scholarly journals Role of nitrate and nitrite for production and consumption of nitric oxide during denitrification in soil

1992 ◽  
Vol 101 (1) ◽  
pp. 59-65 ◽  
Author(s):  
Manfred Baumgärtner ◽  
Ralf Conrad
2008 ◽  
Vol 295 (4) ◽  
pp. F912-F922 ◽  
Author(s):  
Gamika A. Prathapasinghe ◽  
Yaw L. Siow ◽  
Zhibin Xu ◽  
Karmin O

Our recent study (Prathapasinghe GA, Siow YL, O K. Am J Physiol Renal Physiol 292: F1354–F1363, 2007) indicates that homocysteine (Hcy) plays a detrimental role in ischemia-reperfusion-induced renal injury. Elevation of renal Hcy concentration during ischemia-reperfusion is attributed to reduced activity of cystathionine-β-synthase (CBS) that catalyzes the rate-limiting step in the transsulfuration pathway for the metabolism of the majority of Hcy in the kidney. However, the mechanisms of impaired CBS activity in the kidney are unknown. The aim of this study was to investigate the effects of pH and nitric oxide (NO) on the CBS activity in the kidney during ischemia-reperfusion. The left kidney of a Sprague-Dawley rat was subjected to ischemia-reperfusion. The CBS activity was significantly reduced in kidneys subjected to ischemia alone (15–60 min) or subjected to ischemia followed by reperfusion for 1–24 h. The pH was markedly reduced in kidneys upon ischemia. Injection of alkaline solution into the kidney partially restored the CBS activity during ischemia. Further analysis revealed that reduction of CBS activity during reperfusion was accompanied by an elevation of NO metabolites (nitrate and nitrite) in the kidney tissue. Injection of a NO scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), restored the CBS activity in the kidneys subjected to ischemia-reperfusion. Treatment with PTIO could abolish ischemia-reperfusion-induced lipid peroxidation and prevent cell death in the kidney. These results suggested that metabolic acidosis during ischemia and accumulation of NO metabolites during reperfusion contributed, in part, to reduced CBS activity leading to an elevation of renal Hcy levels, which in turn, played a detrimental role in the kidney.


2016 ◽  
Vol 95 (13) ◽  
pp. 1452-1456 ◽  
Author(s):  
X.M. Qu ◽  
Z.F. Wu ◽  
B.X. Pang ◽  
L.Y. Jin ◽  
L.Z. Qin ◽  
...  

The salivary glands and oral bacteria play an essential role in the conversion process from nitrate (NO3-) and nitrite (NO2-) to nitric oxide (NO) in the human body. NO is, at present, recognized as a multifarious messenger molecule with important vascular and metabolic functions. Besides the endogenous L-arginine pathway, which is catalyzed by complex NO synthases, nitrate in food contributes to the main extrinsic generation of NO through a series of sequential steps (NO3--NO2--NO pathway). Up to 25% of nitrate in circulation is actively taken up by the salivary glands, and as a result, its concentration in saliva can increase 10- to 20-fold. However, the mechanism has not been clearly illustrated until recently, when sialin was identified as an electrogenic 2NO3-/H+ transporter in the plasma membrane of salivary acinar cells. Subsequently, the oral bacterial species located at the posterior part of the tongue reduce nitrate to nitrite, as catalyzed by nitrate reductase enzymes. These bacteria use nitrate and nitrite as final electron acceptors in their respiration and meanwhile help the host to convert nitrate to NO as the first step. This review describes the role of salivary glands and oral bacteria in the metabolism of nitrate and in the maintenance of NO homeostasis. The potential therapeutic applications of oral inorganic nitrate and nitrite are also discussed.


1999 ◽  
Vol 5 (5) ◽  
pp. 335-341 ◽  
Author(s):  
Gavin Giovannoni ◽  
N C Silver ◽  
J O'Riordan ◽  
R F Miller ◽  
S J.R. Heales ◽  
...  

