodialysis (HD). In this study, we evaluated the correlations between plasma levels of AOPP (measured by size exclusion/gel filtration high performance liquid chromatography) and those of protein-bound di-tyrosines, protein carbonyls, albumin and fibrinogen in 50 nondiabetic ESRD patients on maintenance HD. Considering that AOPP could represent the bridge between oxidative stress and inflammation, having been identified as proinflammatory mediators, we also evaluated the association between AOPP levels, C-reactive protein concentration and white blood cells count. Finally, we assessed the associations between plasma level of AOPP and serum concentrations of creatinine and urea, both of which showed a strong dependence on the chronological age of haemodialysed patients. Taken together, our results confirm the robust relationship between uraemia and oxidative stress, especially when measured as biomarkers of severe protein oxidative damage (e.g. plasma AOPP).

Placental disease and later dementia: Is there a connection?

To determine the level of advanced oxidation protein products (AOPPs) in children with chronic otitis media with effusion (COME), in an effort to elucidate the multifactorial etiology of this disease.This study involved 25 COME patients and 30 healthy children (control group) recruited from the Ear, Nose and Throat (ENT) and Pediatric Departments, respectively, of the Haseki Research and Training Hospital. In the COME group, blood samples were collected before a middle ear operation, and middle ear fluid was sampled during the operation. Blood samples were also obtained from the control subjects. AOPP levels in the plasma and effusion fluid were measured by the spectrophotometric method.In the COME group, the mean AOPP levels in plasma and effusion fluid were 168.08 μmol/l and 412.75 μmol/l, respectively. In the control group, the mean plasma AOPP level was 141.54 μmol/l. The plasma AOPP levels did not significantly differ between the COME and control groups (p > 0.05). In the COME group, however, the effusion fluid AOPP level (412.75 ± 204.54 μmol/l) was significantly higher than the plasma AOPP level (168.08 ± 68.45 μmol/l; p < 0.01).We found that AOPP levels were elevated in the effusion fluid, but not in the plasma, of COME patients. Thus, COME was associated with protein oxidation abnormalities. Oxidative stress may play a role in the etiopathogenesis of COME, and AOPPs may be used as markers of oxidative stress; however, further studies are required to confirm these findings.

Advanced oxidation protein products induce G1 phase arrest in intestinal epithelial cells via a RAGE/CD36-JNK-p27kip1 mediated pathway

Intestinal epithelial cell (IEC) cycle arrest has recently been found to be involved in the pathogenesis of Crohn's disease (CD). However, the mechanism underlying the regulation of this form of cell cycle arrest, remains unclear. Here, we investigated the roles that advanced oxidation protein products (AOPPs) may play in regulating IEC cycle arrest. Plasma AOPPs levels and IEC cycle distributions were evaluated in 12 patients with CD. Molecular changes in various cyclins, cyclin-dependent kinases (CDKs), and other regulatory molecules were examined in cultured immortalized rat intestinal epithelial (IEC-6) cells after treatment with AOPPs. The in vivo effects exerted by AOPPs were evaluated using a normal C57BL/6 mouse model with an acute AOPPs challenge. Interestingly, plasma AOPPs levels were elevated in active CD patients and correlated with IEC G1 phase arrest. In addition, IEC treatment with AOPPs markedly reduced the expression of cyclin E and CDK2, thus sensitizing epithelial cells to cell cycle arrest both in vitro and in vivo. Importantly, we found that AOPPs induced IEC G1 phase arrest by modulating two membrane receptors, RAGE and CD36. Furthermore, phosphorylation of c-jun N-terminal kinase (JNK) and the expression of p27kip1 in AOPPs-treated cells were subsequently increased and thus affected cell cycle progression. Our findings reveal that AOPPs influence IEC cycle progression by reducing cyclin E and CDK2 expression through RAGE/CD36-depedent JNK/p27kip1 signaling. Consequently, AOPPs may represent a potential therapeutic molecule. Targeting AOPPs may offer a novel approach to managing CD.

