scholarly journals Thioredoxin shapes the C. elegans sensory response to Pseudomonas produced nitric oxide

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Yingsong Hao ◽  
Wenxing Yang ◽  
Jing Ren ◽  
Qi Hall ◽  
Yun Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Calcium Transients ◽  
Sensory Response ◽  
No Production ◽  
Phasic Response ◽  
No Donors ◽  
C Elegans ◽  
Chemosensory Neuron ◽  
Sensory Cue ◽  
Redox Sensing

Nitric oxide (NO) is released into the air by NO-producing organisms; however, it is unclear if animals utilize NO as a sensory cue. We show that C. elegans avoids Pseudomonas aeruginosa (PA14) in part by detecting PA14-produced NO. PA14 mutants deficient for NO production fail to elicit avoidance and NO donors repel worms. PA14 and NO avoidance are mediated by a chemosensory neuron (ASJ) and these responses require receptor guanylate cyclases and cyclic nucleotide gated ion channels. ASJ exhibits calcium increases at both the onset and removal of NO. These NO-evoked ON and OFF calcium transients are affected by a redox sensing protein, TRX-1/thioredoxin. TRX-1’s trans-nitrosylation activity inhibits the ON transient whereas TRX-1’s de-nitrosylation activity promotes the OFF transient. Thus, C. elegans exploits bacterially produced NO as a cue to mediate avoidance and TRX-1 endows ASJ with a bi-phasic response to NO exposure.

scholarly journals C. elegans avoidance of Pseudomonas: thioredoxin shapes the sensory response to bacterially produced nitric oxide

2018 ◽  
Author(s):  
Yingsong Hao ◽  
Wenxing Yang ◽  
Jing Ren ◽  
Qi Hall ◽  
Yun Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bacterial Pathogen ◽  
Calcium Transients ◽  
Sensory Response ◽  
No Production ◽  
Phasic Response ◽  
No Donors ◽  
C Elegans ◽  
Redox Sensing ◽  
No Sensor

AbstractWe show that C. elegans avoids a bacterial pathogen Pseudomonas aeruginosa (PA14) by detecting PA14-produced nitric oxide (NO). PA14 mutants deficient for NO production fail to elicit avoidance and NO donors repel worms. PA14 and NO avoidance are mediated by the ASJ chemosensory neurons, which respond to NO with intracellular calcium rises. PA14 avoidance and NO-evoked calcium responses require receptor guanylate cyclases (DAF-11 and GCY-27), and cyclic nucleotide gated ion channels (TAX-2 and -4). ASJ exhibits calcium increases at both the onset and removal of NO. These NO-evoked ON and OFF calcium transients are affected by a redox sensing protein, TRX-1/thioredoxin. TRX-1’s trans-nitrosylation activity inhibits the ON transient whereas TRX-1’s de-nitrosylation activity promotes the OFF transient. Thus, C. elegans exploits bacterially produced NO as a cue to mediate avoidance and TRX-1 functions as an NO-sensor that endows ASJ with a bi-phasic response to NO exposure.

Hypoxia compared with normoxia alters the effects of nitric oxide in ischemia-reperfusion lung injury

1997 ◽  
Vol 273 (3) ◽  
pp. L504-L512 ◽  
Author(s):  
Y. C. Huang ◽  
P. W. Fisher ◽  
E. Nozik-Grayck ◽  
C. A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Average Rate ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
No Production ◽  
Protective Effects ◽  
Lung Weight ◽  
Edema Formation ◽  
No Donors

Because both the biosynthesis of nitric oxide (NO.) and its metabolic fate are related to molecular O2, we hypothesized that hypoxia would alter the effects of NO. during ischemia-reperfusion (IR) in the lung. In this study, buffer-perfused lungs from rabbits underwent either normoxic IR (AI), in which lungs were ventilated with 21% O2 during ischemia and reperfusion, or hypoxic IR (NI), in which lungs were ventilated with 95% N2 during ischemia followed by reoxygenation with 21% O2. Lung weight gain (WG) and pulmonary artery pressure (Ppa) were monitored continuously, and microvascular pressure (Pmv) was measured after reperfusion to calculate pulmonary vascular resistance. We found that both AI and NI produced acute lung injury, as shown by increased WG and Ppa during reperfusion. In AI, where perfusate PO2 was > 100 mmHg, the administration of the NO. synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) before ischemia worsened WG and Ppa. Pmv also increased, suggesting a hydrostatic mechanism involved in edema formation. The effects of L-NAME could be attenuated by giving L-arginine and exogenous NO. donors before ischemia or before reperfusion. Partial protection was also provided by superoxide dismutase. In contrast, lung injury in NI at perfusate PO2 of 25-30 mmHg was attenuated by L-NAME; this effect could be reversed by L-arginine. Exogenous NO. donors given either before ischemia or before reperfusion, however, did not increase lung injury. NO. production was measured by quantifying the total nitrogen oxides (NOx) accumulating in the perfusate. The average rate of NOx accumulation was greater in AI than in NI. We conclude that hypoxia prevented the protective effects of NO on AI lung injury. The effects of hypoxia may be related to lower NO. production relative to oxidant stress during IR and/or altered metabolic fates of NO.-mediated production of peroxynitrite by hypoxic ischemia.

