The Investigation of Oxidative/nitrosative Stress and DNA Damage in Patients with Permanent Tunnel Port Catheters with Ultrasound Access to Bed

2019 ◽  
Vol 145 ◽  
pp. S78-S79
Keyword(s):  
Dna Damage ◽  
Nitrosative Stress ◽  
Port Catheters

Assessment of oxidative/nitrosative stress biomarkers and DNA damage in Haemonchus contortus, following exposure to zinc oxide nanoparticles

2018 ◽  
Vol 63 (3) ◽  
pp. 563-571 ◽  
Author(s):  
Bijan Esmaeilnejad ◽  
Awat Samiei ◽  
Yousef Mirzaei ◽  
Farhad Farhang-Pajuh
Keyword(s):  
Dna Damage ◽  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Metallic Nanoparticles ◽  
Nitrosative Stress ◽  
Total Antioxidant Status ◽  
Parasitic Infections ◽  
Oxide Nanoparticles ◽  
Helminth Parasites ◽  
Zno Nps

Abstract Drug resistance in helminth parasites has incurred several difficulties to livestock industry and ranked among the top public health concerns. Therefore, seeking for new agents to control parasites is an urgent strategy. In the recent years, metallic nanoparticles have been considerably evaluated for anthelmintic effects. The current research was conducted to assess possible anthelmintic impacts of zinc oxide nanoparticles (ZnO-NPs) on a prevalent gastrointestinal nematode, H. contortus. Moreover, several biomarkers of oxidative/nitrosative stress and DNA damage were measured. Various concentrations of the nanoparticle were prepared and incubated with the worms for 24 hours. The parasite mobility, mortality rate, antioxidant enzymes activities (SOD, Catalase and GSH-Px), lipid peroxidation, total antioxidant status as well as nitric oxide (NO) contents and DNA damage were determined. ZnO-NPs exerted significant wormicidal effects via induction of oxidative/nitrosative stress and DNA damage. Conclusively, ZnO-NPs can be utilized as a novel and potential agent to control and treatment of helminth parasitic infections.

Oxidative and nitrosative stress in acute renal ischemia

2001 ◽  
Vol 281 (5) ◽  
pp. F948-F957 ◽  
Author(s):  
Eisei Noiri ◽  
Akihide Nakao ◽  
Koji Uchida ◽  
Hirokazu Tsukahara ◽  
Minoru Ohno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Nitrosative Stress ◽  
Oxidative And Nitrosative Stress ◽  
Reperfusion Period ◽  
Series Of Experiments ◽  
Acute Renal Ischemia ◽  
Oxide Synthase

First Published July 12, 2001; 10.1152/ajprenal.0071.2001.—Generation of reactive oxygen species and nitric oxide in hypoxia-reperfusion injury may form a cytotoxic metabolite, peroxynitrite, which is capable of causing lipid peroxidation and DNA damage. This study was designed to examine the contribution of oxidative and nitrosative stress to the renal damage in ischemic acute renal failure (iARF). iARF was initiated in rats by 45-min renal artery clamping. This resulted in lipid peroxidation, DNA damage, and nitrotyrosine modification confirmed both by Western and immunohistochemical analyses. Three groups of animals were randomly treated with an inhibitor of inducible nitric oxide synthase (NOS),l- N 6-(1-iminoethyl)lysine (l-Nil), cell-permeable lecithinized superoxide dismutase (SOD), or both. Each treatment resulted in amelioration of renal dysfunction, as well as reduced nitrotyrosine formation, lipid peroxidation, and DNA damage, thus suggesting that peroxynitrite rather than superoxide anion is responsible for lipid peroxidation and DNA damage. Therefore, in a separate series of experiments, a scavenger of peroxynitrite, ebselen, was administered before the reperfusion period. This treatment resulted in a comparable degree of amelioration of iARF. In conclusion, the present study provides the first attempt to elucidate the role of peroxynitrite in initiation of the cascade of lipid peroxidation and DNA damage to ischemic kidneys. The results demonstrate that l-Nil , lecithinized SOD, and ebselen treatments improve renal function due to their suppression of peroxynitrite production or its scavenging, consequently preventing lipid peroxidation and oxidative DNA damage.

