PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Nitrites”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

Mechanisms of nitrite accumulation occurring in soilnitrification.

Because low concentration of nitrite could be toxic to biological systems and high amounts of nitrite have been observed in a river of northern China since 1990, nitrite from agricultural soil sources should be investigated. In this paper, effects of levels of ammonium-N (NH4+-N), soil pH and nitrification inhibitors on NO2- accumulation, and duration of nitrite in soils were studied. Application of 11.2 mg of nitrapyrin kg(-1) soil or 11.2 mg of sodium azide kg(-1) soil dramatically suppressed nitrite occurrence. Within all incubation times and at all levels of ammonium-N input, we did not detect any measurable NO2-N accumulation in samples of Yellow-brown earth (pH 5.67), but observed huge accumulation in the 2 alkaline soils, Fluvo-aquic loam (pH 7.89) and Fluvo-aquic sand (pH 8.20). The concentrations of nitrite in both alkaline soils were related to ammonium-N levels. The effect of pH on nitrite accumulation was demonstrated by using slurries of Fluvo-aquic sand under continuous aeration and buffers of different pH. Data showed that nitrite concentration increased with the elevated pH, yet that ammonia oxidizers from the original soil (pH 8.2) could adapt to the new medium of low pH (pH 5.35). Dynamic changes of nitrite in soils amended with different rates of nitrite-N were also measured in 6 days. Thereby, we concluded that nitrite was unstable in acid soils, but durable in alkaline soils. The authors suggested that NO2- accumulation in field soils and its subsequent environmental impact should receive more attention.

Air↗

Organic nitrites and NO: inhibition of lipid peroxidation and radical reactions.

Organic nitrites, such as i-amyl nitrite (IAN), are nitrovasodilator drugs used both clinically and recreationally. Nitrites are also chemically reasonable biological products of NO metabolism, in particular in both inhibition of lipid peroxidation by NO and induction of lipid peroxidation by peroxynitrite and NO2. Nitrites are also potential products of biomolecule nitrosation and intermediates in biotransformation of nitrate vasodilators. Although mechanisms can be drawn for both prooxidant and antioxidant activity, IAN has been observed to inhibit lipid peroxidation in a variety of systems. To test if the antioxidant activity of nitrites results from NO release alone, inhibition of lipid peroxidation was studied for four organic nitrites and four NO donor NONOates. Iron-induced lipid peroxidation in synaptosomal tissue homogenates and azo compound-initiated lipid peroxidation in liposomes and linoleic acid SDS comicelles were examined. Lipid peroxidation was quantified by TBARS and oxygen uptake analysis. A good correlation of rate of NO release with IC50 for inhibition of lipid peroxidation was observed for the NONOates, compatible with lipid radical chain termination by NO, for which a chain termination stoichiometry of 0.4-0.5 mol of lipid peroxyl radicals per mole of NO was determined. In neutral aqueous solution, nitrites also spontaneously released NO as measured by chemiluminescence; however, no correlation was observed between the rate constants of NO release for the nitrites and their inhibitor potency toward lipid peroxidation. Long chain nitrites were seen to be relatively good inhibitors of lipid peroxidation by mechanisms that must involve factors in addition to simple homolysis to release NO. Evidence for direct alpha-hydrogen atom abstraction from the nitrite by peroxyl radicals was obtained by analysis of aldehyde products and supported by MO calculations. The data suggest that lipid nitrites formed as NO chain termination products have the capacity to further inhibit lipid peroxidation and to release NO.

Animals↗

Intragastric nitric oxide is abolished in intubated patients and restored by nitrite.

