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Advanced Oxidation Protein Products (advanced + oxidation_protein_products)
Selected AbstractsEnhanced formation of advanced oxidation protein products in IBDINFLAMMATORY BOWEL DISEASES, Issue 6 2008Malgorzata Krzystek-Korpacka PhD Abstract Background: Advanced oxidation protein products (AOPPs) are new protein markers of oxidative stress with pro-inflammatory properties, accumulated in many pathological conditions. The issue of their enhanced formation in IBD has not been addressed yet. Methods: The concentration of relative AOPPs (rAOPP; concentration of AOPPs divided by albumin level) were measured in 68 subjects with ulcerative colitis (UC), 50 subjects with Crohn's disease (CD) and 45 healthy volunteers, and related to disease phenotype, clinical and biochemical activity, and therapeutic strategy. Diagnostic utility of rAOPP was evaluated by ROC analysis. Results: In comparison with controls (1.367 ,mol/g), rAOPP were increased in inactive (1.778 ,mol/g, P = 0.053) and active (1.895 ,mol/g, P = 0.013) UC and in active (1.847 ,mol/g, P = 0.003) CD. In CD, but not UC, rAOPP correlated with disease activity (r = 0.42, P = 0.013). Significant correlations with the inflammatory/malnutrition indices-erythrocyte sedimentation rate (ESR) (r = 0.53), leukocytes (r = 0.33), platelets (r = 0.38), IL-6 (r = 0.36), and transferrin (r = ,0.35) were demonstrated in CD. In UC, rAOPP correlated only with ESR (r = 0.35) and IL-6 (r = 0.30). Instead, associations with antioxidant dismutase (r = 0.29) and catalase (r = 0.22) were observed. The diagnostic power of rAOPP in discriminating diseased from non-diseased subjects was less than that of C-reactive protein (CRP). Simultaneous determination of rAOPP and CRP did not significantly improve the power of single CRP determination. Conclusions: IBD was associated with enhanced formation of AOPP, which differed between C and UC with respect to the relationship between rAOPP and disease activity, inflammatory and antioxidant response. These differences may reflect divergent ways that oxidative stress develops in CD and UC. The diagnostic power of rAOPP was insufficient for its clinical application. (Inflamm Bowel Dis 2008) [source] Renal, vascular and cardiac fibrosis in rats exposed to passive smoking and industrial dust fibre amositeJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 11-12 2009Peter Boor Abstract Passive smoking is an independent risk factor for cardiovascular diseases. Industrial fibrous dust, e.g. the asbestos group member, amosite, causes lung cancer and fibrosis. No data are available on renal involvement after inhalational exposure to these environmental pollutants or of their combination, or on cardiovascular and renal toxicity after exposure to amosite. Male Wistar rats were randomized into four groups (n= 6): control and amosite group received initially two intratracheal instillations of saline and amosite solution, respectively. Smoking group was subjected to standardized daily exposure to tobacco smoke for 2 hrs in a concentration resembling human passive smoking. Combined group was exposed to both amosite and cigarette smoke. All rats were killed after 6 months. Rats exposed to either amosite or passive smoking developed significant glomerulosclerosis and tubulointerstitial fibrosis. Combination of both exposures had additive effects. Histomorphological changes preceded the clinical manifestation of kidney damage. In both groups with single exposures, marked perivascular and interstitial cardiac fibrosis was detected. The additive effect in the heart was less pronounced than in the kidney, apparent particularly in changes of vascular structure. Advanced oxidation protein products, the plasma marker of the myeloperoxidase reaction in activated monocytes/macrophages, were increased in all exposed groups, whereas the inflammatory cytokines did not differ between the groups. In rats, passive smoking or amosite instillation leads to renal, vascular and cardiac fibrosis potentially mediated via increased myeloperoxidase reaction. Combination of both pollutants shows additive effects. Our data should be confirmed in subjects exposed to these environmental pollutants, in particular if combined. [source] Advanced oxidation protein products inhibit differentiation and activate inflammation in 3T3-L1 preadipocytes,JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010Qiu Gen Zhou Accumulation of advanced oxidation protein products (AOPPs) is prevalent in metabolic syndromes, a condition with impaired preadipocytes differentiation. In the present study, we tested the hypothesis that AOPPs disturb preadipocyte differentiation. Exposure of 3T3-L1 preadipocytes to increased levels of AOPPs inhibited accumulation