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PubMed2001

Characterization of the magnitude and kinetics of xanthine oxidase-catalyzed nitrite reduction. Evaluation of its role in nitric oxide generation in anoxic tissues.

Xanthine oxidase (XO)-catalyzed nitrite reduction with nitric oxide (NO) production has been reported to occur under anaerobic conditions, but questions remain regarding the magnitude, kinetics, and biological importance of this process. To characterize this mechanism and its quantitative importance in biological systems, electron paramagnetic resonance spectroscopy, chemiluminescence NO analyzer, and NO electrode studies were performed. The XO reducing substrates xanthine, NADH, and 2,3-dihydroxybenz-aldehyde triggered nitrite reduction to NO, and the molybdenum-binding XO inhibitor oxypurinol inhibited this NO formation, indicating that nitrite reduction occurs at the molybdenum site. However, at higher xanthine concentrations, partial inhibition was seen, suggesting the formation of a substrate-bound reduced enzyme complex with xanthine blocking the molybdenum site. Studies of the pH dependence of NO formation indicated that XO-mediated nitrite reduction occurred via an acid-catalyzed mechanism. Nitrite and reducing substrate concentrations were important regulators of XO-catalyzed NO generation. The substrate dependence of anaerobic XO-catalyzed nitrite reduction followed Michaelis-Menten kinetics, enabling prediction of the magnitude of NO formation and delineation of the quantitative importance of this process in biological systems. It was determined that under conditions occurring during no-flow ischemia, myocardial XO and nitrite levels are sufficient to generate NO levels comparable to those produced from nitric oxide synthase. Thus, XO-catalyzed nitrite reduction can be an important source of NO generation under ischemic conditions.

Catalysis↗

PubMedDate not supplied

A rapid method for the determination of nitrate and nitrite by chemiluminescence.

Nitrite and nitrate + nitrite can be determined by selective chemical reduction to nitric oxide which is measured using a chemiluminescence analyser. The reducing agents are sodium iodide in acetic acid for nitrite and ferrous ammonium sulphate-ammonium molybdate for nitrate + nitrite. The concentrations of the reducing agents have been optimized to obtain the maximum yield of nitric oxide and the minimum coefficient of variation. Under these conditions, it is possible to inject repeated samples into the refluxing reducing agents and to obtain rapid evolutions of nitric oxide from which the determinations can be made. Nitric oxide has also been produced using the nitrite reagents from organic nitrites, a S-nitrosothiol, a pseudonitrole and N-nitrosamines. Similarly, an organic nitrate and some C-nitroso compounds respond to the method for nitrate but only to the extent of a yield of nitric oxide of about 10% of the theoretical. Very low or zero responses were evident from aliphatic and aromatic C-nitro compounds but not omega-N-nitroarginine which gave a large yield of nitric oxide using the reagents for nitrate. In general, however, concentrations of nitrate will be in considerable excess of those of related compounds which would interfere with the determinations. Nitrate can be determined either by difference in its mixtures with nitrite or by prior removal of the nitrite using ascorbic acid provided oxygen and nitric oxide are removed by degassing with nitrogen.

Indicators and Reagents↗

PubMedDate not supplied

Microbiological aspects and technological need: technological needs for nitrates and nitrites.

Nitrate and nitrite are used in meat and fish curing, and in the manufacture of certain cheeses. Nitrate itself has little antimicrobial effect and in most applications could be replaced by lower concentrations of nitrite. Further, improved hygiene diminishes the need for nitrite. The antimicrobial activity and technological needs for nitrate and nitrite are reviewed. It is concluded that the technological needs for nitrite in meat products stored at < 10 degrees C could be met by added nitrite concentrations of 50 mg/kg. The overall effect of nitrate in salted fish appears to be marginal. In such products, Vibrio parahaemolyticus does not grow at salt concentrations of 10% and food poisoning by this organism is not related to the absence of nitrate or nitrite; growth of Clostridium botulinum Type E (the predominant cause of botulism from fish products) is arrested by salt concentrations of 3-4%. Listeria monocytogenes in seafood cannot be controlled by nitrite. The use of nitrate in cheese production could be avoided, or at least reduced to a low level by avoiding silage with a high count of gas-producing Clostridia and hygienic milk collection.