OBJECTIVE: Nitrite in saliva is reduced to nitric oxide (NO) in the acidic stomach, and this NO may serve gastroprotective functions. We studied intragastric NO levels in healthy controls and in intubated intensive care unit patients before and after supplementation with nitrite. DESIGN: Prospective observational study involving patients and controls. SETTING: A mixed intensive care unit and a university laboratory. PATIENTS AND SUBJECTS: Eight healthy volunteers and ten intubated, mechanically ventilated intensive care unit patients. INTERVENTIONS: A tonometric catheter was first evaluated in vitro and then used for all NO measurements. In fasting controls, gastric NO levels were measured repeatedly during periods of saliva depletion and after an intragastric nitrite infusion. In patients, changes in levels of intragastric NO, nitrite in plasma and gastric juice, and S-nitrosothiols in gastric juice were measured in response to an intragastric nitrite infusion. MEASUREMENTS AND MAIN RESULTS: The tonometric catheter had a recovery of 80% with a high intraclass and interclass correlation. Median baseline NO levels in healthy volunteers were 21.6 ppm (interquartile range, 11.4-22.3 ppm) and decreased by 90% to 3.3 ppm (2.0-5.2 ppm) during 25-50 mins of saliva depletion. The NO level was restored by an intragastric nitrite infusion. Baseline NO levels in patients were almost abolished (0.1 ppm [0.07-0.4 ppm]) but increased rapidly to 124 ppm (range, 65-180 ppm) during intragastric nitrite infusion. Nitrite levels in plasma increased from 0.18 +/- 0.03 to 1.3 +/- 0.2 microM (p < .01), and levels of S-nitrosothiols in gastric juice increased from 0.12 +/- 0.09 to 6.7 +/- 1.8 microM. CONCLUSIONS: Intragastric generation of NO requires continuous delivery of nitrite-containing saliva and is almost abolished in critically ill, intubated patients. Enteral supplementation with nitrite could however fully restore gastric NO levels. Future studies will reveal if low NO levels contribute to stress ulcers and gastric overgrowth of bacteria often seen in these patients and in turn if restoring gastric NO with nitrite could be a useful therapeutic approach.

Adult↗

Nitrate- and nitrite-reducing bacteria in the achlorhydric stomach.

The microbial composition of samples of gastric juice from eight achlorhydric patients was determined by aerobic and rigorously anaerobic culture techniques. Bacteria from 16 genera were commonly isolated, but representatives of only three genera, (streptococci, neisseriae and haemophili) were isolated from every patient. Nitrate and nitrite were both reduced by veillonellae, haemophili, staphylococci, corynebacteria, lactobacilli, flavobacteria and fusobacteria, but the potential rate of nitrate reduction by suspensions of veillonellae, Haemophilus parainfluenzae and members of the Enterobacteriaceae were up to ten times more rapid than the rate of nitrite reduction. Conversely, although all Neisseria spp. reduced nitrite only some strains reduced nitrate. Streptococci did not reduce nitrate. Streptococcus sanguis reduced nitrite when grown with haematin; other streptococci did not reduce nitrite. Bacterial nitrate and nitrite reduction were active over the pH range 6-8, similar to the pH range of the achlorhydric stomach. From a knowledge of the composition of the bacterial flora and their potential rates of nitrate and nitrite reduction under prevailing conditions, predictions were made about the tendency of nitrite to accumulate during nitrate reduction. Studies of the transient accumulation of nitrite by mixed cultures of H. parainfluenzae and N. subflava were consistent with these predictions. Haemophili and veillonellae could be responsible for the accumulation of nitrite in the gastric juice of some patients, whereas streptococci and neisseriae would tend to remove nitrite from the stomach as rapidly as it formed.

Achlorhydria↗

Immunological identification and distribution of dissimilatory heme cd1 and nonheme copper nitrite reductases in denitrifying bacteria.

