Nitric oxide synthase and oxidative-nitrosative stress play a key role in placental infection byTrypanosoma cruzi

2018 ◽  
Vol 80 (1) ◽  
pp. e12852 ◽  
Author(s):  
María Fernanda Triquell ◽  
Cintia Díaz-Luján ◽  
María Cristina Romanini ◽  
Juan Carlos Ramirez ◽  
Patricia Paglini-Oliva ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Placental Infection ◽  
Oxide Synthase

Stimulation of the endogenous hydrogen sulfide synthesis suppresses oxidative–nitrosative stress and restores endothelial-dependent vasorelaxation in old rats

2020 ◽  
Vol 98 (5) ◽  
pp. 275-281 ◽  
Author(s):  
L.A. Mys ◽  
N.A. Strutynska ◽  
Y.V. Goshovska ◽  
V.F. Sagach
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Nitrosative Stress ◽  
Rat Aorta ◽  
Aortic Tissue ◽  
Old Rats ◽  
Oxide Synthase ◽  
Stimulation Of

Hydrogen sulfide (H2S) is an endogenous gas transmitter with profound effects on the cardiovascular system. We hypothesized that stimulation of H2S synthesis might alleviate age-associated changes in vascular reactivity. Pyridoxal-5-phosphate (PLP), the coenzyme of H2S-synthesizing enzymes, was administrated to old male Wistar rats per os at a dose of 0.7 mg/kg body mass once a day for 2 weeks. H2S content in the aortic tissue, markers of oxidative stress, inducible nitric oxide synthase (iNOS) and constitutive nitric oxide synthase (cNOS), arginase activities, and endothelium-dependent vasorelaxation of the aortic rings were studied. Our results showed that PLP restored endogenous H2S and low molecular weight S-nitrosothiol levels in old rat aorta to the levels detected in adults. PLP significantly reduced diene conjugate content, hydrogen peroxide and peroxynitrite generation rates, and iNOS and arginase activity in the aortic tissue of old rats. PLP also greatly improved acetylcholine-induced relaxation of old rat aorta (47.7% ± 4.8% versus 18.4% ± 4.1% in old rats, P < 0.05) that was abolished by NO inhibition with N-nitro-l-arginine methyl ester hydrochloride (L-NAME) or H2S inhibition with O-carboxymethylhydroxylamine (O-CMH). Thus, PLP might be used for stimulation of endogenous H2S synthesis and correction of oxidative and nitrosative stress and vessel tone dysfunction in aging and age-associated diseases.

scholarly journals Low-Dose Ribavirin Treatments Attenuate Neuroinflammatory Activation of BV-2 Cells by Interfering with Inducible Nitric Oxide Synthase

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Iva Bozic ◽  
Danijela Savic ◽  
Marija Jovanovic ◽  
Ivana Bjelobaba ◽  
Danijela Laketa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Low Dose ◽  
Nitrosative Stress ◽  
Morphological Changes ◽  
Necrosis Factor Alpha ◽  
External Threats ◽  
Cytokine Tumor Necrosis Factor ◽  
Induced Apoptosis ◽  
Oxide Synthase

Microglia play a key role in defending central nervous system from various internal and external threats. However, their excessive and/or chronic activation is associated with deleterious effects in a variety of neurodegenerative diseases. Previously, we have shown that ribavirin when applied in clinically relevant dosage (10 μM) modulates activated microglia in complex fashion inducing both anti- and proinflammatory effects, simultaneously causing cytotoxicity. Here, we examined potential of low-dose ribavirin (0.1 and 1 μM) to modulate activated BV-2 microglia. Morphological and functional activation of BV-2 cells was achieved with lipopolysaccharide (LPS) stimulation. Our results demonstrated that low-dose ribavirin did not induce cell death, while 10 μM ribavirin promoted LPS induced apoptosis. We determined that 1 μM ribavirin was equally efficient in deactivation of LPS induced morphological changes as 10 μM ribavirin treatment. Ribavirin showed halfway success in reducing markers of functional activation of microglia. Namely, none of the doses had effect on LPS triggered production of proinflammatory cytokine tumor necrosis factor alpha. On the other hand, low-dose ribavirin proved its effectiveness in reduction of another inflammatory mediator, nitric oxide, by inhibiting inducible form of nitric oxide synthase. Our results imply that low-dose ribavirin may alleviate nitrosative stress during neuroinflammation.

