Rhizobia: highways to NO

2021 ◽  
Author(s):  
Bryan Ruiz ◽  
Åsa Frostegård ◽  
Claude Bruand ◽  
Eliane Meilhoc
Keyword(s):  
Nitric Oxide ◽  
Nitrogen Fertilizer ◽  
Host Plants ◽  
Nitrate Assimilation ◽  
No Synthase ◽  
No Production ◽  
Enzymatic Reactions ◽  
Atmospheric Nitrogen ◽  
Legume Symbiosis

The interaction between rhizobia and their legume host plants conduces to the formation of specialized root organs called nodules where rhizobia differentiate into bacteroids which fix atmospheric nitrogen to the benefit of the plant. This beneficial symbiosis is of importance in the context of sustainable agriculture as legumes do not require the addition of nitrogen fertilizer to grow. Interestingly, nitric oxide (NO) has been detected at various steps of the rhizobium–legume symbiosis where it has been shown to play multifaceted roles. Both bacterial and plant partners are involved in NO synthesis in nodules. To better understand the role of NO, and in particular the role of bacterial NO, at all steps of rhizobia–legumes interaction, the enzymatic sources of NO have to be elucidated. In this review, we discuss different enzymatic reactions by which rhizobia may potentially produce NO. We argue that there is most probably no NO synthase activity in rhizobia, and that instead the NO2− reductase nirK, which is part of the denitrification pathway, is the main bacterial source of NO. The nitrate assimilation pathway might contribute to NO production but only when denitrification is active. The different approaches to measure NO in rhizobia are also addressed.

Nitrate reductases and hemoglobins control nitrogen-fixing symbiosis by regulating nitric oxide accumulation

2020 ◽  
Author(s):  
Antoine Berger ◽  
Alexandre Boscari ◽  
Alain Puppo ◽  
Renaud Brouquisse
Keyword(s):  
Nitric Oxide ◽  
Defense Responses ◽  
Nodule Formation ◽  
No Production ◽  
Degradation Pathways ◽  
Atmospheric Nitrogen ◽  
Metabolic Intermediate ◽  
Hypoxic Environment ◽  
Nitrate Reductases

Abstract The interaction between legumes and rhizobia leads to the establishment of a symbiotic relationship between plant and bacteria. This is characterized by the formation of a new organ, the nodule, which facilitates the fixation of atmospheric nitrogen (N2) by nitrogenase through the creation of a hypoxic environment. Nitric oxide (NO) accumulates at each stage of the symbiotic process. NO is involved in defense responses, nodule organogenesis and development, nitrogen fixation metabolism, and senescence induction. During symbiosis, either successively or simultaneously, NO regulates gene expression, modulates enzyme activities, and acts as a metabolic intermediate in energy regeneration processes via phytoglobin-NO respiration and the bacterial denitrification pathway. Due to the transition from normoxia to hypoxia during nodule formation, and the progressive presence of the bacterial partner in the growing nodules, NO production and degradation pathways change during the symbiotic process. This review analyzes the different source and degradation pathways of NO, and highlights the role of nitrate reductases and hemoproteins of both the plant and bacterial partners in the control of NO accumulation.

Role of airway nitric oxide on the regulation of pulmonary circulation by carbon dioxide

2001 ◽  
Vol 91 (3) ◽  
pp. 1121-1130 ◽  
Author(s):  
Yasushi Yamamoto ◽  
Hitoshi Nakano ◽  
Hiroshi Ide ◽  
Toshiyuki Ogasa ◽  
Toru Takahashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
No Synthase ◽  
No Production ◽  
Pulmonary Vasoconstriction ◽  
Exhaled No ◽  
Progressive Hypoxia ◽  
Pulmonary Arterial

The effects of hypercapnia (CO2) confined to either the alveolar space or the intravascular perfusate on exhaled nitric oxide (NO), perfusate NO metabolites (NOx), and pulmonary arterial pressure (Ppa) were examined during normoxia and progressive 20-min hypoxia in isolated blood- and buffer-perfused rabbit lungs. In blood-perfused lungs, when alveolar CO2concentration was increased from 0 to 12%, exhaled NO decreased, whereas Ppa increased. Increments of intravascular CO2levels increased Ppa without changes in exhaled NO. In buffer-perfused lungs, alveolar CO2 increased Ppa with reductions in both exhaled NO from 93.8 to 61.7 (SE) nl/min ( P < 0.01) and perfusate NOx from 4.8 to 1.8 nmol/min ( P < 0.01). In contrast, intravascular CO2 did not affect either exhaled NO or Ppa despite a tendency for perfusate NOx to decline. Progressive hypoxia elevated Ppa by 28% from baseline with a reduction in exhaled NO during normocapnia. Alveolar hypercapnia enhanced hypoxic Ppa response up to 50% with a further decline in exhaled NO. Hypercapnia did not alter the apparent K m for O2, whereas it significantly decreased the V max from 66.7 to 55.6 nl/min. These results suggest that alveolar CO2 inhibits epithelial NO synthase activity noncompetitively and that the suppressed NO production by hypercapnia augments hypoxic pulmonary vasoconstriction, resulting in improved ventilation-perfusion matching.

