scholarly journals Investigation of DNA damage and protein damage caused by oxidative stress in canine visceral leishmaniasis

2021 ◽  
Vol 77 (08) ◽  
pp. 6559-2021
Author(s):  
FUNDA KIRAL ◽  
SELIM SEKKIN ◽  
SERDAR PASA ◽  
HATICE ERTABAKLAR ◽  
PINAR ALKIM ULUTAS ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Antioxidant Capacity ◽  
Leishmania Infantum ◽  
Protein Carbonyl ◽  
World Health ◽  
Protein Damage ◽  
Control Group ◽  
Protein Carbonyl Content ◽  
Plasma Malondialdehyde

Leishmaniasis, considered by the World Health Organization as one of the most important zoonotic diseases, causes death when it is not treated in its self-healing skin form. The aim of this study was to investigate DNA damage and oxidative protein damage that occurs in dogs infected with Leishmania infantum. The study group consisted of 25 dogs, including 10 clinically healthy dogs aged 2 to 6 years and 15 dogs infected with Leishmania infantum diagnosed by means of the rk39 dipstick test and the immunofluorescence antibody test (IFAT). The effects of oxidative stress on protein were evaluated in the dogs infected with Leishmania infantum by determining plasma malondialdehyde, protein carbonyl groups, nitrotyrosine, and total antioxidant capacity in blood. DNA damage, on the other hand, was determined by the COMET method. Plasma protein carbonyl content (PCO) and nitrotyrosine (NT) levels, which are considered as indicators of protein damage, were found to be higher in the dogs infected with Leishmania infantum compared to the control group, but the difference in both values was not statistically significant (p > 0.05). Plasma malondialdehyde (MDA), an indicator of lipid peroxidation, was significantly higher in the dogs infected with Leishmania infantum than in the control group. TAC levels, however, were lower in the leishmanial dogs (p < 0.05). According to the results of the COMET assay, lymphocyte cells were damaged in the leishmanial dogs, and both tail intensity (TI) and tail moment (TM) values were higher in those dogs than they were in the control group (p < 0.05, p < 0.01). The parasites caused oxidative stress through protein and DNA damage in the host and decreased the antioxidant capacity concentration that prevents destructive effects.

Alteration in the oxidative status of Drosophila melanogaster Meigen (Diptera: Drosophilidae) fed with a diet containing Centaurea depressa M. Bieb. (Asteraceae)

2020 ◽  
Vol 70 (2) ◽  
pp. 227-237
Author(s):  
Eda Güneş
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Total Protein ◽  
Protein Carbonyl ◽  
Control Group ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Freeze Dried ◽  
Dried Extract

Abstract The aim of the this study was to evaluate the effects of fresh, dried and freeze-dried Centaurea depressa M. Bieb. (Asteraceae) on the oxidant and antioxidant status of the model organism D. melanogaster Meigen (Diptera: Drosophilidae) experimentally. The study was carried out from 2016 to 2019, and plant leaf extracts (0-50 mg/l) were added to insect standard artificial diets. The total protein, protein carbonyl content and glutathione-S-transferase, superoxide dismutase and catalase activities were quantified at the insect’s third larval stage. Our data showed that protein carbonyl content varied from 2.70 nmol/mg protein in the control group to 59.11 nmol/mg protein in the group fed with fresh leaf extract signifying induction of oxidative stress. All extracts increased the levels of all antioxidant enzymes and decreased the amounts of total protein. Meanwhile, the group fed with the freeze-dried extract showed no significant difference in the levels of total protein and protein carbonyl content except at the 50 mg/l concentration of the extract. Moreover, this group had superoxide dismutase and catalase activities 4 to 5 times higher than in the control group. In conclusion, induction of oxidative stress indicates that the fresh form of C. depressa leaves may have potential as a natural pesticide, whereas induction of endogenous antioxidant enzymes by the freeze-dried extract suggest its potential as an antioxidant.

scholarly journals DNA Damage in Lymphocytes in Hypertensive Subjects in Bangladesh