Malondialdehyde and advanced oxidation protein products are not increased in psoriasis: a controlled study

This study investigated oxidative stress in patients with psoriasis of low and medium disease activity. We measured advanced oxidation protein products (AOPP) and malondialdehyde (MDA) in plasma using UV-spectrophotometry and high performance liquid chromatography connected to a fluorescence detector in 84 patients and 84 matched healthy subjects. AOPP is a marker of protein oxidation due to inflammation, whereas MDA is a hydroxyl radical initiated lipid peroxidation product. Clinico-demographic variables including age, gender, disease severity, and fatigue were assessed in relation to AOPP and MDA. Disease severity was evaluated with the Psoriasis Area and Severity Index and the Dermatology Life Quality Index. Median (interquartile range, IQR) AOPP concentrations were 66µmol/l (IQR 54-102) in patients and 69µmol/l (IQR 55-87) in healthy subjects (P = 0.75). Median plasma MDA concentrations were significantly lower in patients than in healthy subjects (0.68µM, IQR 0.54-0.85 vs. 0.76µM, IQR 0.60-0.97; P = 0.03). Plasma levels of AOPP and MDA did not indicate oxidative stress in patients with mild psoriasis. Higher AOPP concentrations were associated with male gender, high body mass index, and high hemoglobin values. Elevated MDA concentrations were associated with advanced age and male gender. No associations with disease severity were detected. Although, the two selected biomarkers do not provide a complete measure of oxidative damage, our study demonstrates that a number of physiological and methodological factors influence the levels of MDA and AOPP. Such methodological issues are important to consider when interpreting results using these biomarkers in patients with psoriasis.

Association of plasma level of advanced oxidation protein products with Framingham risk score in type 2 diabetic patients without vascular diseases

To explore the association of plasma level of advanced oxidation protein products (AOPPs) with Framingham risk score in type 2 diabetic patients without vascular diseases. This cross-sectional study was conducted among type 2 diabetic patients without vascular diseases recruited from 3 affiliated hospitals of Southern Medical University between March, 2010 and May, 2011, with age- and gender-matched healthy individuals as the control group. The demographic data were collected from all the participants, and the biochemical indexes and plasma levels of AOPPs were examined. The risk of cardiovascular disease in 10 years was assessed for all the participants based on their Framingham risk scores. A total of 112 diabetic patients and 49 healthy subjects were enrolled in this study. The diabetic patients had significantly higher body mass index (BMI), blood glucose, triglyceride, low-density lipoprotein (LDL), plasma AOPPs and Framingham risk score but lower high-density lipoprotein level than the control subjects. Spearman correlation analysis showed that plasma level of AOPPs was positively correlated with the Framingham risk score (r=-0.44, P<0.001), and further multiple linear regression analysis suggested that plasma AOPPs level was independently correlated with the Framingham risk score (β0.305, P<0.001). Type 2 diabetic patients without vascular diseases have significantly higher plasma levels of AOPPs and are at a greater risk of cardiovascular events in 10 years than healthy individuals. Plasma AOPPs are positively correlated with the Framingham risk score, suggesting the value of plasma AOPPs level in predicting the risk of cardiovascular events in these patients.

The effect of resveratrol on glycation and oxidation products in plasma and liver of chronic methylglyoxal-treated rats.

Methylglyoxal (MG) is a highly reactive dicarbonyl compound. It is produced by processes like glycolysis, glucose autooxidation, lipid peroxidation, and protein glycation. It is a major precursor of advanced glycation end products (AGE). It also exacerbates oxidative stress in the organism. Although there are some in vitro studies investigating the effect of resveratrol (RES) as an antioxidant and antiglycating agent on MG-induced toxicity, in vivo effect of RES is unknown. Therefore, we aimed to investigate the efficiency of RES in chronic MG-treated rats. Rats were given incrementally increased doses (100-300 mg/kg) of MG in drinking water for ten weeks. RES (10 mg/kg ip) was administered together with MG. Reactive oxygen species (ROS) formation, thiobarbituric reactive substances (TBARS), protein carbonyl (PC), advanced oxidation protein products (AOPP) and AGE levels as well as ferric reducing antioxidant power (FRAP) values were determined in plasma and liver. Significant increases in plasma TBARS, PC, AOPP and AGE and fructosamine levels were detected in MG-treated rats. However, plasma ROS and FRAP levels remained unchanged. Hepatic ROS, TBARS, PC and AOPP, but not AGE and FRAP levels were also increased in MG-treated rats. RES treatment diminished high levels of plasma PC, AOPP and AGE levels in MG-treated rats. Additionally, significant decreases in hepatic ROS, TBARS, PC and AOPP levels together with histopatological amelioration were detected due to RES treatment in MG-treated rats. Our results indicate that RES may be considered as a protective agent against glycoxidative stress generated by in vivo MG treatment.