scholarly journals Salt-induced hypertension in Dahl salt-resistant and salt-sensitive rats with NOS II inhibition

1999 ◽  
Vol 277 (2) ◽  
pp. H732-H739 ◽  
Author(s):  
M. Audrey Rudd ◽  
Maria Trolliet ◽  
Susan Hope ◽  
Anne Ward Scribner ◽  
Geraldine Daumerie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
No Synthase ◽  
No Production ◽  
Induced Hypertension ◽  
Blood Pressures ◽  
Diameter Change ◽  
Inducible Nos ◽  
Tail Cuff

Although recent evidence suggests that reduced nitric oxide (NO) production may be involved in salt-induced hypertension, the specific NO synthase (NOS) responsible for the conveyance of salt sensitivity remains unknown. To determine the role of inducible NOS (NOS II) in salt-induced hypertension, we treated Dahl salt-resistant (DR) rats with the selective NOS II inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) for 12 days. Tail-cuff systolic blood pressures rose 29 ± 6 and 42 ± 8 mmHg in DR rats given 150 and 300 nmol AMT/h, respectively ( P < 0.01, 2-way ANOVA) after 7 days of 8% NaCl diet. We observed similar results with two other potent selective NOS II inhibitors, S-ethylisourea (EIT) and N-[3-(aminomethyl)benzyl]acetamidine hydrochloride (1400W). Additionally, AMT effects were independent of alterations in endothelial function as assessed by diameter change of mesenteric arterioles in response to methacholine using videomicroscopy. We, therefore, conclude from these data that NOS II is important in salt-induced hypertension.

scholarly journals Gastrointestinal nitric oxide generation in germ-free and conventional rats

2004 ◽  
Vol 287 (5) ◽  
pp. G993-G997 ◽  
Author(s):  
Tanja Sobko ◽  
Claudia Reinders ◽  
Elisabeth Norin ◽  
Tore Midtvedt ◽  
Lars E. Gustafsson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastrointestinal Tract ◽  
Intestinal Microflora ◽  
No Synthase ◽  
No Production ◽  
Germ Free ◽  
Qualitative And Quantitative ◽  
Nitrate Load ◽  
Nos Inhibitor

Nitric oxide (NO) is a central mediator of various physiological events in the gastrointestinal tract. The influence of the intestinal microflora for NO production in the gut is unknown. Bacteria could contribute to this production either by stimulating the mucosa to produce NO, or they could generate NO themselves. Using germ-free and conventional rats, we measured gaseous NO directly in the gastrointestinal tract and from the luminal contents using a chemiluminescence technique. Mucosal NO production was studied by using an NO synthase (NOS) inhibitor, and to evaluate microbial contribution to the NO generation, nitrate was given to the animals. In conventional rats, luminal NO differed profoundly along the gastrointestinal tract with the greatest concentrations in the stomach [>4,000 parts per billion (ppb)] and cecum (≈200 ppb) and lower concentrations in the small intestine and colon (≤20 ppb). Cecal NO correlated with the levels in incubated luminal contents. NOS inhibition lowered NO levels in the colon, without affecting NO in the stomach and in the cecum. Gastric NO increased greatly after a nitrate load, proving it to be a substrate for NO generation. In germ-free rats, NO was low (≤30 ppb) throughout the gastrointestinal tract and absent in the incubated luminal contents. NO also remained low after a nitrate load. Our results demonstrate a pivotal role of the intestinal microflora in gastrointestinal NO generation. Distinctly compartmentalized qualitative and quantitative NO levels in conventional and germ-free rats reflect complex host microbial cross talks, possibly making NO a regulator of the intestinal eco system.

scholarly journals Crowding-Induced Alterations in Vascular System of Wistar-Kyoto Rats: Role of Nitric Oxide

2007 ◽  
pp. 667-669
Author(s):  
I Bernátová ◽  
A Púzserová ◽  
J Navarová ◽  
Z Csizmadiová ◽  
M Zeman
Keyword(s):  
Nitric Oxide ◽  
Mesenteric Artery ◽  
Vascular System ◽  
Plasma Corticosterone ◽  
No Synthase ◽  
No Production ◽  
Increasing Trend ◽  
Wistar Kyoto ◽  
Plasma Nitrate