2013 ◽  
Vol 5 (3) ◽  
pp. 535-543
Author(s):  
M. Saiedullah ◽  
S. Hayat ◽  
M. R. Zamir ◽  
M. Arif ◽  
Z. H. Howlader ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Dna Damage ◽  
Superoxide Dismutase ◽  
Oxidative Dna Damage ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Ribonucleic Acids ◽  
Stress Oxidative ◽  
Bangladeshi Population

Oxidative stress due to imbalance between the production of reactive oxygen species and their dismutation is claimed to be higher in hypertensive subjects than normotensive subjects. In hypertensive subjects oxidative stress may damage deoxy-ribonucleic acids (DNA). In this study plasma superoxide dismutase (SOD) activities, protein carbonyl contents (PCCs) and extent of DNA damage in lymphocytes were measured in specimens obtained from 86 subjects to compare oxidative stress and oxidative DNA damage between normotensive and hypertensive subjects and to assess their relationship with the degree of blood pressure. Results were expressed as mean±SD. Two-tailed unpaired t test and Pearson’s correlation test were done to compare or to determine the relationship between groups or variables. SOD activities were 2.85±0.12 unit/mg protein and 3.84±0.45 unit/mg protein (p<0.05) in hypertensive and normotensive groups respectively. PCCs were 4.77±0.36 nmol/mg protein and 3.75±0.23 nmol/mg protein in hypertensive and normotensive groups respectively. Olive tail moments (OTM) were 124.7±11.69 units and 108.9±9.27 units in hypertensive and normotensive groups respectively. The correlation coefficient of OTM was 0.3924 (p<0.05) for diastolic blood pressure and 0.3618 (p<0.05) for systolic blood pressure. Oxidative stress and DNA damage was higher in hypertensives than normotensives and DNA damage correlated positively with blood pressure. Keywords: Superoxide dismutase, Protein carbonyl content, Oxidative stress, Oxidative DNA damage, Hypertension, Bangladeshi population. © 2013 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved. doi: http://dx.doi.org/10.3329/jsr.v5i3.15022 J. Sci. Res. 5 (3), 535-543 (2013)  

scholarly journals Assessment of oxidative stress in lymphocytes with exercise

2011 ◽  
Vol 111 (1) ◽  
pp. 206-211 ◽  
Author(s):  
James E. Turner ◽  
Jos A. Bosch ◽  
Mark T. Drayson ◽  
Sarah Aldred
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Peripheral Blood ◽  
Lipid Peroxides ◽  
Protein Carbonyl ◽  
Treadmill Running ◽  
Effector Memory ◽  
Cellular Composition ◽  
Protein Carbonyl Content ◽  
Thiol Content

This study investigated whether changes in the cellular composition of blood during exercise could partly account for observations of exercise-induced changes in lymphocyte oxidative stress markers. Markers of oxidative stress were assessed before and after 60 min of intense treadmill running. Samples were collected from 16 men (means ± SD: age 33 ± 13 yr; body mass index 23.8 ± 2.5 kg/m2; maximal oxygen uptake 59.7 ± 5.2 ml·kg−1·min−1). Peripheral blood lymphocytes were assayed for protein carbonyl concentration, and plasma was assessed for lipid peroxides and antioxidant capacity. In a separate study, intracellular thiol concentration was determined in lymphocyte subsets from eight characteristically similar men by flow cytometry, of which T-cell memory populations were further identified on the basis of CD27, CD28, and CD45RA expression. Total lymphocyte protein carbonyls were transiently increased with exercise and returned to baseline within 15 min ( P < 0.001). This change was accompanied by an increase in plasma lipid peroxides ( P < 0.05) and total antioxidant capacity ( P < 0.001). Correlation analyses showed that lymphocyte protein carbonyl content was not related to changes in the cellular composition of peripheral blood during exercise. Natural killer cells (CD3−CD56+) and late-differentiated/effector memory cells (CD4+/CD8+CD27−CD28−/CD45RA+), which mobilized most with exercise, showed high intracellular thiol content ( P < 0.001). High thiol content suggests a lower oxidative load carried by these lymphocytes. Thus vigorous exercise resulted in a transient increase in lymphocyte oxidative stress. Results suggest this was unrelated to the alterations in the cellular composition of peripheral blood.

scholarly journals Oxidative Stress Induced in Nurses by Exposure to Preparation and Handling of Antineoplastic Drugs in Mexican Hospitals: A Multicentric Study