Bacteria↗

PubMed1999

The oral nitrate and nitrite intake in The Netherlands: evaluation of the results obtained by HPIC analysis of duplicate 24-hour diet samples collected in 1994.

In spring and autumn of 1994 duplicates of 24-h diets were collected from 123 respondents. One of the goals of this study was to determine the amount of nitrite and nitrate in the duplicates of 24-h diets to establish the oral daily intake of these analytes. For this purpose an HPIC/UV method for the determination of nitrate and nitrite in duplicate diets was developed and validated. The sample preparation procedure was derived from the in-house method used for the determination of nitrate and nitrite in human blood plasma. The sample is diluted with water, deproteinized with Carrez reagent, followed by chromatographic clean-up on an SPE C18-column. Both the nitrate and the nitrite results are quantitative. The recovery for nitrite was on average 104% (n = 21, spiking levels: 0.84-95 mg/kg) and for nitrate on average 103% (N = 21, spiking levels: 1.8-404 mg/kg). Samples of duplicates of 24-h diets were analysed according to the method developed. The median intake of nitrite calculated from the samples collected in spring 1994 was 0.6 mg/person day (range < 0.1-6.1 mg/person/day). For the samples collected in autumn 1994 these figures were < 0.2 mg/person/day (range < 0.1-16 mg/person/day). The mean intake of nitrate was 73 mg/person/day (range 7-322 mg/person/day) in spring 1994 and 87 mg/person/day (range 1-310 mg/person/day) in autumn 1994. The overall mean intake of nitrate in 1994 was 80 mg/person/day. The daily intake for nitrate was higher than that found in the duplicate diet study carried out in 1984/1985, when an average daily intake of 52 mg/person was measured. The intake of nitrite was also higher than found in the duplicate diets collected in 1984/1985. The findings of the study are discussed in the context of the ADI for nitrate and nitrite as well as the outcome of other recent European intake studies.

Adolescent↗

PubMed2001

Increased urinary nitrite, a marker of nitric oxide, in active inflammatory bowel disease.

BACKGROUND: Nitric oxide (NO) production is increased in inflammatory bowel disease (IBD), and measurement of NO metabolites may be useful for monitoring disease activity. AIMS AND OBJECTIVES: To characterise urinary nitrite levels, a stable metabolite of NO, in IBD and to evaluate its potential as a marker of disease activity. METHODS: Twelve-hour urinary nitrites were measured by the microplate assay method in 46 patients with IBD (active; n = 32). Urinary samples from 16 healthy individuals served as controls. RESULTS: Increased levels of urinary nitrites were found in patients with active IBD compared with those with inactive IBD. Twenty-eight out of 32 patients (87.5%) with active IBD had detectable levels of nitrite in their urine as compared with 2/14 (14.3%) patients with inactive IBD. None of the 16 healthy controls had detectable urinary nitrite. Twelve-hour urinary nitrite in active compared with inactive IBD: 5 0.7 versus 0.1+/-0.04 micromol (P < 0.05). There was good correlation between urinary nitrite and some markers of disease activity in IBD such as C-reactive protein and microalbuminuria but not with erythrocyte sedimentation rate. CONCLUSIONS: Increased levels of nitrite were detected in urine of patients with active IBD, consistent with increased NO synthesis. This simple assay may be exploited as a potential marker of disease activity in IBD.

Albuminuria↗

PubMed2005

Methods of quantitative analysis of the nitric oxide metabolites nitrite and nitrate in human biological fluids.

In human organism, the gaseous radical molecule nitric oxide (NO) is produced in various cells from L-arginine by the catalytic action of NO synthases (NOS). The metabolic fate of NO includes oxidation to nitrate by oxyhaemoglobin in red blood cells and autoxidation in haemoglobin-free media to nitrite. Nitrate and nitrite circulate in blood and are excreted in urine. The concentration of these NO metabolites in the circulation and in the urine can be used to measure NO synthesis in vivo under standardized low-nitrate diet. Circulating nitrite reflects constitutive endothelial NOS activity, whereas excretory nitrate indicates systemic NO production. Today, nitrite and nitrate can be measured in plasma, serum and urine of humans by various analytical methods based on different analytical principles, such as colorimetry, spectrophotometry, fluorescence, chemiluminescence, gas and liquid chromatography, electrophoresis and mass spectrometry. The aim of the present article is to give an overview of the most significant currently used quantitative methods of analysis of nitrite and nitrate in human biological fluids, namely plasma and urine. With minor exception, measurement of nitrite and nitrate by these methods requires method-dependent chemical conversion of these anions. Therefore, the underlying mechanisms and principles of these methods are also discussed. Despite the chemical simplicity of nitrite and nitrate, accurate and interference-free quantification of nitrite and nitrate in biological fluids as indicators of NO synthesis may be difficult. Thus, problems associated with dietary and laboratory ubiquity of these anions and other preanalytical and analytical factors are addressed. Eventually, the important issue of quality control, the use of commercially available assay kits, and the value of the mass spectrometry methodology in this area are outlined.