Administration of Selenium Decreases Lipid Peroxidation and Increases Vascular Endothelial Growth Factor in Streptozotocin Induced Diabetes Mellitus.

The imbalance in oxidant/antioxidant status plays a pivotal role in diabetes mellitus (DM). Selenium is a integral component of the antioxidant enzyme glutathione peroxidase. Se treatment induces angiogenesis and improves endothelial function through increased expression of vascular endothelial growth factor (VEGF). The aim of this study is to investigate the effect of selenium on oxidative stress, VEGF, and endothelin 1 (ET1) in a DM rat model. We performed an experimental animal study with 64 adult male Wistar-Albino rats. Rats were divided into the following groups (n=8): control (C)7, C21, C+sodium selenite (Se)7, and C+Se21 (control rats), and DM7, DM21, DM+Se7, and DM+Se21 (diabetic rats). Diabetes was induced by 2-deoxy-2-(3-methyl-3-nitrosoureido)- D-glucopyranose [streptozotocin (STZ)]. Three weeks after STZ, DM+Se7 rats received intraperitoneal (i.p.) injections of 0.4 mg/kg Se for 7 days. The DM+Se21 rats received these injections for 21 days. The same dose/duration of Se was administered to the C+Se7 and C+Se21 groups. The remaining rats (C7, C21, DM7, DM21) received physiologic saline injections for 7 or 21 days. Ferric reducing antioxidant power (FRAP), malondialdehyde (MDA), advanced oxidation protein products (AOPP), and endothelial function markers (VEGF and ET1) in plasma samples were measured. Diabetic rats (DM7 and DM21) had significantly increased plasma FRAP (P=0.002, P=0.001), AOPP (P=0.024, P=0.01), MDA (P=0.004, P=0.001), and ET1 (P=0.028, P=0.003) levels compared with C7 and C21 control rats. VEGF (P=0.02, P=0.01) significantly decreased in DM7 and DM21 diabetic rats compared with their controls (C7, C21). Se administration reversed the increased MDA and decreased VEGF levels, and lowered plasma glucose levels in the DM+Se7 and DM+Se21 diabetic groups compared with diabetic rats (DM7, DM21). We observed positive correlations between FRAP-AOPP (r=0.460), FRAP-ET1 (r=0.510), AOPP-MDA (r=0.270), and AOPP-ET1 (r=0.407), and a negative correlation between MDA-VEGF (r=-0.314). We observed accentuated oxidative stress and impaired endothelial function in diabetes. Se treatment reduced lipid peroxidation and hyperglycemia. Se probably improved endothelial dysfunction in diabetic rats because of the increased VEGF levels.

Levels of renalase and advanced oxidation protein products with regard to catecholamines in haemodialysed patients.

The main mediators of the sympathetic nervous system in the effectors part are catecholamines (CA). An increased sympathetic nerve activity observed in chronic kidney disease (CKD), is due to a raised level of CA in plasma. Renalase is a protein secreted by the kidneys, composed of 342 amino acids, which is able to metabolize the circulating CA and possibly play an important role in the regulation of sympathetic tone and blood pressure. Also, oxidative stress, defined as a disruption of the equilibrium between the generation of oxidants, is a crucial factor in the development of the inflammatory syndrome associated with CKD. The advanced oxidation protein products (AOPP) represent exquisite markers of phagocyte-derived oxidative stress. The aim of the study was to investigate the concentration of renalase and explore the associations between AOPP with regards to CA in haemodialysis (HD) patients. The study was conducted among 50 residents of the municipality and neighbouring villages in the province of Lublin, central-eastern Poland. In the studied patients, it was found that an average concentration of renalase was 44.8 ± 6.5 μg/mL, whereas of AOPP plasma levels - 57.5 ± 21.5 μmol/L. The results demonstrated the correlation between levels of renalase and AOPP in the HD patients. Indeed, elevated levels of renalase and AOPP in HD may be due to the presence of uremic toxins in blood. The concentration of urea affects the plasma concentrations of AOPP and renalase causing a direct relationship between renalase and AOPP. However, there is no clear relationship between renalase and circulating catecholamines in HD patients.