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Leobardo Manuel Gómez-Oliván ◽  
Gerardo Daniel Miranda-Mendoza ◽  
Paula Anel Cabrera-Galeana ◽  
Marcela Galar-Martínez ◽  
Hariz Islas-Flores ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biochemical Analysis ◽  
Protein Carbonyl ◽  
Control Group ◽  
Antineoplastic Drugs ◽  
Multicentric Study ◽  
Protein Carbonyl Content ◽  
Occupationally Exposed ◽  
Study Participants ◽  
The Impact

The impact of involuntary exposure to antineoplastic drugs (AD) was studied in a group of nurses in diverse hospitals in Mexico. The results were compared with a group of unexposed nurses. Anthropometric characteristics and the biochemical analysis were analyzed in both groups. Also, lipid peroxidation level (LPX), protein carbonyl content (PCC), and activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were evaluated in blood of study participants as oxidative stress (OS) biomarkers. The group of occupationally exposed (OE) nurses consisted of 30 individuals ranging in age from 25 to 35 years. The control group included 30 nurses who were not occupationally exposed to the preparation and handling of AD and whose anthropometric and biochemical characteristics were similar to those of the OE group. All biomarkers evaluated were significantly increased (P<0.5) in OE nurses compared to the control group. Results show that the assessment of OS biomarkers is advisable in order to evaluate exposure to AD in nurses.

Acrylamide attenuated immune tissues’ function via induction of apoptosis and oxidative stress: Protection by l-carnitine

2017 ◽  
Vol 37 (8) ◽  
pp. 859-869 ◽  
Author(s):  
E Zamani ◽  
M Shokrzadeh ◽  
A Ziar ◽  
S Abedian-Kenari ◽  
F Shaki
Keyword(s):  
Oxidative Stress ◽  
Blood Cells ◽  
Annexin V ◽  
Protein Carbonyl ◽  
Pathological Examination ◽  
Control Group ◽  
Protein Carbonyl Content ◽  
Organ Weights ◽  
Immune Tissues ◽  
Body Organ

Acrylamide (ACR), with high prevalence in starchy food, has been associated with the development of several organ toxicities such as immunotoxicity. This study aimed to demonstrate the role of oxidative stress and apoptosis as the mechanisms involved in ACR-induced immunotoxicity in mice. Mice were randomly assigned to six groups and treated as follows: control (normal saline), cyclophosphamide (200 mg kg–1), ACR groups (12.5, 25 and 50mg kg–1, orally), and l-carnitine (l-CAR; 100 mg kg–1) + ACR (50 mg kg–1). After 30 days of exposure, mice were killed and immunotoxic response was evaluated via immune blood cells count and body/organ weights. Oxidative stress parameters and pathological examination were done in thymus and spleen. Also, the apoptosis was evaluated via flow cytometric by annexin V/FITC kit in the splenocytes. Our results indicated that ACR could induce immunotoxicity characterized by reduction in immune blood cells, body/organ weights, and pathological changes in spleen. The assessment of oxidative stress markers revealed increase in lipid peroxidation, protein carbonyl content, and depletion of glutathione level. Also, increased apoptosis was observed in splenocytes after ACR administration compared to the control group. These alterations were markedly normalized by coadministration of l-CAR (as a potent antioxidant). Taken together, the results of this study showed the potential of ACR to induce immunotoxicity through provoking oxidative stress and inducing apoptosis and the protective effect of l-CAR to attenuate this toxicity. These findings will help in elucidating the toxicity mechanism induced by ACR.

scholarly journals Antioxidant activity of Lactobacillus plantarum NJAU-01 in an animal model of aging

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qingfeng Ge ◽  
Bo Yang ◽  
Rui Liu ◽  
Donglei Jiang ◽  
Hai Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Lactobacillus Plantarum ◽  
Meat Product ◽  
The Other ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Intragastric Administration ◽  
Aging Effects ◽  
Sterile Saline