Humans↗

PubMed2006

Dynamic response of denitrifying poly-P accumulating organisms batch culture to increased nitrite concentration as electron acceptor.

Despite the fact that, in practice, enhanced biological phosphorus removal (EBPR) is often combined with biological nitrogen removal (BNR), the feasibility of nitrite (an intermediate in BNR) utilization, by denitrifying poly-P accumulating organisms (DPAO) is still unclear. In this study, the effect of nitrite on the EBPR was evaluated by investigating the dynamic response of DPAO to the gradual change of electron acceptor from nitrate to nitrite in an anaerobic/anoxic sequencing batch reactor (SBR). Under the nitrate condition, excellent EBPR was achieved, characterized by the DPAO biomass dominating in the sludge (51%-72% of VSS). Of the DPAO, 34% was the DPAOnitrate that could only use nitrate as electron acceptor, and 66% was the DPAOnitrite that could use nitrate/nitrite as electron acceptor. Nitrite in excess of 12 mg N/L had inhibition effect on the anoxic phosphorus uptake. As the electron acceptor changed, EBPR degraded slowly due to the gradual exclusion of the DPAOnitrate out of the reactor. The DPAOnitrite, therefore, became the single type of DPAO under the nitrite condition, and finally occupied only 33%-49% of the total sludge of VSS. Simultaneously, glycogen accumulating organisms (GAO), the competitor to the DPAO for substrate in the anaerobic phase, was significantly enhanced and grew to dominance in the reactor (46-62% of VSS). Also, the periodical exposure of sludge to the increased nitrite concentration elevated the inhibition level of nitrite for the anoxic phosphorus uptake (80 mg N/L). More attention should be paid to nitrite accumulation at full-scale wastewater treatment plants from the perspective of the stability of EBPR performance.

Biomass↗

PubMed2004

Honey increased saliva, plasma, and urine content of total nitrite concentrations in normal individuals.

This study investigated effects of oral honey solution on total nitrite, a stable nitric oxide metabolite, in saliva, plasma, and urine samples collected from normal subjects. Fourteen adult healthy volunteers, 25-50 years old, nine males and three females, were enrolled in the study. Total nitrite was estimated in saliva, plasma, and urine after 14 hours of food fasting. Each subject was then asked to drink honey solution (80 g of raw honey dissolved in 250 mL of water). Saliva and blood samples were collected at 1, 2, and 3 hours after ingestion of honey solution for total nitrite assay, while urine samples were collected after 3 hours for total nitrite assay. The mean total fasting nitrite in saliva was 108 +/- 61.3 micromol/L, which was increased to 130 +/- 62.9, 131.2 +/- 59, and 135.1 +/- 64.3 micromol/L at 1, 2, and 3 hours, respectively. Plasma total nitrite was 22.41 +/- 16.22 micromol/L before drinking honey, which was increased to 34.71 +/- 18.13, 29.38 +/- 14.29, and 33 +/- 13.09 micromol/L at 1, 2, and 3 hours, respectively, after drinking honey. Urine total nitrite before drinking honey was 75.8 +/- 54.79 micromol/L, which was increased to 107.8 +/- 70.83 micromol/L 3 hours after ingestion of honey solution. Although not statistically significant, honey solution showed a tendency to increase total nitrite concentration in different biological fluids from humans, including saliva, plasma, and urine.

Administration, Oral↗

PubMed1978

Urinary nitrite and urinary-tract infection.