of intracellular triglyceride and decreased the expression of the essential markers of matured adipocytes, such as adipocyte fatty-acid-binding protein (aP2), CAAT/enhancer-binding protein (C/EBP)-,, and peroxisome proliferator-activated receptor (PPAR)-,, in response to standard adipogenic induction. Inhibitory effects of AOPPs on preadipocytes differentiation was time sensitive, which occurred at the early stage of differentiation. In the presence of AOPPs, induction of preadipocytes differentiation resulted in upregulated expression of C/EBP homologous protein (CHOP) and CUG-Triplet repeat-binding protein (CUGBP), two important inhibitors of preadipocytes differentiation. In addition, treatment with AOPPs increased abundance of C/EBP-,-liver enriched inhibitory protein (C/EBP-,-LIP), a truncated C/EBP-, isoform without adipogenic activity. Moreover, AOPPs-treated preadipocytes expressed a macrophage marker F4/80 and overexpressed tumor necrosis factor-, and interleukin-6 via nuclear factor-,B (NF-,B)-dependent pathway. However, blocking inflammation with NF-,B inhibitor failed to improve AOPPs-induced inhibition of preadipocytes differentiation. These data suggest that accumulation of AOPPs may inhibit differentiation of preadipocytes and activate inflammation in these cells. This information might have implication for understanding the impairment of preadipocytes differentiation and fat inflammation seen in metabolic syndrome. J. Cell. Physiol. 225: 42,51, 2010. © 2010 Wiley-Liss, Inc. [source] Enhanced formation of advanced oxidation protein products in IBDINFLAMMATORY BOWEL DISEASES, Issue 6 2008Malgorzata Krzystek-Korpacka PhD Abstract Background: Advanced oxidation protein products (AOPPs) are new protein markers of oxidative stress with pro-inflammatory properties, accumulated in many pathological conditions. The issue of their enhanced formation in IBD has not been addressed yet. Methods: The concentration of relative AOPPs (rAOPP; concentration of AOPPs divided by albumin level) were measured in 68 subjects with ulcerative colitis (UC), 50 subjects with Crohn's disease (CD) and 45 healthy volunteers, and related to disease phenotype, clinical and biochemical activity, and therapeutic strategy. Diagnostic utility of rAOPP was evaluated by ROC analysis. Results: In comparison with controls (1.367 ,mol/g), rAOPP were increased in inactive (1.778 ,mol/g, P = 0.053) and active (1.895 ,mol/g, P = 0.013) UC and in active (1.847 ,mol/g, P = 0.003) CD. In CD, but not UC, rAOPP correlated with disease activity (r = 0.42, P = 0.013). Significant correlations with the inflammatory/malnutrition indices-erythrocyte sedimentation rate (ESR) (r = 0.53), leukocytes (r = 0.33), platelets (r = 0.38), IL-6 (r = 0.36), and transferrin (r = ,0.35) were demonstrated in CD. In UC, rAOPP correlated only with ESR (r = 0.35) and IL-6 (r = 0.30). Instead, associations with antioxidant dismutase (r = 0.29) and catalase (r = 0.22) were observed. The diagnostic power of rAOPP in discriminating diseased from non-diseased subjects was less than that of C-reactive protein (CRP). Simultaneous determination of rAOPP and CRP did not significantly improve the power of single CRP determination. Conclusions: IBD was associated with enhanced formation of AOPP, which differed between C and UC with respect to the relationship between rAOPP and disease activity, inflammatory and antioxidant response. These differences may reflect divergent ways that oxidative stress develops in CD and UC. The diagnostic power of rAOPP was insufficient for its clinical application. (Inflamm Bowel Dis 2008) [source] Advanced oxidation protein products inhibit differentiation and activate inflammation in 3T3-L1 preadipocytes,JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010Qiu Gen Zhou Accumulation of advanced oxidation protein products (AOPPs) is prevalent in metabolic syndromes, a condition with impaired preadipocytes differentiation. In the present study, we tested the hypothesis that AOPPs disturb preadipocyte differentiation. Exposure of 3T3-L1 preadipocytes to increased levels of AOPPs inhibited accumulation of intracellular triglyceride and decreased the expression of the essential markers of matured adipocytes, such as adipocyte fatty-acid-binding protein (aP2), CAAT/enhancer-binding protein (C/EBP)-,, and peroxisome proliferator-activated receptor (PPAR)-,, in response to standard adipogenic induction. Inhibitory effects of AOPPs on preadipocytes differentiation was time sensitive, which occurred at the early stage of differentiation. In the presence of AOPPs, induction of preadipocytes differentiation resulted in upregulated expression of C/EBP homologous protein (CHOP) and CUG-Triplet repeat-binding protein (CUGBP), two important inhibitors of