In-vivo effects of nociceptin and its structural analogue [Orn9] nociceptin on the antioxidant status of rat blood and liver after carrageenan-induced paw inflammation

Open Medicine ◽  
2010 ◽  
Vol 5 (1) ◽  
pp. 123-131 ◽  
Author(s):  
Lubomir Petrov ◽  
Elina Tzvetanova ◽  
Almira Pavlova ◽  
Albena Alexandrova ◽  
Rositsa Zamfirova ◽  
...  

AbstractThe production of reactive oxygen species (ROS) in cells is well balanced with their elimination by the antioxidant defence system. This balance is essential for maintenance of physiological conditions, and its disturbance (oxidative stress) has been suggested as a potential pathogenic mechanism in a variety of diseases, accompanied by inflammation. In this study, the in-vivo effects of nociceptin (N/OFQ(1–13)NH2) and its structure analogue [Orn9]N/OFQ(1–13)NH2 were studied on markers of oxidative stress in erythrocytes and liver of rats 4 hours after subplantar administration of carrageenan (CG) (1%, 100 µl) in the right hind paw. A considerable inflammatory oedema of the paw was observed. CG did not change blood haemoglobin content, hematocrit value, glutathione level and antioxidant enzyme activities in the erythrocytes, but there was an increase in lipid peroxidation. In liver, CG-induced imbalance was manifested by an increase in lipid peroxidation and a decrease in glutathione level. Both peptides (20 µg, i.p.), when administered alone, had no effect on all parameters tested. When either [Orn9]N/OFQ(1–13)NH2 or N/OFQ(1–13)NH2 was injected simultaneously with CG or 15 minutes before it, they did not affect the CG-induced changes in the antioxidant status of the erythrocytes and liver. Our results suggest that the peptides tested did not play a role in the free radical processes that accompany CG-induced paw inflammation.

2009 ◽  
Vol 25 (8) ◽  
pp. 545-550 ◽  
Author(s):  
Ismail Karabulut ◽  
Z. Dicle Balkanci ◽  
Bilge Pehlivanoglu ◽  
Aysen Erdem ◽  
Ersin Fadillioglu

Toluene, an organic solvent used widely in the industry, is highly lipophilic and accumulates in the cell membrane impeding transport through it. Its metabolites cause oxygen radical formation that react with unsaturated fatty acids and proteins in erythrocytes leading to lipid peroxidation and protein breakdown. In this study, we aimed to investigate the membrane stabilizing and the oxidative stress—inducing effects of toluene in human erythrocytes. Measurements of osmotic fragility, mean corpuscular volume (MCV), oxidative stress parameters and antioxidant enzyme activities were performed simultaneously both in individuals exposed to toluene professionally (in vivo) and human erythrocytes treated with toluene (in vitro). To measure osmotic fragility, erythrocytes were placed in NaCl solutions at various concentrations (0.1% [blank], 0.38%, 0.40%, 0.42%, 0.44%, 0.46%, 0.48% and 1% [stock]). Percentage of haemolysis in each solution was calculated with respect to the 100% haemolysis in the blank solution. The erythrocyte packs prepared at the day of the above-mentioned measurements were kept at —80°C until the time for determination of malonyldialdehyde and protein carbonyl levels, and catalase (CAT) and glutathione peroxidase activities as indicators of oxidative stress. Toluene increased oxidative stress parameters significantly both in vivo and in vitro; it also caused a significant decrease in the activities of antioxidant enzymes. Osmotic fragility was altered only in the case of in vitro exposure. In conclusion, toluene exposure resulted in increased lipid peroxidation and protein damage both in vivo and in vitro. Although, it is natural to expect increased osmotic fragility due to oxidative properties of toluene, its membrane-stabilizing effect overcame the oxidative properties leading to decreased osmotic fragility or preventing its deterioration in vitro and in vivo toluene exposures, respectively, in the present study.


2018 ◽  
Vol 19 (3) ◽  
pp. 287-291 ◽  
Author(s):  
Ashish Verma ◽  
Vivek Tripathi ◽  
Sahib T Singh ◽  
Chetan D Singh ◽  
Jaspreet S Gill

ABSTRACT Introduction Periodontitis is a common problem affecting a significant population of the world. For the assessment of oxidative stress of an individual, total oxidation status (TOS) and total antioxidant capacity (TAOC) are the significant biomarkers. Hence, we planned the present study to assess malondialdehyde (MDA), TOS, TAOC levels, and oxidative stress index (OSI) in generalized aggressive periodontitis (GP) and chronic periodontitis (CP) patients. Materials and methods The present study included assessment of 40 CP patients, 40 GP patients, and 40 healthy controls. Clinical assessment of all the subjects was done by measuring the probing depth (PD), clinical attachment (CL), gingival index (GI), gingival bleeding index (GBI), and plaque index (PI). Salivary and serum samples were taken and assessed by standard procedures as described previously in the literature. All the values were assessed and compared. Results Significant results were obtained while comparing all the periodontal parameters in between various study groups. Mean serum MDA levels in the CP, GP, and control group were found to be 0.68, 0.65, and 0.61 µM respectively. Statistically nonsignificant results were obtained while comparing the serum MDA levels in between the three study groups. Significant results were obtained while comparing the mean serum and salivary TOS values, TAOC values, and OSI in between various study groups. Conclusion In periodontitis patients, oxidative stress was significantly higher in comparison with healthy subjects. Clinical significance Oxidative parameters do play a significant role in the pathologic profile of periodontitis. How to cite this article Tripathi V, Singh ST, Sharma V, Verma A, Singh CD, Gill JS. Assessment of Lipid Peroxidation Levels and Total Antioxidant Status in Chronic and Aggressive Periodontitis Patients: An in vivo Study. J Contemp Dent Pract 2018;19(3):287-291.