Two dipstick procedures and an automated quantitative urinary nitrite assay were used to study nitrite in 786 samples of urine submitted to the bacteriology laboratory for routine culture and sensitivity testing. Many samples that had more than 100,000 nitrite-reducing organisms/ml and no detectable nitrite were studied. Limited nitrate concentration in urine was not a significant cause of false-negative nitrite results. However, in some urine samples nitrite added in vitro was lost during a four-hour incubation in vitro at 37 C in the presence of more than 100,000 nitrite-reducing organisms/ml. Ascorbic acid, abnormal amounts of urobilinogen, and urinary pH below 6.0 are all possible causes of false-negative nitrite determinations.

Autoanalysis↗

PubMed1986

Metabolic nitrite formation from N-nitrosamines: are there other pathways than reductive denitrosation by cytochrome P-450?

To demonstrate whether there are any pathways of nitrite formation from N-nitrosamines other than reductive denitrosation by cytochrome P-450 we performed the following experiments. An esterified alpha-hydroxylated nitrosamine was incubated in a microsomal system to test if nitrite generation is coupled with or linked to the oxidative bioactivation pathway. Simultaneously, inhibitors of microsomal esterases were added to test if the intact molecule or a metabolite from the oxidative metabolism was responsible for nitrite formation. To check if the superoxide radical anion could be related to the mechanism of nitrite generation, nitrosamines were incubated with a xanthine oxidase/hypoxanthine system. To test if the OH radical was involved in nitrite formation, nitrosamines were incubated with an artificial hydroxy-radical generating system (xanthine oxidase/hypoxanthine system supplemented with Fe2+/EDTA). Measurable amounts of nitrite were detected after incubation of the esterified-hydroxylated N-nitrosamine when the hydrolysis by microsomal esterases was inhibited by diisopropylfluorophosphate or paraoxon and when the N-nitrosamines were incubated with the artificial hydroxy-radical generating system. Nitrite formation could not be detected in the O2(-)-generating system (xanthine oxidase/hypoxanthine) or when the esterified alpha-hydroxylated N-nitrosamine was incubated without inhibition of the microsomal esterases. These results demonstrate that besides reductive denitrosation by cytochrome P-450, nitrite generation from N-nitrosamines can also be caused by hydroxy-radicals. The importance of this possible pathway for the in vivo situation of nitrosamine metabolism is discussed.

Animals↗

PubMed2003

The presence of nitrite during UVA irradiation protects from apoptosis.

Nitrite occurs ubiquitously in biological fluids such as blood and sweat, representing an oxidation product of nitric oxide. Nitrite has been associated with a variety of adverse effects such as mutagenicity, carcinogenesis, and toxicity. In contrast, here we demonstrate that the presence of nitrite, but not nitrate, during irradiation of endothelial cells in culture exerts a potent and concentration-dependent protection against UVA-induced apoptotic cell death. Protection is half-maximal at a concentration of 3 mM, and complete rescue is observed at 10 mM. Nitrite-mediated protection is mediated via inhibition of lipid peroxidation in a similar manner as seen with butylated hydroxytoluene, a known inhibitor of lipid peroxidation. Interestingly, nitrite-mediated protection is completely abolished by coincubation with the NO scavenger cPTIO. Using electron paramagnetic resonance (EPR) spectroscopy or Faraday modulation spectroscopy, we directly prove UVA-induced NO formation in solutions containing nitrite. In conclusion, evidence is presented that nitrite represents a protective agent against UVA-induced apoptosis due to photodecomposition of nitrite and subsequent formation of NO.

Apoptosis↗

PubMed2003

Gastric juice nitrite and vitamin C in patients with gastric cancer and atrophic gastritis: is low acidity solely responsible for cancer risk?

BACKGROUND: N-nitroso compounds are carcinogens formed from nitrite, a process that is inhibited by vitamin C in gastric juice. Helicobacter pylori infection has been reported to increase nitrite and decrease vitamin C in gastric juice. Therefore, susceptibility to gastric cancer in H. pylori-infected patients may be derived from increased N-nitroso compounds in gastric juice. However, most H. pylori-infected patients do not develop gastric cancer. OBJECTIVE: To investigate additional factors that may affect susceptibility to gastric cancer, we compared nitrite and vitamin C levels in gastric juice from H. pylori-infected patients with and without gastric cancer. METHODS: Serum and gastric juice were obtained from 95 patients undergoing diagnostic endoscopy, including those with normal findings, duodenal ulcer, gastric ulcer, atrophic gastritis and gastric cancer. Serum was analysed for H. pylori antibody, nitrate and nitrite, gastrin and pepsinogens; gastric juice was analysed for pH, nitrite and vitamin C. RESULTS: pH and nitrite levels were increased and vitamin C levels decreased in the gastric juice of patients with atrophic gastritis and gastric cancer compared with other patients. However, in patients with a similar gastric acidity (pH 5-8), nitrite concentrations in the gastric juice were significantly higher and vitamin C levels significantly lower in patients with gastric cancer than in those with atrophic gastritis. CONCLUSION: Although hypochlorhydria increases intraluminal nitrite and decreases intraluminal vitamin C, which increases the intraluminal formation of N-nitroso compounds, our results indicate that patients with gastric cancer may have additional factors that emphasize these changes.