Assessment of oxidative/nitrosative stress biomarkers and DNA damage in Teladorsagia circumcincta following exposure to zinc oxide nanoparticles

2020 ◽  
Vol 94 ◽  
Author(s):  
Z. Baghbani ◽  
B. Esmaeilnejad ◽  
S. Asri-Rezaei
Keyword(s):  
Dna Damage ◽  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Nitrosative Stress ◽  
Gastrointestinal Nematodes ◽  
Parasitic Infections ◽  
Oxide Nanoparticles ◽  
Helminth Parasites ◽  
Zno Nps ◽  
Teladorsagia Circumcincta

Abstract Drug resistance to helminth parasites is one of the most serious problems to threaten the livestock industry. The problem also poses a major threat to public health. Therefore, novel and safe agents should urgently be investigated to control parasitic infections. The current study was conducted to evaluate the possible antiparasitic effects of zinc oxide nanoparticles (ZnO-NPs) on one of the most prevalent gastrointestinal nematodes, Teladorsagia circumcincta. The worms were incubated with various concentrations of ZnO-NPs: 1, 4, 8, 12 and 16 ppm for 24 hours. Mobility and mortality of the parasites were recorded at four-hour intervals. At the endpoint, several biomarkers of oxidative/nitrosative stress, including superoxide dismutase, glutathione peroxidase and catalase, as well as lipid peroxidation, protein carbonylation, total antioxidant status, nitric oxide contents and DNA damage, were measured in the homogenized samples. ZnO-NPs showed significant anthelminthic effects, depending on time and concentration. Furthermore, the nanoparticle induced severe oxidative/nitrosative stress and DNA damage. ZnO-NPs could be considered as a novel and potent anthelminthic agent.

scholarly journals DNA Alkylation Damage as a Sensor of Nitrosative Stress in Mycobacterium tuberculosis

2003 ◽  
Vol 71 (2) ◽  
pp. 997-1000 ◽  
Author(s):  
Steven I. Durbach ◽  
Burkhard Springer ◽  
Edith E. Machowski ◽  
Robert J. North ◽  
K. G. Papavinasasundaram ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mycobacterium Tuberculosis ◽  
Nitrosative Stress ◽  
Dna Alkylation ◽  
Genotoxic Effects ◽  
Alkylation Damage ◽  
Damage Repair

ABSTRACT One of the cellular consequences of nitrosative stress is alkylation damage to DNA. To assess whether nitrosative stress is registered on the genome of Mycobacterium tuberculosis, mutants lacking an alkylation damage repair and reversal operon were constructed. Although hypersensitive to the genotoxic effects of N-methyl-N′-nitro-N-nitrosoguanidine in vitro, the mutants displayed no phenotype in vivo, suggesting that permeation of nitrosative stress to the level of cytotoxic DNA damage is restricted.

scholarly journals The Salutary Effects of Catalpol on Diesel Exhaust Particles-Induced Thrombogenic Changes and Cardiac Oxidative Stress, Inflammation and Apoptosis

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 99
Author(s):  
Abderrahim Nemmar ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Salem Alblooshi ◽  
Saleh Alseiari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Dna Damage ◽  
Diesel Exhaust ◽  
Nitrosative Stress ◽  
Antioxidant Properties ◽  
Diesel Exhaust Particles ◽  
Cardiovascular Toxicity ◽  
Particulate Air Pollution ◽  
Exhaust Particles

