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.

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.

Effect of l-NAME on oxygen uptake kinetics during heavy-intensity exercise in the horse

2001 ◽  
Vol 91 (2) ◽  
pp. 891-896 ◽  
Author(s):  
Casey A. Kindig ◽  
Paul McDonough ◽  
Howard H. Erickson ◽  
David C. Poole
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Electron Transport Chain ◽  
Slow Component ◽  
Oxygen Uptake Kinetics ◽  
No Synthase ◽  
Metabolic Rates ◽  
Transport Chain ◽  
Synthase Inhibitor ◽  
Reduced Time

There is evidence that oxidative enzyme inertia plays a major role in limiting/setting the O2 uptake (V˙o 2) response at the transition to higher metabolic rates and also that nitric oxide (NO) competitively inhibits V˙o 2 within the electron transport chain. To investigate whether NO is important in setting the dynamic response of V˙o 2 at the onset of high-intensity (heavy-domain) running in horses, five geldings were run on a treadmill across speed transitions from 3 m/s to speeds corresponding to 80% of peak V˙o 2with and without nitro-l-arginine methyl ester (l-NAME), an NO synthase inhibitor (20 mg/kg; order randomized). l-NAME did not alter (both P> 0.05) baseline (3 m/s, 15.4 ± 0.3 and 16.2 ± 0.5 l/min for control and l-NAME, respectively) or end-exerciseV˙o 2 (56.9 ± 5.1 and 55.2 ± 5.8 l/min for control and l-NAME, respectively). However, in the l-NAME trial, the primary on-kinetic response was significantly ( P < 0.05) faster (i.e., reduced time constant, 27.0 ± 2.7 and 18.7 ± 3.0 s for control andl-NAME, respectively), despite no change in the gain ofV˙o 2 ( P > 0.05). The faster on-kinetic response was confirmed independent of modeling by reduced time to 50, 63, and 75% of overallV˙o 2 response (all P < 0.05). In addition, onset of the V˙o 2 slow component occurred earlier (124.6 ± 11.2 and 65.0 ± 6.6 s for control and l-NAME, respectively), and the magnitude of the O2 deficit was attenuated (both P < 0.05) in the l-NAME compared with the control trial. Acceleration of the V˙o 2kinetics by l-NAME suggests that NO inhibition of mitochondrial V˙o 2 may contribute, in part, to the intrinsic metabolic inertia evidenced at the transition to higher metabolic rates in the horse.

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.

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.

scholarly journals Comparative Physiological Analysis Reveals the Role of NR-Derived Nitric Oxide in the Cold Tolerance of Forage Legumes

2019 ◽  
Vol 20 (6) ◽  
pp. 1368 ◽  
Author(s):  
Peipei Zhang ◽  
Shuangshuang Li ◽  
Pengcheng Zhao ◽  
Zhenfei Guo ◽  
Shaoyun Lu
Keyword(s):  
Nitric Oxide ◽  
Nitrate Reductase ◽  
Cold Acclimation ◽  
Cold Tolerance ◽  
Cold Treatment ◽  
No Production ◽  
Forage Legumes ◽  
Model Legume ◽  
Nr Activity

The role of nitric oxide (NO) signaling in the cold acclimation of forage legumes was investigated in this study. Medicago sativa subsp. falcata (L.) Arcang. (hereafter M. falcata) is a forage legume with a higher cold tolerance than Medicago truncatula, a model legume. Cold acclimation treatment resulted in increased cold tolerance in both M. falcata and M. truncatula, which was suppressed by pretreatment with tungstate, an inhibitor of nitrate reductase (NR), and 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO), a scavenger of NO. Likely, NITRATE REDUCTASE 1 (NIA1), but not NIA2 transcript, NR activity, and NO production were increased after cold treatment. Treatments with exogenous NO donors resulted in increased cold tolerance in both species. Superoxide dismutase (SOD), catalase (CAT), and ascorbate-peroxidase (APX) activities and Cu,Zn-SOD2, Cu,Zn-SOD3, cytosolic APX1 (cAPX1), cAPX3 and chloroplastic APX1 (cpAPX1) transcript levels were induced in both species after cold treatment, which was suppressed by tungstate and 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO). Treatment with exogenous NO resulted in enhanced activities of SOD, CAT, and APX. Moreover, higher levels of NIA1 transcript, NR activity, NO production, and antioxidant enzyme activities and transcripts were observed in M. falcata as compared with M. truncatula after cold treatment. The results suggest that NR-derived NO production and upregulated antioxidant defense are involved in cold acclimation in both species, while the higher levels of NO production and its derived antioxidant enzymes are associated with the higher cold tolerance in M. falcata as compared with M. truncatula.

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.

scholarly journals Clustering as a Means To Control Nitrate Respiration Efficiency and Toxicity in Escherichia coli

mBio ◽  
2019 ◽  
Vol 10 (5) ◽  
Author(s):  
Suzy Bulot ◽  
Stéphane Audebert ◽  
Laetitia Pieulle ◽  
Farida Seduk ◽  
Emilie Baudelet ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Electron Transport ◽  
Nitrate Reductase ◽  
Electron Transport Chain ◽  
Electron Flux ◽  
Redox Activity ◽  
Nitrate Respiration ◽  
Multiprotein Complex ◽  
Gut Colonization ◽  
Transport Chain

ABSTRACT Respiration is a fundamental process that has to optimally respond to metabolic demand and environmental changes. We previously showed that nitrate respiration, crucial for gut colonization by enterobacteria, is controlled by polar clustering of the nitrate reductase increasing the electron flux through the complex. Here, we show that the formate dehydrogenase electron-donating complex, FdnGHI, also clusters at the cell poles under nitrate-respiring conditions. Its proximity to the nitrate reductase complex was confirmed by its identification in the interactome of the latter, which appears to be specific to the nitrate-respiring condition. Interestingly, we have identified a multiprotein complex dedicated to handle nitric oxide resulting from the enhanced activity of the electron transport chain terminated by nitrate reductase. We demonstrated that the cytoplasmic NADH-dependent nitrite reductase NirBD and the hybrid cluster protein Hcp are key contributors to regulation of the nitric oxide level during nitrate respiration. Thus, gathering of actors involved in respiration and NO homeostasis seems to be critical to balancing maximization of electron flux and the resulting toxicity. IMPORTANCE Most bacteria rely on the redox activity of respiratory complexes embedded in the cytoplasmic membrane to gain energy in the form of ATP and of an electrochemical gradient established across the membrane. Nevertheless, production of harmful and toxic nitric oxide by actively growing bacteria as either an intermediate or side-product of nitrate respiration challenges how homeostasis control is exerted. Here, we show that components of the nitrate electron transport chain are clustered, likely influencing the kinetics of the process. Nitric oxide production from this respiratory chain is controlled and handled through a multiprotein complex, including detoxifying systems. These findings point to an essential role of compartmentalization of respiratory components in bacterial cell growth.

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