Polyclonal antibodies were used to identify heme or copper nitrite reductases in the following groups: 23 taxonomically diverse denitrifiers from culture collections, 100 numerically dominant denitrifiers from geographically diverse environments, and 51 denitrifiers from a culture collection not selected for denitrification. Antisera were raised against heme nitrite reductases from Pseudomonas aeruginosa and Pseudomonas stutzeri and against copper nitrite reductase from Achromobacter cycloclastes. Nitrite reductases were identified by Western immunoblot. Diethyldithiocarbamate, which specifically inhibits copper nitrite reductases, was used to confirm the immunological characterization and determine which type was present in strains nonreactive with any antiserum. For groups in which the type of nitrite reductase has not been previously described, we found that Alcaligenes eutrophus, Bacillus azotoformans, Bradyrhizobium japonicum, Corynebacterium nephridii, and Rhizobium spp. contained copper nitrite reductase, while Aquaspirillum itersonii, Flavobacterium spp., and Pseudomonas fluorescens contained heme nitrite reductase. Heme nitrite reductases dominated, regardless of soil type or geographic origin. They occurred in 64 and 92%, respectively, of denitrifiers in the numerically dominant and nonselected collections. The two nitrite reductase types were mutually exclusive in individual bacteria, but both appeared in different strains from the Alcaligenes and Pseudomonas genera. The heme type predominated in Pseudomonas strains. The heme-type nitrite reductase appeared more conserved if judged by similarities in molecular weights and immunological reactions. The Cu type was found in more taxonomically unrelated strains and varied in molecular weight and antiserum recognition.

Animals↗

Effect of nitrite and nitrate on toxin production by Clostridium botulinum and on nitrosamine formation in perishable canned comminuted cured meat.

Comminuted ham was formulated with different levels of sodium nitrite and nitrate, inoculated with Clostridium botulinum, and pasteurized to an internal temperature of 68.5 C. When added to the meat, nitrite concentrations decreased, and cooking had little effect on them. Nitrite concentrations decreased more rapidly during storage at 27 than at 7 C; however they remained rather constant at formulated levels throughout the experiment at both incubation temperatures. The level of nitrite added to the meat greatly influenced growth and toxin production of C. botulinum. The concentration of nitrite necessary to effect complete inhibition was dependent on the inoculum level. With 90 C. botulinum spores/g of meat, botulinum toxin developed in samples formulated with 150 but not with 200 mug of nitrite per g of meat. At a spore level of 5,000/g, toxin was detected in samples with 400 but not with 500 mug of nitrite per g of the product incubated at 27 C. At lower concentrations of nitrite, growth was retarded at both spore levels. No toxin developed in samples incubated at 7 C. Nitrate showed a statistically significant inhibitory effect at a given nitrite level; however, the effect was insufficient to be of practical value. Analyses for 14 volatile nitrosamines from samples made with varying levels of nitrite and nitrate were negative at a detection level of 0.01 mug of nitrite or nitrate per g of meat.

Animals↗

Nitrite reductase of Escherichia coli specific for reduced nicotinamide adenine dinucleotide.

Kemp, John D. (University of California, Los Angeles), and Daniel E. Atkinson. Nitrite reductase of Escherichia coli specific for reduced nicotinamide adenine dinucleotide. J. Bacteriol. 92:628-634. 1966.-A nitrite reductase specific for reduced nicotinamide adenine dinucleotide (NADH(2)) appears to be responsible for in vivo nitrite reduction by Escherichia coli strain Bn. In extracts, the reduction product is ammonium, and the ratio of NADH(2) oxidized to nitrite reduced or to ammonium produced is 3. The Michaelis constant for nitrite is 10 mum. The enzyme is induced by nitrite, and the ability of intact cells to reduce nitrite parallels the level of NADH(2)-specific nitrite reductase activity demonstrable in cell-free preparations. Crude extracts of strain Bn will also reduce hydroxylamine, but not nitrate or sulfite, at the expense of NADH(2). Kinetic observations indicate that hydroxylamine and nitrite may both be reduced at the same active site. The high apparent Michaelis constant for hydroxylamine (1.5 mm), however, seems to exclude hydroxylamine as an intermediate in nitrite reduction. In vitro activity is enhanced by preincubation with nitrite, and decreased by preincubation with NADH(2).

Enzyme Induction↗

Origin of nitrite and nitrate in nasal and exhaled breath condensate and relation to nitric oxide formation.