Transiently, paralleled upregulation of arginase and nitric oxide synthase and the effect of both enzymes on the pathology of asthma

2007 ◽  
Vol 293 (6) ◽  
pp. L1419-L1426 ◽  
Author(s):  
Kei Takemoto ◽  
Keiki Ogino ◽  
Masafumi Shibamori ◽  
Toshikazu Gondo ◽  
Yoshiaki Hitomi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Nitrosative Stress ◽  
Dermatophagoides Farinae ◽  
Cell Hyperplasia ◽  
Bronchial Epithelial ◽  
Nitrite Nitrate ◽  
Oxide Synthase ◽  
Arginase I

Changes in the expression of arginase and their association with nitrosative stress were investigated using an asthmatic model previously established in NC/Nga mice with mite extract. Mite crude extract (100 μg/day) from Dermatophagoides farinae was administered intranasally for 5 consecutive days ( day 0–4), and a single challenge was performed on day 11. On day 12, upregulation of the mRNA expression of inducible types of nitric oxide synthase (iNOS) and increases in immunohistochemical staining for iNOS and nitrotyrosine were observed. However, the level of nitrite + nitrate was unchanged. An increase in enzymatic activity, upregulation of mRNA expression, and immunostaining for arginase I was detected in the lung tissue and serum. Moreover, increases in both arginase I and II were revealed by immunoblotting. Goblet cell hyperplasia in bronchial epithelial cells and increasing collagen synthesis around the bronchus were also observed. These results suggested that an increase in arginase may lead to decreased availability of arginine for nitric oxide synthase and may contribute to the remodeling of the lung.

scholarly journals INHIBITION OF TRANSCRIPTION FACTORS NF KAPPA B AND AP-1 LIMITS THE PROGRESSION OF OXIDATIVE-NITROSATIVE STRESS IN THE TISSUE OF CEREBRAL HEMISPHERES IN RATS AFTER MODELLED TRAUMATIC BRAIN INJURY

2020 ◽  
Vol 20 (1) ◽  
pp. 80-85 ◽  
Author(s):  
I.V. Yavtushenko ◽  
V.O. Kostenko
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Transcription Factors ◽  
Brain Injury ◽  
Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Cerebral Hemispheres ◽  
Male Rats ◽  
Nf Kappa B ◽  
Oxide Synthase

The study was aimed as investigating the effects of inhibitors of transcription factors NF kappa B and AP-1 activation on the development of oxidative-nitrosative stress in rat cerebral hemispheres following experimental traumatic brain injury (TBI). The study included 60 white Wistar male rats weighing 180-220 g, divided into 4 groups of 7 animals in each: the 1st group included pseudo-injured animals subjected to the same manipulations (ether anaesthesia, fixation) as the animals  in the experimental groups, except for TBI modelling, the 2nd group included the animals exposed to modelled TBI, the 3rd and 4th groups involved the rats who received ammonium pyrolidine dithiocarbamate, the nuclear translocation inhibitor NF kappa B in a dose of 76 mg/kg and the inhibitor AP-1 SR 11302 in a dose of 1 mg/kg, respectively for 7 days following the TBI modelling. On the 7th day after the simulation of a moderate TBI in rat cerebral hemisphere tissue, the following signs of oxidative-nitrosative stress have been detected: increased production of superoxide radical anion by NADPH and NADH-dependent electron transport chains, increased activity of nitric oxide synthase (total and inducible), a decrease and impairment of the coupling of its constitutive isoform, growth in the concentration of peroxynitrite, the development of decompensated lipid peroxidation. The application of transcription factor inhibitors NF kappa B (PDTC) and AP-1 (SR 11302) significantly reduces the signs of oxidative-nitrosative stress in the tissue of rat cerebral hemispheres on the 7th day of the experiment, reduces the production of superoxide anion radical and the activity of nitric oxide synthase (total and inducible), improves the coupling of its constitutive isoform, limits the peroxynitrite concentration, and enhances the antioxidant potential.

scholarly journals Nitrosative Stress and Its Association with Cardiometabolic Disorders

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2555 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Linaloe Manzano-Pech ◽  
María Esther Rubio-Ruíz ◽  
María Elena Soto ◽  
Verónica Guarner-Lans
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Current Knowledge ◽  
Redox System ◽  
Nitrogen Species ◽  
Irreversible Damage ◽  
Cardiometabolic Diseases ◽  
Cardiometabolic Disorders ◽  
Oxide Synthase

Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS). The presence of high concentrations of superoxide anions (O2−) is also necessary for their formation. RNS react three times faster than O2− with other molecules and have a longer mean half life. They cause irreversible damage to cell membranes, proteins, mitochondria, the endoplasmic reticulum, nucleic acids and enzymes, altering their activity and leading to necrosis and to cell death. Although nitrogen species are important in the redox imbalance, this review focuses on the alterations caused by the RNS in the cellular redox system that are associated with cardiometabolic diseases. Currently, nitrosative stress (NSS) is implied in the pathogenesis of many diseases. The mechanisms that produce damage remain poorly understood. In this paper, we summarize the current knowledge on the participation of NSS in the pathology of cardiometabolic diseases and their possible mechanisms of action. This information might be useful for the future proposal of anti-NSS therapies for cardiometabolic diseases.