2015 ◽  
Vol 3 (3) ◽  
pp. 12-16
Author(s):  
Raju Kumar Dubey ◽  
Narayan Gautam ◽  
Niraj Dhakal ◽  
Nirmal Baral ◽  
Madhab Lamsal ◽  
...  

INTRODUCTION: Brain is particularly vulnerable to oxidative free radicals. Oxidative stress might primarily or secondarily be involved in the pathogenesis of Bipolar Affective Disorder. Therefore this study was aimed to estimate & compare parameters of oxidative stress and antioxidant levels in patients with Bipolar Affective Disorder and healthy controls. MATERIAL AND METHODS: A total of 32 Bipolar Affective Disorder patients and 30 healthy subjects were recruited in this study. Plasma MDA level was measured as indicator of lipid peroxidation and SOD and CAT activities were determined as a measure of antioxidant status. RESULT: Out of total Bipolar Affective Disorder patients 21 were in mania with psychotic symptoms, 8 were in mania without psychotic symptoms and only 3 were in mixed episode. Significantly (p<0.001) elevated MDA level (nmol/ml) was found in before treatment patient group (7.11 ± 1.62) as compared to control (3.02 ± 1.30) group. Patients on follow-up also had significantly increased MDA level (nmol/ml) (5.37 ± 1.36) as compared to control group and decrease in level was significant (p<0.001) in comparison to before treatment patients. CAT and SOD activities (U/gm Hb) were significantly decreased in both before treatment (87.57 ± 28.79 & 1341 ± 167.18) and after treatment (77.12 ± 29.48 & 1305.56 ± 154.86) patients group compared to the control (155.92 ± 29.43 & 1408.14 ± 78.82) group respectively. CAT and MDA were negatively correlated in the before treatment patients group (r = -0.356, p<0.05).  CONCLUSION: The findings suggest that there is increased oxidative stress in Bipolar Affective Disorder patients in comparison to controls.


Signals ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 138-158
Author(s):  
Hsiang-Wei Wang ◽  
Cameron Bringans ◽  
Anthony J. R. Hickey ◽  
John A. Windsor ◽  
Paul A. Kilmartin ◽  
...  

Oxidative stress plays a pivotal role in the pathogenesis of many diseases, but there is no accurate measurement of oxidative stress or antioxidants that has utility in the clinical setting. Cyclic Voltammetry is an electrochemical technique that has been widely used for analyzing redox status in industrial and research settings. It has also recently been applied to assess the antioxidant status of in vivo biological samples. This systematic review identified 38 studies that used cyclic voltammetry to determine the change in antioxidant status in humans and animals. It focusses on the methods for sample preparation, processing and storage, experimental setup and techniques used to identify the antioxidants responsible for the voltammetric peaks. The aim is to provide key information to those intending to use cyclic voltammetry to measure antioxidants in biological samples in a clinical setting.


2016 ◽  
pp. 75-78
Author(s):  
Liliia Babynets ◽  
Tetiana Maevska

The study proved that patients with combined progress of osteoarthritis and chronic pancreatitis have reliable top-level activation of lipid peroxidation in terms of malonyc aldehyde and tissue destruction in terms of oxyproline, weakening of the antioxidant level (in terms of superoxide dismutase and SH-groups) and activation parameters of catalase and ceruloplasmin (p<0,05). The authentic predictority of patients biological age, duration of combined clinical courses, the functional capacity of the pancreas in terms of fecal α-elastase, structural state by ultrasound criteria for progression effects of oxidative stress, accumulation oxyproline activation parameters catalase and ceruloplasmin, which statistically was reflected by the presence of mainly moderate of significant correlations between these groups of indicators have been identified.


2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.


2009 ◽  
Vol 4 (2) ◽  
pp. 170-178 ◽  
Author(s):  
Rositsa Zamfirova ◽  
Elina Tzvetanova ◽  
Albena Alexandrova ◽  
Lubomir Petrov ◽  
Polina Mateeva ◽  
...  