BACKGROUND: Raised concentrations of nitrate and nitrite have been found in exhaled breath condensate (EBC) in airway disease, and it has been postulated that this reflects increased nitric oxide (NO) metabolism. However, the chemical and anatomical origin of nitrate and nitrite in the airways has not yet been sufficiently studied. METHODS: The fraction of exhaled NO at an exhalation flow rate of 50 ml/s (FE(NO)) and nitrite and nitrate in EBC, nasal condensate, and saliva were measured in 17 tracheostomised and 15 non-tracheostomised subjects, all of whom were non-smokers without respiratory disease. Tracheal and oral samples were taken from the tracheostomised subjects and nasal (during velum closure) and oral samples from the non-tracheostomised subjects. Measurements were performed before and after sodium nitrate ingestion (10 mg/kg) and use of antibacterial mouthwash (chlorhexidine 0.2%). RESULTS: In tracheostomised subjects oral FE(NO) increased by 90% (p<0.01) while tracheal FE(NO) was not affected 60 minutes after nitrate ingestion. Oral EBC nitrite levels were increased 23-fold at 60 minutes (p<0.001) whereas the nitrite levels in tracheal EBC showed only a minor increase (fourfold, p<0.05). Nitrate was increased the same amount in oral and tracheal EBC at 60 minutes (2.5-fold, p<0.05). In non-tracheostomised subjects oral FE(NO) and EBC nitrite increased after nitrate ingestion and after chlorhexidine mouthwash they approached baseline levels again (p<0.001). Nasal NO, nitrate, and nitrite were not affected by nitrate intake or mouthwash. At baseline, mouthwash with deionised water did not affect nitrite in oral EBC or saliva, whereas significant reductions were seen after antibacterial mouthwash (p<0.05 and p<0.001, respectively). CONCLUSIONS: Besides the salivary glands, plasma nitrate is taken up by the lower airways but not the nasal airways. Nitrate levels in EBC are thus influenced by dietary intake. Nitrate is reduced to nitrite by bacterial activity which takes place primarily in the oropharyngeal tract of healthy subjects. Only oropharyngeal nitrite seems to contribute to exhaled NO in non-inflamed airways, and there is also a substantial contribution of nitrite from the oropharyngeal tract during standard collection of EBC.

Adult↗

Nitrite uptake and metabolism and oxidant stress in human erythrocytes.

Nitric oxide, when released into the bloodstream, is quickly scavenged by Hb in erythrocytes or oxidized to nitrite. Nitrite can also enter erythrocytes and oxidize Hb. The goals of this work were to determine the mechanism of erythrocyte nitrite uptake and whether this uptake causes oxidant stress in these cells. Erythrocytes took up 0.8 mM nitrite with a half-time of 11 min. Nitrite uptake was sensitive to temperature and to the pH and ionic composition of the medium but was not inhibited by the specific anion-exchange inhibitor DIDS. About 25% of nitrite uptake occurred on the sodium-dependent phosphate transporter and the rest as diffusion of nitrous acid or other species across the plasma membrane. Methemoglobin formation increased in proportion to the intracellular nitrite concentration. Nitrite reacted with erythrocyte ascorbate, but ascorbate loading of cells decreased nitrite-induced methemoglobin formation only at high nitrite concentrations. In conclusion, nitrite rapidly enters erythrocytes and reacts with oxyhemoglobin but does not exert a strong oxidant stress on these cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver.

Nitrite represents a circulating and tissue storage form of NO whose bioactivation is mediated by the enzymatic action of xanthine oxidoreductase, nonenzymatic disproportionation, and reduction by deoxyhemoglobin, myoglobin, and tissue heme proteins. Because the rate of NO generation from nitrite is linearly dependent on reductions in oxygen and pH levels, we hypothesized that nitrite would be reduced to NO in ischemic tissue and exert NO-dependent protective effects. Solutions of sodium nitrite were administered in the setting of hepatic and cardiac ischemia-reperfusion (I/R) injury in mice. In hepatic I/R, nitrite exerted profound dose-dependent protective effects on cellular necrosis and apoptosis, with highly significant protective effects observed at near-physiological nitrite concentrations. In myocardial I/R injury, nitrite reduced cardiac infarct size by 67%. Consistent with hypoxia-dependent nitrite bioactivation, nitrite was reduced to NO, S-nitrosothiols, N-nitros-amines, and iron-nitrosylated heme proteins within 1-30 minutes of reperfusion. Nitrite-mediated protection of both the liver and the heart was dependent on NO generation and independent of eNOS and heme oxygenase-1 enzyme activities. These results suggest that nitrite is a biological storage reserve of NO subserving a critical function in tissue protection from ischemic injury. These studies reveal an unexpected and novel therapy for diseases such as myocardial infarction, organ preservation and transplantation, and shock states.