The Characteristics and Roles of Advanced Oxidation Protein Products in Atherosclerosis.

Advanced oxidation protein products (AOPPs) are novel biomarkers of oxidative damage to proteins and a novel class of inflammatory mediators. AOPPs can promote oxidative stress (OS) and inflammation and thus participate in many pathophysiological disease processes. Atherosclerosis is a chronic inflammatory disease of blood vessels that is characterized by low-density lipoprotein infiltration into the endothelial intima and the formation of atherosclerotic plaques. Inflammation and OS are established risk factors for the formation of atherosclerosis. Accumulated studies show that AOPPs can accelerate the progression of atherosclerosis through OS and inflammation. Additionally, AOPPs can accelerate the formation of atherosclerotic plaques by inhibiting high-density lipoprotein receptor scavenger receptor class B type I-mediated high-density lipoprotein cholesterol reverse transport, leading to metabolic disturbances. Some studies have suggested that plasma AOPPs levels are independently positively correlated with blood pressure and are also independent risk factors for cardiovascular disease. AOPPs can trigger oxidative bursts of neutrophils, monocytes and phagocytic cells, increase the generation of reactive oxygen species and promote the secretion of cytokines to accelerate endothelial cell injury. Detecting the levels and inhibiting the formation of AOPPs may provide a novel approach to monitor the progress and improve the prognosis of atherosclerosis.

Advanced oxidation protein products and malondialdehyde - the new biological markers of oxidative stress - are elevated in postmenopausal women.

The aim of the study was to measure advanced oxidation protein products (AOPPs) as markers for oxidative stress to evaluate cardiovascular risk in pre- and postmenopausal women and to compare the results with malondialde-hyde (MDA) levels. Twenty premenopausal women and 84 naturally postmenopausal patients were enrolled in the study. AOPP and MDA plasma levels were measured. The postmenopausal group was further subdivided into two groups: postmenopausal age of 40-49 and of 50-59 years. AOPP and MDA levels were compared between premenopausal, 40-49 and 50-59 year old menopausal women. Plasma AOPP and MDA levels in postmenopausal women were increased when compared with their premeno-pausal peers (123.83 ± 55.51 μmol/L vs. 61.59 ± 16.42 μmol/L and 6.50 ± 1.05 μmol/L vs. 5.98 ± 0.77 μmol/L; respectively). Mean plasma AOPP levels in the two menopausal age groups were both significantly higher from the premenopausal group (118.64 ± 59.1 μmol/L vs. 61.59 ± 16.42 μmol/L and 132.31 ± 48.97 μmol/L vs. 61.59 ± 16.42 μmol/L; respectively). No significant difference was found in mean AOPP levels between postmenopausal subjects of 40-49 and 50-59 years age (118.64 ± 59.12 μmol/L vs. 132.31 ± 48.97 μmol/L). Mean plasma MDA levels of each of two postmenopausal age groups were both significantly higher from the premenopausal group (6.50 ± 1.04 μmol/L vs. 5.98 ± 0.77 μmol/L and 6.50 ± 1.10 μmol/L vs. 5.98 ± 0.77 μmol/L; respectively). However, no statistically significant difference between the two postmenopausal age groups (6.50 ± 1.04 μmol/L vs. 6.50 ± 1.10 μmol/L) was found. AOPP and MDA levels are elevated in postmenopausal women as compared to their premenopausal peers, suggesting they can be used as markers for cardiovascular risk in postmenopausal women.

Plasma levels of oxidative stress in children with steroid-sensitive nephrotic syndrome and their predictive value for relapse frequency.