preadipocytes differentiation. In addition, treatment with AOPPs increased abundance of C/EBP-,-liver enriched inhibitory protein (C/EBP-,-LIP), a truncated C/EBP-, isoform without adipogenic activity. Moreover, AOPPs-treated preadipocytes expressed a macrophage marker F4/80 and overexpressed tumor necrosis factor-, and interleukin-6 via nuclear factor-,B (NF-,B)-dependent pathway. However, blocking inflammation with NF-,B inhibitor failed to improve AOPPs-induced inhibition of preadipocytes differentiation. These data suggest that accumulation of AOPPs may inhibit differentiation of preadipocytes and activate inflammation in these cells. This information might have implication for understanding the impairment of preadipocytes differentiation and fat inflammation seen in metabolic syndrome. J. Cell. Physiol. 225: 42,51, 2010. © 2010 Wiley-Liss, Inc. [source] Advanced oxidative protein products are independently associated with endothelial function in peritoneal dialysis patientsNEPHROLOGY, Issue 3 2009HUSEYIN KOCAK SUMMARY Aim: Oxidative stress (OS) and asymmetric dimethylarginine (ADMA) are accepted as non-classical cardiovascular risk factors in end-stage renal disease patients. To clarify the role of these factors in the atherosclerotic process, we investigated if OS and ADMA are associated with endothelial function (EF) in peritoneal dialysis (PD) patients. Methods: Fifty-two non-diabetic PD patients without known atherosclerotic disease as well as 30 age- and sex-matched healthy individuals were included. We measured serum thiobarbituric acid-reactive substances (TBARS), malondialdehyde (MDA), advanced glycation end-product (AGE), pentosidine, advanced oxidation protein products (AOPP), ADMA and EF as described by Celermejer et al. in all subjects. Results: TBARS, MDA, AOPP, AGE, pentosidine and ADMA levels were significantly higher in PD patients than in controls (P < 0.001). Flow-mediated dilatation (FMD)% and nitrate mediated dilatation (NMD)% in PD patients were lower than in the control group (7.7 ± 4.0% vs 11.70 ± 5.50%, P < 0.01 and 17.6 ± 8.3% vs 26.4 ± 4.6%, P < 0.01). Additionally, it was found that AOPP are independently correlated with FMD% and NMD% in PD patients (, = ,463, P < 0.01 and , = ,420, P < 0.05). Conclusion: This study shows that PD patients without known atherosclerotic disease can also be characterized by endothelial dysfunction and AOPP levels independently predict endothelial function level in PD patients. [source] Natural surfactant combined with beclomethasone decreases oxidative lung injury in the preterm lambPEDIATRIC PULMONOLOGY, Issue 12 2009Carlo Dani MD Abstract We performed a randomized study in preterm lambs to assess the hypothesis that the treatment with natural surfactant combined with beclomethasone might decrease pulmonary oxidative stress in an animal model of respiratory distress syndrome (RDS). Animals received 200,mg/kg of porcine natural surfactant or 200,mg/kg of natural surfactant combined with 400 or 800,µg/kg of beclomethasone. Lung tissue oxidation was studied by measuring total hydroperoxide (TH), advanced oxidation protein products (AOPP), and non-protein bound iron (NPBI) in bronchial aspirate samples. In addition, lung mechanics was evaluated. TH was lower in the groups treated with surfactant plus 400 or 800,µg/kg of beclomethasone than in the surfactant group; AOPP was lower in the group treated with surfactant plus 800,µg/kg of beclomethasone than in the other groups; NPBI was similar in all groups. Surfactant treatment was followed by a sustained improvement of tidal volume (TV) and airway resistance, while dynamic compliance did not vary. However, the mean airway pressure needed to obtain similar values of TV was lower in the group treated with surfactant plus 800,µg/kg of beclomethasone than in other groups. We concluded that natural surfactant combined with beclomethasone at 800,µg/kg is effective in reducing the oxidative lung stress and improving the respiratory function in an animal model of RDS. Pediatr Pulmonol. 2009; 44:1159,1167. © 2009 Wiley-Liss, Inc. [source] Bilirubin influence on oxidative lung damage and surfactant surface tension propertiesPEDIATRIC PULMONOLOGY, Issue 3 2004Carlo Dani MD Abstract To study the hypothesis that hyperbilirubinemia might reduce in vivo oxidative lung damage while also diminishing lung surfactant surface tension properties during acute lung injury, we performed a randomized study in a rabbit model of acute lung injury. Twenty rabbits were randomized to receive bilirubin or saline intravenously. Acute lung injury was induced by lung lavages with saline. Lung tissue oxidation was evaluated by measuring total hydroperoxide (TH), advanced oxidation protein products (AOPP), and protein carbonyls (PC) in bronchial