Animals↗

Formation of DNA-damaging and mutagenic activity in the reaction systems containing nitrite and butylated hydroxyanisole, tryptophan, or cysteine.

It was confirmed by the procedure of rec-assay that DNA-damaging activities were formed in the reaction systems containing nitrite and phenol derivatives including BHA, tryptophan or cysteine under gastric pH conditions. The mutagenic action of the nitrite-BHA, nitrite-tryptophan and nitrite-cysteine systems was also tested according to Ames' method using Salmonella typhimurium TA 1535 and TA 98. The mutagenic activity was observed in the nitrite-tryptophan and nitrite-cysteine systems, though the nitrite-BHA system did not show the activity. The DNA-damaging products were generally labile, i.e., the activity decreased significantly after 1.5 to 2 hours of the reaction, except in the case of the nitrite-BHA system. The DNA-damaging activity in the nitrite-BHA system did not decrease even after 48 hours of the reaction. Nitrosophenol derivatives themselves showed the DNA-damaging activity at pH 1. The active product in the nitrite-BHA system was isolated and the structure was determined to be 2-tert-butyl-quinone. This compound gave a positive rec-assay test, and showed no mutagenesis by Ames' method. The active product from the nitrite-cysteine system was infered to be nitrosocysteine, and the product showed both DNA-damaging and mutagenic activity.

Anisoles↗

[Influence of thermal processing and storage on the content of nitrates and nitrites in chosen vegetables from the Podlasie province].

The dangerous for health nitrate and nitrite can penetrate with food human organism for this reason in study the influence of thermal processing and storage on the level of these compounds in the vegetables was determined. The content of nitrates and nitrites was determined in such vegetables as carrot, parsley-root, celery and potatoes growing by farmers in the Podlasie province. Nitrates and nitrites were assessed in fresh and boiled vegetables as well as in the stock and in carrot juice. These compounds were also determined after storage of vegetables at +4 degrees C for 2 weeks and at -15 degrees C for 1 and 3 months. Nitrates and nitrites concentrations were assayed colorimetrically by the Griess method modified to food investigation. Boiling reduced nitrate content in the vegetables. Considerable part (about 50%) of these compounds passed into stock during boiling. Storage of these vegetables at +4 degrees C resulted in slight lowering of nitrate content in carrot and parsley-root and marked elevation in celery. Cold storage of vegetables through 1 and 3 months had no important influence on nitrate content. Boiling decreased the content of nitrites similarly as nitrates. Storage of the vegetables at +4 degrees C through 2 weeks led to an increase in nitrite content in carrot and parsley-root while in celery the content of nitrites was reduced. Storage of vegetables at -15 degrees C resulted in lowering content of nitrite. The study revealed that the vegetable-roots (carrot, parsley and celery) and potatoes cultivated in the Podlasie province as well as in the other provinces were excessively contaminated by nitrates and nitrites. Moreover, it has been shown that thermal processing such as boiling considerably reduced the content of nitrates and nitrites in these vegetables while freezing changed mainly nitrite content.

Environmental Monitoring↗

Disappearance of nitrite from the rat stomach: contribution of emptying and other factors.