The aim of this study was to determine the effect of chronic crowding on the cardiovascular system of Wistar-Kyoto (WKY) rats. Rats were randomly divided into the control (480 cm(2) per rat) or crowded (200 cm(2) per rat) group for eight weeks. Body weight, blood pressure (BP), heart rate and plasma nitrate/nitrite levels of the crowded rats were not different from controls at the end of the experiment. Plasma corticosterone exhibited an increasing trend (5.7+/-1.8 vs. 12.6+/-3.7 ng/ml, p=0.08) while blood glucose was significantly reduced in the crowded rats in comparison with the controls. Nitric oxide (NO) synthase activity and nitrate/nitrite levels of the crowded rats were significantly elevated in the aorta by 80 % and 20 %, respectively, but unchanged in the left ventricle. Moreover, acetylcholine-induced relaxation was significantly increased in the crowded rats in both the femoral artery (61+/-5 % vs. 76+/-5 %, p<0.001) and mesenteric artery (51+/-6 % vs. 72+/-7 %, p<0.001). In conclusion, results suggest that chronic crowding may increase vasorelaxation and vascular NO production in normotensive rats. This may be considered as an adapting mechanism preventing the development of the stress-related elevation of BP. Additionally, results also suggest caution in the housing of rats because an inappropriate crowding may affect results of the experiment significantly.

scholarly journals Role of Nitrate Reductase in NO Production in Photosynthetic Eukaryotes

Plants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 56 ◽  
Author(s):  
Manuel Tejada-Jimenez ◽  
Angel Llamas ◽  
Aurora Galván ◽  
Emilio Fernández
Keyword(s):  
Nitric Oxide ◽  
Nitrate Reductase ◽  
Electron Transport Chain ◽  
No Synthase ◽  
No Production ◽  
Cell Responses ◽  
Secondary Messenger ◽  
Photosynthetic Eukaryotes ◽  
Transport Chain

Nitric oxide is a gaseous secondary messenger that is critical for proper cell signaling and plant survival when exposed to stress. Nitric oxide (NO) synthesis in plants, under standard phototrophic oxygenic conditions, has long been a very controversial issue. A few algal strains contain NO synthase (NOS), which appears to be absent in all other algae and land plants. The experimental data have led to the hypothesis that molybdoenzyme nitrate reductase (NR) is the main enzyme responsible for NO production in most plants. Recently, NR was found to be a necessary partner in a dual system that also includes another molybdoenzyme, which was renamed NO-forming nitrite reductase (NOFNiR). This enzyme produces NO independently of the molybdenum center of NR and depends on the NR electron transport chain from NAD(P)H to heme. Under the circumstances in which NR is not present or active, the existence of another NO-forming system that is similar to the NOS system would account for NO production and NO effects. PII protein, which senses and integrates the signals of the C–N balance in the cell, likely has an important role in organizing cell responses. Here, we critically analyze these topics.

scholarly journals Fasting-induced intestinal apoptosis is mediated by inducible nitric oxide synthase and interferon-γ in rat

2010 ◽  
Vol 298 (6) ◽  
pp. G916-G926 ◽  
Author(s):  
Junta Ito ◽  
Hiroyuki Uchida ◽  
Takayuki Yokote ◽  
Kazuo Ohtake ◽  
Jun Kobayashi
Keyword(s):  
Nitric Oxide ◽  
Protein Expression ◽  
Interferon Γ ◽  
No Synthase ◽  
Histological Evaluation ◽  
No Production ◽  
Ros Production ◽  
Nitrite Production ◽  
Ifn Γ

Nitric oxide (NO) is associated with intestinal apoptosis in health and disease. This study aimed to investigate the role of intestinal NO in the regulation of apoptosis during fasting in rats. Male Wistar rats were divided into two groups and subcutaneously injected with saline (SA) or aminoguanidine (AG), followed by fasting for 24, 48, 60, and 72 h. At each time point, the jejunum was subjected to histological evaluation for enterocyte apoptosis by histomorphometric assessment and TUNEL analysis. We performed immunohistochemistry for inducible NO synthase (iNOS) expression in the jejunum and measured tissue nitrite levels using HPLC and 8-hydroxydeoxyguanosine adduct using ELISA, indicative of endogenous NO production and reactive oxygen species (ROS) production, respectively. Jejunal transcriptional levels of iNOS, neuronal NO synthase (nNOS), and interferon-γ (IFN-γ) were also determined by RT-PCR. Fasting caused significant jejunal mucosal atrophy due to attenuated cell proliferation and enhanced apoptosis with increase in iNOS transcription, its protein expression in intestinal epithelial cells (IEC), and jejunal nitrite levels. However, AG treatment histologically reduced apoptosis with inhibition of fasting-induced iNOS transcription, protein expression, and nitrite production. We also observed fasting-induced ROS production and subsequent IFN-γ transcription, which were all inhibited by AG treatment. Furthermore, we observed reduced transcriptional levels of nNOS, known to suppress iNOS activation physiologically. These results suggest that fasting-induced iNOS activation in IEC may induce apoptosis mediators such as IFN-γ via a ROS-mediated mechanism and also a possible role of nNOS in the regulation of iNOS activity in fasting-induced apoptosis.