Sex differences in nitrosative stress during renal ischemia

2010 ◽  
Vol 299 (5) ◽  
pp. R1387-R1395 ◽  
Author(s):  
Francisca Rodríguez ◽  
Susana Nieto-Cerón ◽  
Francisco J. Fenoy ◽  
Bernardo López ◽  
Isabel Hernández ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sex Differences ◽  
Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Differential Pulse ◽  
Sprague Dawley ◽  
Oxidative And Nitrosative Stress ◽  
Sprague Dawley Rats ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Females. suffer a less severe ischemic acute renal failure than males, apparently because of higher nitric oxide (NO) bioavailability and/or lower levels of oxidative stress. Because the renal ischemic injury is associated with outer medullary (OM) endothelial dysfunction, the present study evaluated sex differences in OM changes of NO and peroxynitrite levels (by differential pulse voltammetry and amperometry, respectively) during 45 min of ischemia and 60 min of reperfusion in anesthetized Sprague-Dawley rats. Endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) protein expression and their phosphorylated forms [peNOS(Ser1177) and pnNOS(Ser1417)], 3-nitrotyrosine, reduced sulfhydryl groups (-SH), and glomerular filtration rate (GFR) were also determined. No sex differences were observed in monomeric eNOS and nNOS expression, NO, or 3-nitrotyrosine levels in nonischemic kidneys, but renal -SH content was higher in females. Ischemia increased dimeric/monomeric eNOS and nNOS ratio more in females, but the dimeric phosphorylated peNOS(Ser1177) and pnNOS(Ser1417) forms rose similarly in both sexes, indicating no sex differences in nitric oxide synthase activation. However, NO levels increased more in females than in males (6,406.0 ± 742.5 and 4,058.2 ± 272.35 nmol/l respectively, P < 0.05), together with a lower increase in peroxynitrite current (5.5 ± 0.7 vs. 12.7 ± 1.5 nA, P < 0.05) and 3-nitrotyrosine concentration, (28.7 ± 3.7 vs. 48.7 ± 3.7 nmol/mg protein, P < 0.05) in females than in males and a better preserved GFR after ischemia in females than in males (689.7 ± 135.0 and 221.4 ± 52.5 μl·min−1·g kidney wt−1, P < 0.01). Pretreatment with the antioxidants N-acetyl-l-cysteine or ebselen abolished sex differences in peroxynitrite, nitrotyrosine, and GFR, suggesting that a greater oxidative and nitrosative stress worsens renal damage in males.

Variation of genes involved in oxidative and nitrosative stresses in depression

2018 ◽  
Vol 48 (1) ◽  
pp. 38-48 ◽  
Author(s):  
Paulina Wigner ◽  
Piotr Czarny ◽  
Ewelina Synowiec ◽  
Micha� Bijak ◽  
Katarzyna Białek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Depressive Disorders ◽  
Nitrosative Stress ◽  
Nucleotide Polymorphisms ◽  
Oxidative And Nitrosative Stress ◽  
Increased Risk ◽  
Genes Encoding ◽  
Oxide Synthase ◽  
The Impact

AbstractThe dominating hypothesis among numerous hypotheses explaining the pathogenesis of depressive disorders (DD) is the one involving oxidative and nitrosative stress. In this study, we examined the association between single-nucleotide polymorphisms of the genes encoding SOD2 (superoxide dismutase 2), CAT (catalase), GPx4 (glutathione peroxidase 4), NOS1 (nitric oxide synthase 1), NOS2 (nitric oxide synthase 2), and the development of depressive disorders. Our study was carried out on the DNA isolated from peripheral blood collected from 281 depressed patients and 229 controls. Using TaqMan probes, we genotyped the following six polymorphisms: c.47T > C (p.Val16Ala) (rs4880) in SOD2, c.-89A > T (rs7943316) in CAT, c.660T > C (rs713041) in GPx4, c.-420-34221G > A (rs1879417) in NOS1, c.1823C > T (p.Ser608Leu) (rs2297518), and c.-227G > C (rs10459953) in NOS2. We found that the T/T genotype of the c.47T > C polymorphism was linked with an increased risk of depression. Moreover, the T/T genotype and T allele of c.660T > C increased the risk of DD occurrence, while the heterozygote and C allele decreased this risk. On the other hand, we discovered that the A/A genotype of c.-89A > T SNP was associated with a reduced risk of DD, while the A/T genotype increased this risk. We did not find any correlation between the genotypes/alleles of c.-420-34221G > A, c.1823C > T, and c.-227G > C, and the occurrence of DD. In addition, gene-gene and haplotype analyses revealed that combined genotypes and haplotypes were connected with the disease. Moreover, we found that sex influenced the impact of some SNPs on the risk of depression. Concluding, the studied polymorphisms of SOD2, CAT and GPx4 may modulate the risk of depression. These results support the hypothesis that oxidative and nitrosative stresses are involved in the pathogenesis of depressive disorders.

scholarly journals Myoglobin Protects the Heart from Inducible Nitric-oxide Synthase (iNOS)-mediated Nitrosative Stress

2003 ◽  
Vol 278 (24) ◽  
pp. 21761-21766 ◽  
Author(s):  
Axel Gödecke ◽  
Andre Molojavyi ◽  
Jacqueline Heger ◽  
Ulrich Flögel ◽  
Zhaoping Ding ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide
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