aspirate (BA) samples. Surface surfactant activity was studied in BA samples using a capillary surfactometer. Bilirubin BA concentration increased in bilirubin-treated rabbits, while it remained undetectable in controls. A similar increase in TH, AOPP, and PC bronchial aspirate concentrations was found in both the study and control groups, while surfactant surface activity was lower in the bilirubin than in the control group. We conclude that during hyperbilirubinemia, bilirubin enters the lung tissue, where it can be detected in BA fluid. Bilirubin is not effective as an antioxidant agent and exerts a detrimental effect on lung surfactant surface tension properties. These findings may have relevance to the management of premature neonates suffering from respiratory distress syndrome and hyperbilirubinemia. Pediatr Pulmonol. © 2004 Wiley-Liss, Inc. [source] Effects of antioxidant stobadine on protein carbonylation, advanced oxidation protein products and reductive capacity of liver in streptozotocin-diabetic rats: Role of oxidative/nitrosative stressBIOFACTORS, Issue 3 2007Ahmet Cumao Background: Increased oxidative/nitrosative stress is important in the pathogenesis of diabetic complications, and the protective effects of antioxidants are a topic of intense research. The purpose of this study was to investigate whether a pyridoindole antioxidant stobadine (STB) have a protective effect on tissue oxidative protein damage represented by the parameters such as protein carbonylation (PC), protein thiol (P-SH), total thiol (T-SH) and non-protein thiol (Np-SH), nitrotyrosine (3-NT), and advanced oxidation protein products (AOPP) in streptozotocin-diabetic rats. Methods: Diabetes was induced in male Wistar rats by intraperitonal injection of streptozotocin (55 mg/kg). Some of the non-diabetic (control) and diabetic rats treated with STB (24.7 mg/kg/day) during 16 weeks, and the effects on blood glucose, PC, AOPP, 3-NT, P-SH, T-SH and Np-SH were studied. Biomarkers were assayed by enzyme-linked immunosorbent assay (ELISA) or by colorimetric methods. Results: Administration of stobadine to diabetic animals lowered elevated blood glucose levels by ,16% relative to untreated diabetic rats. Although stobadine decreased blood glucose, poor glycemic control was maintained in stobadine treated diabetic rats during the treatment period. Biochemical analyses of liver proteins showed significant diminution of sulfhydryl groups, P-SH, T-SH, Np-SH, and elevation of carbonyl groups in diabetic animals in comparison to healthy controls. As a biomarker of nitrosative stress, 3-NT levels did not significantly change by diabetes induction or by stobadine treatment when compared to control animals. However, the treatment with stobadine resulted in a significant decrease in PC, AOPP levels and normalized P-SH, T-SH, Np-SH groups in liver of diabetic animals. [source] 3353: Response of the human eye against oxidative stress at high altitudesACTA OPHTHALMOLOGICA, Issue 2010S KARAKUCUK Purpose To evaluate the response of the anterior segment of the eye against oxidative stress during acute exposure to high altitudes. Methods Forty volunteers were examined and measurements performed at Erciyes University Medical Faculty,Ophthalmology Clinic, Kayseri,Turkey(1080m). On the following day, participants were transported to Mt. Erciyes Ski Center by bus(2200m); thereafter they climbed to an altitude of 2800m.with a moderate pace. Central corneal thickness, intraocular pressure,spheric equivalent of refraction, arterial oxygen pressure,blood pressure, pulse rate and body temperature were measured at both altitudes. Venous blood samples were taken from volunteers at both altitudes;total oxidant status (TOS),total antioxidant status(TAS),advanced oxidation protein products (AOPP), xanthine oxidase (XO), thiol, adenosine deaminase(ADA)levels were investigated at 1080m and 2800m. Results TOS(7.02µmol H2O2 equiv/L, range:0.49-22.07) and AOPP(220.74µmol/L,range:103.81-667.35)significantly increased at high altitude, compared to low altitude levels (3.32µmol H2O2 equiv/L range:0.92-18.41,and 195.58µmol/L,range:84.77-663.16, resp; p<0.05).IOP significantly elevated at high altitude (14.45±3.54mmHg vs 13.22±2.74mmHg; p<0.05). There was a significant positive correlation between IOP and TAS levels(p<0.05). No significant correlation was found between spherical equivalent or central corneal thickness with the investigated oxidation parameters at both altitudes Conclusion We conclude that oxidative stress markers, TOS and AOPP are increased along with IOP during acute exposure to hypoxic environment at high altitudes and that antioxidant system may have a limited capacity to counter balance this effect because of acute unacclimatized ascent. [source] | |||||||||||||