Nitric oxide production and signalling in algae

2020 ◽  
Author(s):  
Jeremy Astier ◽  
Jordan Rossi ◽  
Pauline Chatelain ◽  
Agnès Klinguer ◽  
Angélique Besson-Bard ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rapid Development ◽  
Algal Species ◽  
No Synthase ◽  
No Production ◽  
Nitric Oxide Production ◽  
Signalling Molecule ◽  
Oxide Synthase

Abstract Nitric oxide (NO) was the first identified gaseous messenger and is now well established as a major ubiquitous signalling molecule. The rapid development of our understanding of NO biology in embryophytes came with the partial characterization of the pathways underlying its production and with the decrypting of signalling networks mediating its effects. Notably, the identification of proteins regulated by NO through nitrosation greatly enhanced our perception of NO functions. In comparison, the role of NO in algae has been less investigated. Yet, studies in Chlamydomonas reinhardtii have produced key insights into NO production through the identification of NO-forming nitrite reductase and of S-nitrosated proteins. More intriguingly, in contrast to embryophytes, a few algal species possess a conserved nitric oxide synthase, the main enzyme catalysing NO synthesis in metazoans. This latter finding paves the way for a deeper characterization of novel members of the NO synthase family. Nevertheless, the typical NO–cyclic GMP signalling module transducing NO effects in metazoans is not conserved in algae, nor in embryophytes, highlighting a divergent acquisition of NO signalling between the green and the animal lineages.

scholarly journals The emerging role of asymmetric dimethylarginine in cardiovascular disease

2008 ◽  
Vol 14 (4) ◽  
pp. 306-314 ◽  
Author(s):  
R. N. Rodionov ◽  
I. O. Blokhin ◽  
M. M. Galagudza ◽  
E. V. Shlyakhto ◽  
S. R. Lentz
Keyword(s):  
Nitric Oxide ◽  
Risk Factor ◽  
Metabolic Pathways ◽  
Asymmetric Dimethylarginine ◽  
Structural Analog ◽  
No Synthase ◽  
No Production ◽  
Causative Role ◽  
Vascular Events

Asymmetric dimethylarginine (ADMA) is a methylated derivative of the amino acid L-arginine that is receiving increasing attention as a cardiovascular risk factor. As a structural analog of L-arginine, ADMA can inhibit the activity of nitric oxide (NO) synthase, resulting in decreased NO production in blood vessels and other tissues. While substantial epidemiological and experimental evidence links elevated levels of ADMA with endothelial dysfunction and adverse vascular events, the causative role of ADMA in cardiovascular diseases remains still largely unproven. To definitively determine whether ADMA is a biomarker or a causative risk factor, a better understanding of the biochemistry, genetics, and pharmacology of the ADMA metabolic pathways is needed.

The Signaling Pathways in Nitric Oxide Production by Neutrophils Exposed to N-nitrosodimethylamine

2018 ◽  
Vol 16 (2) ◽  
pp. 194-199
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Ewa Jablonska
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Polymorphonuclear Neutrophils ◽  
Microbial Pathogens ◽  
Human Neutrophils ◽  
No Production ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Background: Polymorphonuclear neutrophils (PMNs) play a crucial role in the innate immune system’s response to microbial pathogens through the release of reactive nitrogen species, including Nitric Oxide (NO). </P><P> Methods: In neutrophils, NO is produced by the inducible Nitric Oxide Synthase (iNOS), which is regulated by various signaling pathways and transcription factors. N-nitrosodimethylamine (NDMA), a potential human carcinogen, affects immune cells. NDMA plays a major part in the growing incidence of cancers. Thanks to the increasing knowledge on the toxicological role of NDMA, the environmental factors that condition the exposure to this compound, especially its precursors- nitrates arouse wide concern. Results: In this article, we present a detailed summary of the molecular mechanisms of NDMA’s effect on the iNOS-dependent NO production in human neutrophils. Conclusion: This research contributes to a more complete understanding of the mechanisms that explain the changes that occur during nonspecific cellular responses to NDMA toxicity.

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