Oxidative stress has been reported to play an important role in children with primary nephrotic syndrome (PNS). However, the results of previous studies are controversial. Forty children with steroid-sensitive nephrotic syndrome (SSNS) and 20 age- and sex-matched healthy controls were enrolled. Patients were followed-up for 12-18 months and divided into three subgroups: frequent relapse (n = 10), non-frequent relapse (n = 12), and non-relapse (n = 18). The plasma levels of advanced oxidation protein products (AOPP), malondialdehyde (MDA), and superoxide dismutase (SOD) were tested in controls and patient group at first presentation and after 4 weeks of steroid treatment. Patients had higher AOPP and MDA levels but lower SOD compared with controls. AOPP levels were significantly higher in the frequent relapse subgroup compared with the non-frequent relapse and non-relapse subgroups, respectively. No significant differences were found in the plasma levels of MDA and SOD among the three subgroups. AOPP >87.55 μmol/l before steroid treatment and AOPP >78.5 μmol/l after 4-week steroid treatment were positively correlated with the relapse frequency in patients with SSNS. Children with SSNS have oxidative stress. The plasma levels of AOPP before and after 4-week steroid treatment may predict whether patients with SSNS will relapse frequently.

Advanced oxidation protein products, total thiol levels and total oxidant/antioxidant status in patients with nash.

In this study we aim to evaluate the relationship of advanced oxidation protein products (AOPP), total thiol, total antioxidant status (TAS), total oxidant status (TOS) levels and oxidative stress index (OSI) in patients with nonalcoholic steatohepatitis (NASH). A total of 28 patients with NASH and 19 age-and-gender-matched healthy subjects were enrolled in the study as control group. Plasma AOPP and thiol levels were determined by spectrophotometric methods. Plasma TAS and TOS levels were measured using commercially available kits and OSI was calculated. Plasma AOPP (256.7 vs. 125.8 μmol/L) and TOS levels (8.9 vs. 5.9 μmol H2O2 equiv/L) were higher in patients with NASH than the controls (p<0.019 and p<0.041 respectively). Plasma total thiol levels (235.0 vs. 291.6 μmol/L) were lower in patients with NASH than the controls (p<0.001). TAS levels (1.14 vs. 1.14 mmol Trolox equiv/L) were not significantly different in patients with NASH than the controls (p>0.900). OSI values (8.0 vs. 5.5) were higher in patients with NASH than the controls (p<0.039). Our findings indicate that oxidative stress increases in patients with NASH as shown by increases in TOS level. We think effective antioxidant therapy to inhibit protein oxidation and also to increase of TAS and total thiol levels may be a therapeutic option in patients with NASH who have under increased oxidative stress.

Advanced Oxidation Protein Products as a Novel Marker of Oxidative Stress in Postmenopausal Osteoporosis.

BackgroundAdvanced oxidation protein products (AOPPs) are acknowledged as a novel marker of oxidation-mediated protein damage. This study aimed to investigate the plasma levels of AOPPs in postmenopausal osteoporotic women, and to determine the relationship between AOPPs accumulation and lumbar bone mineral destiny (BMD) or bone turnover markers.Material/MethodsLumbar BMD was measured by dual-energy X-ray absorptiometry. Plasma AOPPs levels as a marker of protein oxidation damage and malondialdehyde (MDA) levels as a marker of lipid peroxidation were measured by spectrophotometry. The concentrations of 2 specific markers of bone turnover, bone-specific alkaline phosphatase (BALP) and tartrate-resistant acid phosphatase5b, (TRACP 5b) were quantified using ELISA kits.ResultsWe recruited 60 postmenopausal women meeting osteoporosis (OP) diagnostic criteria of World Health Organization (WHO) and 60 postmenopausal women without OP. Plasma levels of AOPPs (P<0.001), BALP (P<0.001) and TRACP 5b (P<0.001) were statistically significantly increased in the postmenopausal osteoporotic women compared with controls, but there was no statistically significant difference in MDA (P=0.124) between the 2 groups. Plasma AOPPs levels were negatively correlated with lumbar BMD and positively correlated with bone turnover markers both in postmenopausal osteoporotic women and in all subjects. However, plasma MDA levels were not correlated with lumbar BMD or bone turnover markers.ConclusionsIn postmenopausal osteoporotic women elevated AOPPs is associated with reduced BMD and increased bone turnover markers. Because AOPPs is stable and easy to detect it may be used as a simple plasma marker to predict the severity of postmenopausal OP.