Abstract Background Excessive reactive oxygen species (ROS) can cause serious damage to the human body and may cause various chronic diseases. Studies have found that lactic acid bacteria (LAB) have antioxidant and anti-aging effects, and are important resources for the development of microbial antioxidants. This paper was to explore the potential role of an antioxidant strain, Lactobacillus plantarum NJAU-01 screened from traditional dry-cured meat product Jinhua Ham in regulating D-galactose-induced subacute senescence of mice. A total of 48 specific pathogen free Kun Ming mice (SPF KM mice) were randomly allocated into 6 groups: control group with sterile saline injection, aging group with subcutaneously injection of D-galactose, treatments groups with injection of D-galactose and intragastric administration of 107, 108, and 109 CFU/mL L. plantarum NJAU-01, and positive control group with injection of D-galactose and intragastric administration of 1 mg/mL Vitamin C. Results The results showed that the treatment group of L. plantarum NJAU-01 at 109 CFU/mL showed higher total antioxidant capacity (T-AOC) and the antioxidant enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) than those of the other groups in serum, heart and liver. In contrast, the content of the oxidative stress marker malondialdehyde (MDA) showed lower levels than the other groups (P < 0.05). The antioxidant capacity was improved with the supplement of the increasing concentration of L. plantarum NJAU-01. Conclusions Thus, this study demonstrates that L. plantarum NJAU-01 can alleviate oxidative stress by increasing the activities of enzymes involved in oxidation resistance and decreasing level of lipid oxidation in mice.

scholarly journals Protein carbonyls and protein thiols in rheumatoid arthritis

2018 ◽  
Vol 6 (5) ◽  
pp. 1738 ◽  
Author(s):  
Pullaiah P. ◽  
Suchitra M. M. ◽  
Siddhartha Kumar B.
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Protein Modification ◽  
Antioxidant Properties ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Carbonyl Content ◽  
Protein Thiol ◽  
Protein Carbonyl Content ◽  
Protein Thiols

Background: Oxidative stress (OS) has an important role in the pathogenesis and progression of rheumatoid arthritis (RA). OS causes protein modification, thereby impairing the biological functions of the protein. This study was conducted to assess the oxidatively modified protein as protein carbonyl content and the antioxidant status as protein thiols, and to study the association between protein carbonyls and protein thiols in RA.Methods: Newly diagnosed RA patients who were not taking any disease modifying anti-rheumatic drugs were included into the study group (n=45) along with age and sex matched healthy controls (n=45). Serum protein carbonyl content and protein thiols were estimated.Results: Elevated protein carbonyl content and decreased protein thiol levels (p<0.001) were observed in RA. A significant negative correlation was observed between protein carbonyl content and protein thiol levels (p<0.001).Conclusions: Oxidative stress in RA is evidenced by enhanced protein oxidation and decreased antioxidant protein thiol levels. Decreased protein thiols may also reflect protein modifications leading to compromise in the antioxidant properties. This oxidant and antioxidant imbalance needs to be addressed by therapeutic interventions to prevent disease progression.

scholarly journals Sulforaphane-Mediated Nrf2 Activation Prevents Radiation-Induced Skin Injury through Inhibiting the Oxidative-Stress-Activated DNA Damage and NLRP3 Inflammasome

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1850
Author(s):  
Jinlong Wei ◽  
Qin Zhao ◽  
Yuyu Zhang ◽  
Weiyan Shi ◽  
Huanhuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Western Blotting ◽  
Nlrp3 Inflammasome ◽  
Fibrous Tissue ◽  
Mouse Skin ◽  
Control Group ◽  
Skin Injury ◽  
Antioxidant Genes ◽  
Radiation Induced

This article mainly observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI). In addition, we will discuss the mechanism of SFN’s protection on RISI. The RISI model was established by the irradiation of the left thigh under intravenous anesthesia. Thirty-two C57/BL6 mice were randomly divided into control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group. At eight weeks after irradiation, the morphological changes of mouse skin tissues were detected by H&E staining. Then, the oxidative stress and inflammatory response indexes in mouse skin tissues, as well as the expression of Nrf2 and its downstream antioxidant genes, were evaluated by ELISA, real-time PCR, and Western blotting. The H&E staining showed the hyperplasia of fibrous tissue in the mouse dermis and hypodermis of the IR group. Western blotting and ELISA results showed that the inflammasome of NLRP3, caspase-1, and IL-1β, as well as oxidative stress damage indicators ROS, 4-HNE, and 3-NT, in the skin tissues of mice in the IR group were significantly higher than those in the control group (p < 0.05). However, the above pathological changes declined sharply after SFN treatment (p < 0.05). In addition, the expressions of Nrf2 and its regulated antioxidant enzymes, including CAT and HO-1, were higher in the skin tissues of SFN and IR/SFN groups, but lower in the control and IR groups (p < 0.05). SFN may be able to suppress the oxidative stress by upregulating the expression and function of Nrf2, and subsequently inhibiting the activation of NLRP3 inflammasome and DNA damage, so as to prevent and alleviate the RISI.