To help understand how intragastric nitrosation forms N-nitroso compounds, nitriet disappearance from the rat stomach was measured after food containing nitrite was given. In preliminary experiments, nitrite disappearance from buffered aqueous solutions became more rapid as the pH was lowered from 5 to 1 and, at a given pH, was more rapid in a slurry of commercial rat food. The disappearance of nitrite from buffer was little affected by the addition of pepsin, mucin, albumin, or rat gastric contents. When starved rats were given 5 g food with 1.82 mg nANO3/g, nitrate was not reduced to nitrite in the stomach. Five g food containing 154 mug NaNO2/g was administered similarly, and the total stomach (T) and glandular and nonglandular parts (G and NG) were analyzed after 1.5 hours. Weight and nitrite concentration of the stomach contents dropped linearly and the amount of nitrite dropped exponentially (with a half-life of 1.4 hr). Mean nitrite concentration in G was less than half that in NG. From similar experiments with phenol red, emptying accounted for 60% of nitrite loss from T. In G, nitrite concentration was reduced about 3 times due to dilution and 3 times due to other causes. Conditions in G, e.g., nitrite concentration, pH, and empyting time, were discussed in relation to carcinogenesis experiments with nitrite plus amines and amides.

Albumins↗

Spectrophotometric and electron spin resonance studies on the substrate interactions of ferredoxin-linked nitrite reductase from spinach.

Interactions of ferredoxin-linked nitrite reductase (NiR) from spinach with its substrate were studied by spectrophotometry and electron spin resonance (ESR) spectroscopy. Siroheme was extractable from NiR with 2.5% (W/V) trichloroacetic acid (TCA) and with acetone containing 0.01 N HCl. The addition of nitrite or sulfite to these extracts resulted in shifts of the absorption spectra of siroheme. The HCl-acetone extract showed ESR signals of symmetrical high spin heme, which disappeared on addition of nitrite. Spectral titration indicated a high affinity of extracted siroheme to nitrite and sulfite. The addition of nitrite or sulfite to protoheme dissolved in 0.01 N HCl-acetone did not cause a shift of the absorption spectrum. The extractability of siroheme with 0.01 N HCl-acetone was suppressed by the addition of nitrite to the NiR preparation. Moreover, a substrate-induced difference spectrum with peaks at about 295 and 287 nm was observed on addition of nitrite to NiR. These observations indicated an intrinsic strong affinity of siroheme to nitrite and sulfite, formation of rhombicity of siroheme by binding to the protein moiety, and also a probable conformational change of NiR on binding to the substrate. In agreement with previous reports, ESR signals of the heme-NO complex were observed with NiR in the presence of nitrite, methyl viologen (MV), and dithionite. In the present study, the same signals of similar intensity were also observed on omission of MV, under which conditions no catalytic reduction of nitrite occurred. Furthermore, the signal of the heme-NO complex was not observed when MV was replaced by spinach ferredoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Electron Spin Resonance Spectroscopy↗

Nitrosyl-heme complexes are formed in the ischemic heart: evidence of nitrite-derived nitric oxide formation, storage, and signaling in post-ischemic tissues.

In addition to the generation from specific nitric-oxide (NO) synthases, NO formation from nitrite occurs in ischemic tissues, such as the heart. Although NO binding to heme-centers is the basis for NO-mediated signaling as occurs through guanylate cyclase, it is not known if this process is triggered with physiologically relevant periods of sublethal ischemia and if nitrite serves as a critical substrate. Therefore electron paramagnetic resonance studies were performed to measure nitrosylheme formation during the time course of myocardial ischemia and reperfusion and the role of nitrite in this process. Rat hearts were either partially nitrite-depleted by nitrite-free buffer perfusion or nitrite-enriched by preinfusion with 50 microm nitrite. Ischemic hearts loaded with nitrite showed prominent spectra of six-coordinate nitrosyl-heme complexes, primarily NO-myoglobin, that increased as a function of ischemic duration, whereas in nonischemic-controls these signals were not seen. Total nitrosyl-heme concentrations within the heart were 6.6 +/- 0.7 microm after 30 min of ischemia. Nitrite-depleted hearts also gave rise to NO-heme signals during ischemia, but levels were 8-fold lower. Nitrite-mediated NO-heme complex formation during ischemia was associated with activation of guanylate cyclase. Upon reperfusion, the levels of NO-heme complexes decreased 3-fold by the first 15 min but remained elevated for over 45 min. The decrease in NO-heme complex levels was paralleled by the formation of nitrate, suggesting the oxidation of heme-bound NO upon reperfusion. Thus, nitrite-mediated NO-heme formation occurs progressively during ischemia, with these complexes serving as a store of NO with concordant activation of NO signaling pathways.