Nitric oxide and cerebral blood flow responses to hyperbaric oxygen

2000 ◽  
Vol 88 (4) ◽  
pp. 1381-1389 ◽  
Author(s):  
Ivan T. Demchenko ◽  
Albert E. Boso ◽  
Thomas J. O'Neill ◽  
Peter B. Bennett ◽  
Claude A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Methyl Ester ◽  
No Production ◽  
No Donors ◽  
Mk 801 ◽  
Neuronal Excitation ◽  
Synthase Inhibitor ◽  
Electroencephalogram Eeg

We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O2 (HBO2) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O2 exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor ( N ω-nitro-l-arginine methyl ester), l-arginine, NO donors, or the N-methyl-d-aspartate receptor inhibitor MK-801. After 30 min of O2 exposure at 3 and 4 ATA, rCBF decreased by 26–39% and by 37–43%, respectively, and was sustained for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia nigra by one-third but, thereafter, gradually returned to preexposure levels, preceding the onset of EEG spiking activity. Rats pretreated with N ω-nitro-l-arginine methyl ester and exposed to HBO2 at 5 ATA maintained a low rCBF. MK-801 did not alter the cerebrovascular responses to HBO2at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in control rats but were ineffective during HBO2 exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO2, but, as exposure time is prolonged, NO production increases and augments rCBF in anticipation of neuronal excitation.

Regulation of metalloproteinases by nitric oxide in human trophoblast cells in culture

2001 ◽  
Vol 13 (6) ◽  
pp. 411 ◽  
Author(s):  
Virginia Novaro ◽  
Alejandro Colman-Lerner ◽  
Felipe Vadillo Ortega ◽  
Alicia Jawerbaum ◽  
Dante Paz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Embryo Implantation ◽  
No Production ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
No Donors ◽  
Multinucleated Cells ◽  
Nos Inhibitors ◽  
Spermine Nonoate

The process of embryo implantation requires extensive remodelling of the endometrial extracellular matrix, a function largely performed by matrix-degrading metalloproteinases (MMPs). In the present study, we used trophoblast cells isolated from human term placentas to study the regulation of MMPs by nitric oxide (NO). Using a combination of zymography, Western blot and indirect immunofluorescence, we showed that MMP-2 and MMP-9 are increased during the conversion from low-motile cytotrophoblast cells to the highly motile and differentiated syncytiotrophoblast multinucleated cells. We also observed an increase in NO production and NO synthase (NOS) expression during this cellular differentiation process. In addition, we demonstrated a positive regulatory role of NO on the activity and protein expression of MMP-2 and MMP-9, because NO donors (NOC-18 and spermine-NONOate) or the NOS substrate (L-arginine) stimulate, whereas NOS inhibitors (NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine) reduce the expression and gelatinolytic activity of MMP-2 and MMP-9 in isolated trophoblast cells. Taken together, these results suggest that, in differentiating trophoblasts, NO regulates the induction of matrix-degrading proteases required for invasion during embryo implantation.

scholarly journals Anti-Inflammatory CeO2 Nanoparticles Prevented Cytotoxicity Due to Exogenous Nitric Oxide Donors via Induction Rather Than Inhibition of Superoxide/Nitric Oxide in HUVE Cells

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5416
Author(s):  
Mohd Javed Akhtar ◽  
Maqusood Ahamed ◽  
Hisham Alhadlaq
Keyword(s):  
Nitric Oxide ◽  
Superoxide Radical ◽  
Underlying Mechanism ◽  
No Production ◽  
Oxygen Species ◽  
No Donors ◽  
Mitochondrial Data ◽  
Tnf Α ◽  
Exogenous Nitric Oxide ◽  
O2 Production