Aged↗

PubMed1978

The chromosomal location and pleiotropic effects of mutations of the nirA+ gene of Escherichia coli K12: the essential role of nirA+ in nitrite reduction and in other anaerobic redox reactions.

Cytochrome c552, which has been implicated as an electron carrier for nitrite reduction by Escherichia coli, has been separated from NADH-nitrite oxidoreductase activity. The cytochrome is therefore not required for the reduction of nitrite by NADH in vitro. Nevertheless, some mutants which were selected by their inability to use nitrite as a nitrogen source during anaerobic growth synthesize neither NADH-nitrite oxidoreductase nor cytochrome c552. The defects in these mutants are due to mutations in a single gene, nirA, which is located at about minute 29 on the recalibrated linkage map. Experiments with an F' plasmid which carries a nirA+ allele established that nirA+ is dominant to the defective allele. Other mutants, defective in nitrate reductase activity because of mutations in the chlA or chlB genes, synthesized nitrite reductase and cytochrome c552 in the absence of nitrate or nitrite. A mutant with a defective fnr gene was also NirA- and, conversely, nirA mutants were Fnr-. In a series of transduction experiments, attempts to separate the nirA and fnr defects were unsuccessful. Furthermore, no complementation was observed when an F' plasmid carrying a defective nirA allele was transferred into the fnr strain. It is concluded that the fnr gene described by Lambden & Guest (1976) is identical to the nirA gene and that its product affects the synthesis or assembly of a variety of anaerobic redox enzymes which include nitrite reductase, cytochrome c552, nitrate reductase, fumarate reductase and formate hydrogenlyase.

Chromosome Mapping↗

PubMed1987

Nitrite accumulation during anaerobic nitrate reduction by binary suspensions of bacteria isolated from the achlorhydric stomach.

Binary suspensions of bacteria isolated from the gastric juice of achlorhydric patients were used to determine conditions which favour nitrite accumulation during nitrate reduction. Suspensions of Veillonella parvula and Haemophilus parainfluenzae accumulated nitrite during nitrate reduction in the absence of nitrite-reducing Neisseria subflava or Streptococcus sanguis. The maximum concentration of nitrite that transiently accumulated decreased predictably as the ratio of nitrite-removing bacteria to nitrite-accumulating bacteria increased. This ratio, but more importantly the bacterial density, determined the duration of nitrite accumulation. These results are correlated with the previously reported tendency of nitrite to accumulate in the gastric juice of hypogammaglobulinaemic and pernicious anaemic patients, and with the extremely high incidence of gastric cancer in the two groups.

Achlorhydria↗

PubMed1999

Estimation of oxidative products of nitric oxide (nitrates, nitrites) in preeclampsia.

Oxidative products of nitric oxide, serum nitrates and nitrites were estimated in 50 primigravidas with preeclampsia and in 50 gestation and age-matched normotensive primigravidas. Thirty three (66%) of these women had mild preeclampsia and 17 (34%) had severe preeclampsia. Serum nitrate and nitrite levels were significantly higher in preeclamptic women (nitrates - 15 +/- 1.17; nitrites - 11.82 +/- 1.16 micromol/L) than in the normotensive pregnant women (nitrates 11.82 +/- 1.16; nitrites - 5.08 +/- 0.47 micromol/L, p < 0.001). In preeclamptic women, serum nitrate and nitrite levels correlated with the severity of the disease (mild preeclampsia nitrate - 14.46 +/- 1.98; nitrite 6.21 +/- 0.84 micromol/L, severe preeclampsia nitrate - 16.65 +/- 3.64; Nitrite - 6.87 +/- 1.56 micromol/L). In preeclampsia there was significant positive correlation between nitrate and nitrite levels and diastolic blood pressure and proteinuria.