Inhaled particulate air pollution exerts pulmonary inflammation and cardiovascular toxicity through secondary systemic effects due to oxidative stress and inflammation. Catalpol, an iridiod glucoside, extracted from the roots of Rehmannia glutinosa Libosch, has been reported to possess anti-inflammatory and antioxidant properties. Yet, the potential ameliorative effects of catalpol on particulate air pollution—induced cardiovascular toxicity, has not been studied so far. Hence, we evaluated the possible mitigating mechanism of catalpol (5 mg/kg) which was administered to mice by intraperitoneal injection one hour before the intratracheal (i.t.) administration of a relevant type of pollutant particle, viz. diesel exhaust particles (DEPs, 30 µg/mouse). Twenty-four hours after the lung deposition of DEPs, several cardiovascular endpoints were evaluated. DEPs caused a significant shortening of the thrombotic occlusion time in pial microvessels in vivo, induced platelet aggregation in vitro, and reduced the prothrombin time and the activated partial thromboplastin time. All these actions were effectively mitigated by catalpol pretreatment. Likewise, catalpol inhibited the increase of the plasma concentration of C-reactive proteins, fibrinogen, plasminogen activator inhibitor-1 and P- and E-selectins, induced by DEPs. Moreover, in heart tissue, catalpol inhibited the increase of markers of oxidative (lipid peroxidation and superoxide dismutase) and nitrosative (nitric oxide) stress, and inflammation (tumor necrosis factor α, interleukin (IL)-6 and IL-1β) triggered by lung exposure to DEPs. Exposure to DEPs also caused heart DNA damage and increased the levels of cytochrome C and cleaved caspase, and these effects were significantly diminished by the catalpol pretreatment. Moreover, catalpol significantly reduced the DEPs-induced increase of the nuclear factor κB (NFκB) in the heart. In conclusion, catalpol significantly ameliorated DEPs–induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.

DNA damage and repair in neuropsychiatric disorders. What do we know and what are the future perspectives?

Mutagenesis ◽  
2019 ◽  
Author(s):  
Piotr Czarny ◽  
Katarzyna Bialek ◽  
Sylwia Ziolkowska ◽  
Justyna Strycharz ◽  
Tomasz Sliwinski
Keyword(s):  
Dna Damage ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Nitrosative Stress ◽  
Nuclear Dna ◽  
Neuropsychiatric Disorders ◽  
Dna Lesions ◽  
Major Depressive ◽  
Oxidative And Nitrosative Stress ◽  
Dna Damage And Repair

Abstract Over the past two decades, extensive research has been done to elucidate the molecular etiology and pathophysiology of neuropsychiatric disorders. In majority of them, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), bipolar disorder (BD), schizophrenia and major depressive disorder, increased oxidative and nitrosative stress was found. This stress is known to induce oxidative damage to biomolecules, including DNA. Accordingly, increased mitochondrial and nuclear DNA, as well as RNA damage, were observed in patients suffering from these diseases. However, recent findings indicate that the patients are characterised by impaired DNA repair pathways, which may suggest that these DNA lesions could be also a result of their insufficient repair. In the current systematic, critical review, we aim to sum up, using available literature, the knowledge about the involvement of nuclear and mitochondrial DNA damage and repair, as well as about damage to RNA in pathoetiology of neuropsychiatric disorders, i.e., AD, PD, ALS, BD, schizophrenia and major depressive disorder, as well as the usefulness of the discussed factors as being diagnostic markers and targets for new therapies. Moreover, we also underline the new directions to which future studies should head to elucidate these phenomena.

scholarly journals CSB promoter downregulation via histone H3 hypoacetylation is an early determinant of replicative senescence

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Clément Crochemore ◽  
Cristina Fernández-Molina ◽  
Benjamin Montagne ◽  
Audrey Salles ◽  
Miria Ricchetti
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Nitrosative Stress ◽  
Replicative Senescence ◽  
Histone H3 ◽  
Independent Manner ◽  
Normal Cells ◽  
Age Related ◽  
Damage Response ◽  
P21 Promoter

AbstractCellular senescence has causative links with ageing and age-related diseases, however, it remains unclear if progeroid factors cause senescence in normal cells. Here, we show that depletion of CSB, a protein mutated in progeroid Cockayne syndrome (CS), is the earliest known trigger of p21-dependent replicative senescence. CSB depletion promotes overexpression of the HTRA3 protease resulting in mitochondrial impairments, which are causally linked to CS pathological phenotypes. The CSB promoter is downregulated by histone H3 hypoacetylation during DNA damage-response. Mechanistically, CSB binds to the p21 promoter thereby downregulating its transcription and blocking replicative senescence in a p53-independent manner. This activity of CSB is independent of its role in the repair of UV-induced DNA damage. HTRA3 accumulation and senescence are partially rescued upon reduction of oxidative/nitrosative stress. These findings establish a CSB/p21 axis that acts as a barrier to replicative senescence, and link a progeroid factor with the process of regular ageing in human.

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