The mechanism behind the cytoprotective potential of cerium oxide nanoparticles (CeO2 NPs) against cytotoxic nitric oxide (NO) donors and H2O2 is still not clear. Synthesized and characterized CeO2 NPs significantly ameliorated the lipopolysaccharide (LPS)-induced cytokines IL-1β and TNF-α. The main goal of this study was to determine the capacities of NPs regarding signaling effects that could have occurred due to reactive oxygen species (ROS) and/or NO, since NP-induced ROS/NO did not lead to toxicity in HUVE cells. Concentrations that induced 50% cell death (i.e., IC50s) of two NO donors (DETA-NO; 1250 ± 110 µM and sodium nitroprusside (SNP); 950 ± 89 µM) along with the IC50 of H2O2 (120 ± 7 µM) were utilized to evaluate cytoprotective potential and its underlying mechanism. We determined total ROS (as a collective marker of hydrogen peroxide, superoxide radical (O2•−), hydroxyl radical, etc.) by DCFH-DA and used a O2•− specific probe DHE to decipher prominent ROS. The findings revealed that signaling effects mediated mainly by O2•− and/or NO are responsible for the amelioration of toxicity by CeO2 NPs at 100 µg/mL. The unaltered effect on mitochondrial membrane potential (MMP) due to NP exposure and, again, CeO2 NPs-mediated recovery in the loss of MMP due to exogenous NO donors and H2O2 suggested that NP-mediated O2•− production might be extra-mitochondrial. Data on activated glutathione reductase (GR) and unaffected glutathione peroxidase (GPx) activities partially explain the mechanism behind the NP-induced gain in GSH and persistent cytoplasmic ROS. The promoted antioxidant capacity due to non-cytotoxic ROS and/or NO production, rather than inhibition, by CeO2 NP treatment may allow cells to develop the capacity to tolerate exogenously induced toxicity.

scholarly journals Nitric oxide signalling in plant nanobiology: current status and perspectives

2020 ◽  
Author(s):  
Zsuzsanna Kolbert ◽  
Réka Szőllősi ◽  
Gábor Feigl ◽  
Zoltán Kónya ◽  
Andrea Rónavári
Keyword(s):  
Nitric Oxide ◽  
Basic Research ◽  
Scientific Basis ◽  
Research Field ◽  
Current Status ◽  
Signal Molecules ◽  
No Production ◽  
No Donor ◽  
No Donors ◽  
Agricultural Use

Abstract Plant nanobiology as a novel research field provides a scientific basis for the agricultural use of nanoparticles (NPs). Plants respond to the presence of nanomaterials by synthesizing signal molecules, such as the multifunctional gaseous nitric oxide (NO). Several reports have described the effects of different nanomaterials (primarily chitosan NPs, metal oxide NPs, and carbon nanotubes) on endogenous NO synthesis and signalling in different plant species. Other works have demonstrated the ameliorating effect of exogenous NO donor (primarily sodium nitroprusside) treatments on NP-induced stress. NO-releasing NPs are preferred alternatives to chemical NO donors, and evaluating their effects on plants has recently begun. Previous studies clearly indicate that endogenous NO production in the presence of nanomaterials or NO levels increased by exogenous treatments (NO-releasing NPs or chemical NO donors) exerts growth-promoting and stress-ameliorating effects in plants. Furthermore, an NP-based nanosensor for NO detection in plants has been developed, providing a new and excellent perspective for basic research and also for the evaluation of plants’ health status in agriculture.

scholarly journals The Nitric Oxide (NO) Donor Sodium Nitroprusside (SNP) and Its Potential for the Schizophrenia Therapy: Lights and Shadows

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3196
Author(s):  
Elli Zoupa ◽  
Nikolaos Pitsikas
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Cognitive Deficits ◽  
Negative Symptoms ◽  
Mental Disease ◽  
No Production ◽  
No Donor ◽  
No Donors ◽  
Worldwide Population ◽  
The Brain

Schizophrenia is a severe psychiatric disorder affecting up to 1% of the worldwide population. Available therapy presents different limits comprising lack of efficiency in attenuating negative symptoms and cognitive deficits, typical features of schizophrenia and severe side effects. There is pressing requirement, therefore, to develop novel neuroleptics with higher efficacy and safety. Nitric oxide (NO), an intra- and inter-cellular messenger in the brain, appears to be implicated in the pathogenesis of schizophrenia. In particular, underproduction of this gaseous molecule is associated to this mental disease. The latter suggests that increment of nitrergic activity might be of utility for the medication of schizophrenia. Based on the above, molecules able to enhance NO production, as are NO donors, might represent a class of compounds candidates. Sodium nitroprusside (SNP) is a NO donor and is proposed as a promising novel compound for the treatment of schizophrenia. In the present review, we intended to critically assess advances in research of SNP for the therapy of schizophrenia and discuss its potential superiority over currently used neuroleptics.

scholarly journals Supplementary Nitric Oxide Donors and Exercise as Potential Means to Improve Vascular Health in People with Type 1 Diabetes: Yes to NO?