scholarly journals Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus

2011 ◽  
Vol 34 (3) ◽  
pp. 163 ◽  
Author(s):  
Omur Tabak ◽  
Remise Gelisgen ◽  
Hayriye Erman ◽  
Fusun Erdenen ◽  
Cüneyt Muderrisoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Vascular Complications ◽  
Diabetic Group ◽  
Control Group ◽  
Diabetic Patients ◽  
Serum Samples ◽  
Type 2 Diabetic Patients

Purpose: The purpose of this study was to determine the effects of diabetic complications on oxidation of proteins, lipids, and DNA and to investigate the relationship between oxidative damage markers and clinical parameters. Methods: The study group consisted of 69 type 2 diabetic patients (20 patients without complication, 49 patients with complication) who attended internal medicine outpatient clinics of Istanbul Education and Research Hospital and 19 healthy control subjects. In serum samples of both diabetic patients and healthy subjects, 8-hydroxy-2’deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, Nε-(hexanoyl)lysine (HEL) and 15-F2t-iso-prostaglandin (15-F2t-IsoP). as products of lipooxidative damage, advanced oxidation protein products (AOPP), as markers of protein damage, and paraoxonase1 (PON1) as antioxidant were studied. Results: 15-F2t-IsoP (p < 0.005) and AOPP (p < 0.001) levels were significantly higher in diabetic group than control group while there were no significant differences in levels of 8-OHdG and HEL between the two groups. AOPP (p < 0.001) and 8-OHdG (p < 0.001) were significantly higher in diabetic group with complications compared to diabetic group without complications. Conclusions: Increased formation of free radicals and oxidative stress, under conditions of hyperglycaemia, is one of the probable causes for evolution of complications in diabetes mellitus. Our study supports the hypothesis that oxidant/antioxidant balance is disturbed in diabetic patients.

Lead induced oxidative DNA damage in battery-recycling child workers from Bangladesh

2018 ◽  
Vol 34 (4) ◽  
pp. 213-218 ◽  
Author(s):  
Mohammad Arif ◽  
MM Towhidul Islam ◽  
Hossain Uddin Shekhar
Keyword(s):  
Dna Damage ◽  
Lead Exposure ◽  
Oxidative Dna Damage ◽  
Lead Concentration ◽  
Threshold Level ◽  
Protein Carbonyl ◽  
The Body ◽  
Lipid Peroxidation Product ◽  
Protein Carbonyl Content ◽  
Battery Recycling

Lead exposure can damage cells directly by effecting DNA or indirectly by modifying proteins and enzymes. In Bangladesh, many working children are exposed to a very high level of lead during their early life due to their involvement with lead-oriented professions. This imposes a severe threat to the growth and development of the children. Therefore to study the effect of lead, we enrolled 60 age-matched male children, from an area of old Dhaka city, where battery-recycling shops are located, depending on their blood lead concentration. If the children had a plasma lead concentration above the WHO recommended threshold level of 10 µg/dl, we grouped them as test subjects and others as control subjects to determine the effect of lead on different biochemical parameters of the body. Compared to the controls, acculumlation of the lipid peroxidation product, malondialdehyde, increased significantly in test subjects ( p < 0.01). Lead exposure also increased the protein carbonyl content ( p < 0.05) and significantly decreased the plasma glutathione levels of test subjects compared to the controls ( p < 0.05). While comparing the lead-exposed group against controls, it was found that the percentage of damaged DNA, as measured using the Comet assay, significantly increased in tail ( p < 0.01) and decreased in head regions. All of these results suggest that high-plasma lead content may induce an oxidative stress to the study population, which may lead to DNA damage.

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