An Increase of Plasma Advanced Oxidation Protein Products Levels Is Associated with Cardiovascular Risk in Incident Peritoneal Dialysis Patients: A Pilot Study.

Advanced oxidation protein products (AOPPs) are considered as markers and even mediators of the proinflammatory effect of oxidative stress in uremia. We hypothesized that an increase of oxidative stress associated with peritoneal dialysis (PD), estimated by the variation of plasma AOPPs over time, might be associated with cardiovascular (CV) risk and overall prognosis. In 48 PD patients, blood samples were collected on two occasions: the first one in the first six months after starting PD therapy and the second one, one year after. The plasma AOPPs level variation over the first year on PD was significantly associated with CV antecedents and also with CV prognosis. In those patients in whom the AOPPs levels increased more than 50% above the baseline value, a significant association with past and future CV disease was confirmed. These patients had 4.7 times greater risk of suffering later CV disease than those with a smaller increase, even after adjusting for previous CV history. Our data suggest that the increase of AOPPs plasma level over the first year on PD is conditioned by CV antecedents but also independently predicts CV prognosis. AOPPs plasma levels seem to represent the CV status of PD patients with sufficient sensitivity to identify those with a clearly sustained higher CV risk.

Advanced oxidation protein product level in children with chronic otitis media with effusion

ObjectiveTo determine the level of advanced oxidation protein products (AOPPs) in children with chronic otitis media with effusion (COME), in an effort to elucidate the multifactorial etiology of this disease. MethodsThis study involved 25 COME patients and 30 healthy children (control group) recruited from the Ear, Nose and Throat (ENT) and Pediatric Departments, respectively, of the Haseki Research and Training Hospital. In the COME group, blood samples were collected before a middle ear operation, and middle ear fluid was sampled during the operation. Blood samples were also obtained from the control subjects. AOPP levels in the plasma and effusion fluid were measured by the spectrophotometric method. ResultsIn the COME group, the mean AOPP levels in plasma and effusion fluid were 168.08μmol/l and 412.75μmol/l, respectively. In the control group, the mean plasma AOPP level was 141.54μmol/l. The plasma AOPP levels did not significantly differ between the COME and control groups (p>0.05). In the COME group, however, the effusion fluid AOPP level (412.75±204.54μmol/l) was significantly higher than the plasma AOPP level (168.08±68.45μmol/l; p<0.01). ConclusionWe found that AOPP levels were elevated in the effusion fluid, but not in the plasma, of COME patients. Thus, COME was associated with protein oxidation abnormalities. Oxidative stress may play a role in the etiopathogenesis of COME, and AOPPs may be used as markers of oxidative stress; however, further studies are required to confirm these findings.

The patients with clinically isolated syndrome and relapsing remitting multiple sclerosis show different levels of advanced protein oxidation products and total thiol content in plasma and CSF

Advanced oxidation protein products (AOPP) and total thiol (SH) groups levels in plasma and CSF were studied in a cohort of 50 clinically isolated syndrome (CIS) and 57 relapsing remittent multiple sclerosis (RRMS) patients related to 20 control group (CG) patients’ values. The obtained results were compared regarding patients demographic, biochemical, clinical (EDSS) and MRI features (total T2 weighted lesions number and Gd enhancement lesion volume).Plasma and CSF AOPP levels in CIS and RRMS patients were higher than those in CG, while SH groups showed lower values compared to CG (p<0.05). Both parameters were higher in CIS than in RRMS patients (p<0.05). Related to EDSS median range, all patients were divided into those with slight or mild and those with severe clinical presentation. AOPP and SH group changes were more pronounced in both, CIS and RRMS patients with higher, compared to those with lower EDSS (p<0.05). AOPP, SH group levels and EDSS positive correlations were observed in both study groups (p<0.01). Both parameters showed the same approach regarding the median range of total T2 weighted lesions and Gd enhancement lesion volume mean values (p<0.05), but no correlation was found between AOPP and SH levels and these patients radiological characteristics (p>0.01).The data support the fact that oxidative stress is always involved in CIS and RRMS pathophysiology, but not always as a disease determinant dependent on its intensity, which might be important for new therapeutic strategies based on antioxidant approach in those patients.