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1571 ◽  
Author(s):  
Olivia McCarthy ◽  
Othmar Moser ◽  
Max L. Eckstein ◽  
Stephen C. Bain ◽  
Jason Pitt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Type 1 Diabetes ◽  
Risk Mitigation ◽  
Vascular Dysfunction ◽  
No Production ◽  
Vascular Health ◽  
No Donors ◽  
Oxide Synthase

Type 1 diabetes (T1D) is associated with a greater occurrence of cardiovascular pathologies. Vascular dysfunction has been shown at the level of the endothelial layers and failure to maintain a continuous pool of circulating nitric oxide (NO) has been implicated in the progression of poor vascular health. Biochemically, NO can be produced via two distinct yet inter-related pathways that involve an upregulation in the enzymatic activity of nitric oxide synthase (NOS). These pathways can be split into an endogenous oxygen-dependent pathway i.e., the catabolism of the amino acid L-arginine to L-citrulline concurrently yielding NO in the process, and an exogenous oxygen-independent one i.e., the conversion of exogenous inorganic nitrate to nitrite and subsequently NO in a stepwise fashion. Although a body of research has explored the vascular responses to exercise and/or compounds known to stimulate NOS and subsequently NO production, there is little research applying these findings to individuals with T1D, for whom preventative strategies that alleviate or at least temper vascular pathologies are critical foci for long-term risk mitigation. This review addresses the proposed mechanisms responsible for vascular dysfunction, before exploring the potential mechanisms by which exercise, and two supplementary NO donors may provide vascular benefits in T1D.

Nitric oxide-releasing molecules at the interface of inorganic chemistry and biology: a concise overview

2019 ◽  
Vol 39 (2) ◽  
pp. 91-112 ◽  
Author(s):  
Jan Mohammad Mir ◽  
Bashir Ahmad Malik ◽  
Ram Charitra Maurya
Keyword(s):  
Inorganic Chemistry ◽  
Nitric Oxide ◽  
Amino Acids ◽  
No Production ◽  
No Donors ◽  
Chemically Modified ◽  
Nitrosyl Complexes ◽  
Ability To Act ◽  
Nitric Oxide Releasing ◽  
Biological Milieu

AbstractThe useful aspects of nitric oxide (NO) are nowadays widely known. Due to the need for this molecule in the maintenance of homeostasis, NO-releasing compounds are tested every year to optimize its levels in a patient suffering from low NO production. This manuscript is an update of some important historical concerns about nitrosyl complexes having the ability to act as NO-releasing compounds under the influence of different chemically modified environments. At present, the search for efficient and less harmful NO-releasing molecules at desirable targets and concentrations has gained considerable momentum in nitrosyl chemistry. Iron, ruthenium, and manganese nitrosyls have been investigated elitely to disentangle their electronic transition (excitation) under visible light to act as NO donors without harming the healthy cells of a target. There is much evidence supporting the increase of NO lability if amino acids are used as complexing ligands, the design of a reduction center close to an NO grouping, and the development of porphyrin system-based nitrosyl complexes. From the overall survey, it may be concluded that the desirable properties of such scaffolds need to be evaluated further to complement the biological milieu.

scholarly journals Haem and nitric oxide: synergism in the modulation of the endothelial haem oxygenase-1 pathway

2003 ◽  
Vol 372 (2) ◽  
pp. 381-390 ◽  
Author(s):  
Roberta FORESTI ◽  
Martha HOQUE ◽  
Sandip BAINS ◽  
Colin J. GREEN ◽  
Roberto MOTTERLINI
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Sodium Nitroprusside ◽  
Nitrosative Stress ◽  
No Production ◽  
Oxidative And Nitrosative Stress ◽  
No Donors ◽  
Aortic Endothelial Cells ◽  
Oxygenase Activity ◽  
Haem Oxygenase

NO potently up-regulates vascular haem oxygenase-1 (HO-1), an inducible defensive protein that degrades haem to CO, iron and the antioxidant bilirubin. Since several pathological states are characterized by increased NO production and liberation of haem from haem-containing proteins, we examined how NO influences HO-1 induction mediated by haemin. Aortic endothelial cells treated with S-nitroso-N-acetylpenicillamine (SNAP), sodium nitroprusside (SNP) or diethylenetriamine-NONOate (DETA/NO) and haemin exhibited higher levels of haem oxygenase activity compared with cells exposed to NO donors or haemin alone. This was accompanied by a marked increase in bilirubin production and, notably, by a strong magnification of cellular haem uptake. A role for haem metabolites in modulating HO-1 expression by NO was assessed by exposing cells to SNAP, SNP or DETA/NO in medium derived from cells treated with haemin, which contained increased bilirubin levels. This treatment considerably potentiated HO-1 expression and haem oxygenase activity mediated by NO and the use of a haem oxygenase inhibitor abolished this effect. Both iron liberated during haem breakdown and the formation of nitroxyl anion from NO appeared to partially contribute to the amplifying phenomenon; in addition, medium from haemin-treated cells significantly augmented the release of NO by NO donors. Thus we have identified novel mechanisms related to the induction of HO-1 by NO indicating that the signalling actions of NO vary significantly in the presence of haem and haem metabolites, ultimately increasing the defensive abilities of the endothelium to counteract oxidative and nitrosative stress.

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