Nitric oxide (•NO) has been implicated in the immunopathogenesis of MS as a potential mediator of neuronal loss. To investigate the role of .NO in the development of progressive disease we measured the .NO metabolites (nitrate and nitrite) and neopterin, in the urine of 129 patients with demyelinating disease (DD): 23 with clinically isolated syndromes compatible with demyelination and in 46 relapsing remitting (RR) and 60 patients with progressive MS. Eighty-nine of these 129 patients underwent Gd-enhanced MRI. In addition 58 normal control subjects (NC), 19 AIDS and 35 rheumatoid arthritis (RA) patients were studied. Patients with DD, AIDS and RA had significantly elevated urinary nitrate plus nitrite (nit: creat.urine) and neopterin (neopt: creat.urine) to creatinine ratios compared to NC subjects. (Median[25th-75th%] nit: creat.urine: NC=1183[962-1365] vs DD=1245[875-2403], AIDS=1686[1231-2531], and RA=1950[1214-2726] mmol/mol, P50.001 and median[25th-75th%] neopt: creat.urine: NC=99[76-151] vs DD=163[119-266], AIDS=972[653-1456], and RA=389[257-623] mmol/mol, P50.001). Patients with early DD and RR MS had significantly elevated nit: creat.urine compared to patients with progressive MS (nit: creat.urine: 1612[1020-2733] vs 1159[790-1641] mmol/mol, P=0.006). The nit: creat.urine and neopt: creat.urine did not correlate with clinical relapse or MRI activity. Excretion of .NO metabolites is increased in patients with early or relapsing-remitting disease. .NO appears to be a double-edged sword, mediating tissue damage and modulating complex immunological functions which may be protective in MS.


Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 281
Author(s):  
Emily Margaret Jakubcik ◽  
Kay Rutherfurd-Markwick ◽  
Marsanne Chabert ◽  
Marie Wong ◽  
Ajmol Ali

Background: Nitrate (NO3−)-rich beetroot (BR) juice supplementation has been shown to improve cardiovascular function via reduction to nitrite (NO2−) and then to the bioactive molecule nitric oxide (NO). However, limited research exists for the role of inorganic NO2− that is contained naturally within BR. Objective: As BR juice can naturally contain both NO3− and NO2− the objective of this study was to evaluate the individual effects of NO3− and NO2− consumed from BR on plasma [NO3−]/[NO2−] and their subsequent effects on various cardiovascular measures. Design: In four separate treatments, 11 healthy adults consumed 250 mL of BR containing one of the following: (i) high NO3−, low NO2− (HL; 572 mg NO3−, 32 mg NO2−); (ii) medium NO3−, medium NO2− (MM; 280 mg NO3−, 237 mg NO2−); (iii) low NO3−, medium NO2− (LM; 43 mg NO3−, 262 mg NO2−); (iv) placebo (PL; low NO3−, low NO2−: 8 mg NO3−, 5.8 mg NO2−). Plasma [NO3−]/[NO2−], blood pressure, heart rate, mean arterial pressure (MAP), cardiac output and stroke volume were measured at baseline and every hour or second hour for 6 h post-BR consumption. Outcomes: Ingestion of the HL and MM BR increased plasma [NO2−] and [NO3−] after 2 h, with both remaining elevated after 6 h (p < 0.05). LM increased plasma [NO3−] (p < 0.05) but did not increase plasma [NO2−] compared to PL (p = 0.177). MAP was lower following the consumption of HL at 4 h and LM at 6 h (p < 0.05). Conclusion: Inorganic NO3− consumption is the critical factor in elevating plasma [NO3−] and [NO2−]; however, both NO2− and NO3− show potential to reduce MAP. The known reduction of systolic blood pressure (SBP)/diastolic blood pressure (DBP) following NO3− supplementation was not observed, making it unclear if NO2− contributes to a reduction in SBP/DBP alongside NO3−.


Cephalalgia ◽  
2009 ◽  
Vol 30 (4) ◽  
pp. 486-492 ◽  
Author(s):  
H-J Gruber ◽  
C Bernecker ◽  
A Lechner ◽  
S Weiss ◽  
M Wallner-Blazek ◽  
...  

Nitric oxide (NO) has been implicated in migraine attacks, but the role of NO in migraine remains unclear. We here hypothesize that increased NO in the headache-free period is associated with migraine. One hundred and thirty probands participated in this study. Various parameters of the NO pathway, such as nitrate, nitrite, arginine, citrulline, nitrosylated proteins, asymmetric dimethylarginine, symmetrical dimethylarginine, expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase and two polymorphisms of eNOS were investigated. We found significant increased nitrate and decreased nitrite levels in migraineurs in the headache-free period. Nitrate and nitrite levels showed a significant inverse correlation. Logistic regression revealed an odds ratio of 3.6 for migraine. Other parameters of the NO pathway were neither altered in migraineurs nor correlated with nitrate. We show here that migraine patients suffer under sustained increased nitrosative stress in the headache-free period, which is associated with a 3.6-fold higher risk for migraine.


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