Adult↗

PubMed2007

Selenite-reducing capacity of the copper-containing nitrite reductase of Rhizobium sullae.

Rhizobium sullae strain HCNT1 contains a nitric oxide-producing nitrite reductase of unknown function due to the absence of a complementary nitric oxide reductase. HCNT1 had the ability to grow on selenite concentrations as high as 50 mM, and during growth, selenite was reduced to the less toxic elemental selenium. An HCNT1 mutant lacking nitrite reductase grew poorly in the presence of 5 mM selenite, was unable to grow in the presence of 25 or 50 mM selenite and also showed no evidence of selenite reduction. A naturally occurring nitrite reductase-deficient R. sullae strain, CC1335, also showed little growth on the higher concentrations of selenite. Mobilization of a plasmid containing the HCNT1 gene encoding nitrite reductase into CC1335 increased its resistance to selenite. To confirm that this ability to grow in the presence of high concentrations of selenite correlated with nitrite reductase activity, a new nitrite reductase-containing strain was isolated from the same location where HCNT1 was isolated. This strain was also resistant to high concentrations of selenite. Inactivation of the gene encoding nitrite reductase in this strain increased selenite sensitivity. These data suggest that the nitrite reductase of R. sullae provides resistance to selenite and offers an explanation for the radically truncated denitrification found uniquely in this bacterium.

Bacterial Proteins↗

PubMed1974

Effect of sodium nitrite on toxin production by Clostridium botulinum in bacon.

Pork bellies were formulated to 0, 30, 60, 120, 170, or 340 mug of nitrite per g of meat and inoculated with Clostridium botulinum via pickle or after processing and slicing. Processed bacon was stored at 7 or 27 C and assayed for nitrite, nitrate, and botulinal toxin at different intervals. Nitrite levels declined during processing and storage. The rate of decrease was more rapid at 27 than at 7 C. Although not added to the system, nitrate was detected in samples during processing and storage at 7 and 27 C. The amount of nitrate found was related to formulated nitrite levels. No toxin was found in samples incubated at 7 C throughout the 84-day test period. At 27 C, via pickle, inoculated samples with low inoculum (210 C. botulinum per g before processing and 52 per g after processing) became toxic if formulated with 120 mug of nitrite per g of meat or less. Toxin was not detected in bacon formulated with 170 or 340 mug of nitrite per g of meat under these same conditions. Toxin was detected at all formulated nitrite levels in bacon inoculated via the pickle with 19,000 C. botulinum per g (4,300 per g after processing) and in samples inoculated after slicing. However, increased levels of formulated nitrite decreased the probability of botulinal toxin formation in bacon inoculated by both methods.

Animals↗

PubMed1997

Involvement of NtcB, a LysR family transcription factor, in nitrite activation of the nitrate assimilation operon in the cyanobacterium Synechococcus sp. strain PCC 7942.

Nitrite, either exogenously supplied or endogenously generated by nitrate reduction, activates transcription of the nitrate assimilation operon (nirA-nrtABCD-narB) in Synechococcus sp. strain PCC 7942 cells treated with L-methionine-DL-sulfoximine (an inhibitor of glutamine synthetase), in which there is no negative feedback resulting from fixation of the ammonium generated by nitrite reduction (Kikuchi et al., J. Bacteriol. 178:5822-5825, 1996). Other transcription units related to nitrogen assimilation, i.e., the nirB-ntcB operon, glnA, and ntcA, were not activated by nitrite. Nitrite did not activate nirA operon transcription in a mutant with a deletion of ntcB, an ammonium-repressible gene encoding a LysR-type DNA-binding protein. Introduction of plasmid-borne ntcB into the ntcB deletion mutant restored the response of the cells to nitrite, indicating that NtcB activates the nirA operon in response to nitrite. Supplementation of nitrite or nitrate to nitrogen-starved cultures of the wild-type strain, but not of the ntcB deletion mutant, caused activation of the nirA operon without L-methionine-DL-sulfoximine treatment of the cells. The results suggested that the positive-regulation mechanism of nirA operon transcription plays a role in rapid adaptation of nitrogen-starved cells to changing availability of nitrate and nitrite.

Bacterial Proteins↗