AbstractThe effects of nociceptin(1–13)NH2 (N/OFQ(1–13)NH2) and its structural analogue [Orn9]N/OFQ(1–13)NH2 on acute carrageenan (CG)-induced peripheral inflammation and paw antioxidant status were studied. CG was injected intraplantarly in the right hind paw of rats and the volume of the inflamed paw was measured each 30 min for a period of 4h. When administered simultaneously with CG, N/OFQ(1–13)NH2 decreased the paw volume, whereas if injected 15 min before CG it had no effect. [Orn9]N/OFQ(1–13)NH2 produced the opposite effects at the same time-intervals of its administration. We also investigated whether these neuropeptides influence CG-induced changes in cell antioxidant system, especially at the 4th hour of CG administration. CG alone decreased the glutathione level and superoxide dismutase activity, as measured in post-nuclear homogenate of the inflamed paw. However, CG injection increased glutathione peroxidase and glucose-6-phospate dehydrogenase activities, while the activity of glutathione reductase was unchanged. The peptides themselves did not change all measured parameters. Moreover, neither N/OFQ(1–13)NH2 nor [Orn9]N/OFQ(1–13)NH2 modified CG-induced changes in the antioxidant status, regardless of the time of their injection (simultaneously or 15 min before CG). The present results suggest that N/OFQ(1–13)NH2 and [Orn9]N/OFQ(1–13)NH2 most likely affect the neuronal inflammation, rather than act as pro- or antioxidants.


2013 ◽  
Vol 59 (4) ◽  
pp. 443-451 ◽  
Author(s):  
E.A. Kosenko ◽  
L.A. Tikhonova ◽  
A.C. Poghosyan ◽  
Y.G. Kaminsky

Age of patients and brain oxidative stress may contribute to pathogenesis of Alzheimer's disease (AD). Erythrocytes (red blood cells, RBC) are considered as passive “reporter cells” for the oxidative status of the whole organism and are not well studied in AD. The aim of this work was to assess whether the antioxidant status of RBC changes in aging and AD. Blood was taken from AD and non-Alzheimer's dementia patients, aged-matched and younger controls. In vivo antioxidant status was assessed in each of the study subjects by measuring RBC levels of Н О , organic hydroperoxides, glutathione (GSH) and glutathione disulfide (GSSG), activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, and glucose-6-phosphate dehydrogenase. In both aging and dementia, oxidative stress in RBC was shown to increase and to be expressed in elevated concentrations of H O and organic hydroperoxides, decreased the GSH/GSSG ratio and glutathione S-transferase activity. Decreased glutathione peroxidase activity in RBC may be considered as a new peripheral marker for Alzheimer’s disease while alterations of other parameters of oxidative stress reflect age-related events.


2021 ◽  
Author(s):  
Arnold N. Onyango

Unhealthy diets, such as those high in saturated fat and sugar accelerate the development of non-communicable diseases. The metabolic syndrome is a conglomeration of disorders such as abdominal obesity, hypertension, impaired glucose regulation and dyslipidemia, which increases the risk for diabetes and cardiovascular disease. The prevalence of the metabolic syndrome is increasing globally, and dietary interventions may help to reverse this trend. A good understanding of its pathophysiological mechanisms is needed for the proper design of such interventions. This chapter discusses how lipid peroxidation is associated with the development of this syndrome, mainly through the formation of bioactive aldehydes, such as 4-hydroxy-2-nonenal, malondialdehyde, acrolein and glyoxal, which modify biomolecules to induce cellular dysfunction, including the enhancement of oxidative stress and inflammatory signaling. It gives a current understanding of the mechanisms of formation of these aldehydes and how dietary components such as saturated fatty acids promote oxidative stress, leading to lipid oxidation. It also outlines mechanisms, apart from free radical scavenging and singlet oxygen quenching, by which various dietary constituents prevent oxidative stress and lipid oxidation in vivo.


Blood ◽  
2009 ◽  
Vol 113 (3) ◽  
pp. 744-754 ◽  
Author(s):  
Yixin Tang ◽  
Elizabeth A. Scheef ◽  
Shoujian Wang ◽  
Christine M. Sorenson ◽  
Craig B. Marcus ◽  
...  

Abstract Reactive species derived from cell oxygenation processes play an important role in vascular homeostasis and the pathogenesis of many diseases including retinopathy of prematurity. We show that CYP1B1-deficient (CYP1B1−/−) mice fail to elicit a neovascular response during oxygen-induced ischemic retinopathy. In addition, the retinal endothelial cells (ECs) prepared from CYP1B1−/− mice are less adherent, less migratory, and fail to undergo capillary morphogenesis. These aberrant cellular responses were completely reversed when oxygen levels were lowered or an antioxidant added. CYP1B1−/− ECs exhibited increased oxidative stress and expressed increased amounts of the antiangiogenic factor thrombospondin-2 (TSP2). Increased lipid peroxidation and TSP2 were both observed in retinas from CYP1B1−/− mice and were reversed by administration of an antioxidant. Reexpression of CYP1B1 in CYP1B1−/− ECs resulted in down-regulation of TSP2 expression and restoration of capillary morphogenesis. A TSP2 knockdown in CYP1B1−/− ECs also restored capillary morphogenesis. Thus, CYP1B1 metabolizes cell products that modulate intracellular oxidative stress, which enhances production of TSP2, an inhibitor of EC migration and capillary morphogenesis. Evidence is presented that similar changes occur in retinal endothelium in vivo to limit neovascularization.


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