Animals↗

The anaerobic treatment of nitrite containing wastewater using an expanded granular sludge bed (EGSB) reactor.

The integration of denitrification from nitrite with methanogenesis was studied in this work. Experimental results from the continuous treatment of wastewater containing nitrite, which lasted for 144 days, demonstrated that wastewater containing nitrite could be anaerobically treated in an expanded granular sludge bed (EGSB) reactor. From 92% to 97% of COD was removed at organic COD volumetric loading rates up to 6.5 g COD l(-1) d(-1). Nitrite was denitrified for 97% to 100% at nitrite volumetric loading rates up to 0.9 g NO2-N l(-1) d(-1). Batch tests of 15 days with sludge from the reactor showed that 100% of nitrite and 93 to 95% of COD were removed. Nitrite was denitrified for 92 to 96% to N2. The remaining nitrite might be converted to NO and N2O. The ratio of COD to NO2--N for the denitrification was varied from 2.49 to 5.64. Denitrification from nitrite preceded methanogenesis. Methanogenesis recovered rapidly after the denitrification from nitrite was completed. No dissimilatory reduction of nitrite to ammonium occurred. Some small losses of ammonium could not be accounted for in the process.

Bacteria, Anaerobic↗

Regulation of Nitrite Reductase Activity under CO2 Limitation in the Cyanobacterium Synechococcus sp. PCC7942.

During photoautotrophic growth under CO2-limited conditions, cells of Synechococcus sp. PCC7942 excreted into the medium about 30% of the nitrite produced by reduction of nitrate. No nitrite was excreted under CO2-sufficient conditions. After transfer of high-CO2-grown cells to CO2-limited conditions, nitrite reductase activity started to decline within 0.5 h and decreased to 50% of the initial level in 3 h, whereas nitrate reductase activity was virtually unchanged. Nitrite started to accumulate in the medium about 3 h after the transfer of the cells to CO2-limited conditions and reached a concentration of >0.4 mM at 17 h. These findings suggested that the nitrite excretion was due to an imbalance of the activities of nitrite reductase and nitrate reductase. Since ammonium, the product of nitrite reduction, was not detected in the medium, it was concluded that the step of nitrite reduction limits the rate of nitrate assimilation under CO2-limited conditions. The extent of decrease in nitrite reductase activity under CO2-limited conditions was much larger than that caused by rifampicin (an inhibitor of RNA synthesis) treatment under high-CO2 conditions. Addition of CO2, in the form of sodium bicarbonate, to the CO2-limited culture increased the nitrite reductase activity, but rifampicin inhibited this increase. These findings suggested the presence of a mechanism that irreversibly inactivates nitrite reductase under CO2-limited conditions.

Journal Article↗

Steady-state Growth of the Marine Diatom Thalassiosira pseudonana: UNCOUPLED KINETICS OF NITRATE UPTAKE AND NITRITE PRODUCTION.

Seasonal studies of the vertical distribution of nitrate, nitrite, and phytoplankton in the oceans and studies using (15)N as a tracer of nitrate metabolism indicate that the reduction of nitrate by phytoplankton is a source of nitrite in the upper waters of the ocean. To better understand this process, the relationship between nitrate uptake and nitrite production has been examined with continuous cultures of the small marine diatom Thalassiosira pseudonana. In a turbidostat culture, the rates of nitrite production by T. pseudonana increase with light intensity. This process is only loosely coupled to rates of nitrate assimilation since the ratio of net nitrite production to total nitrate assimilation increases with increased rates of growth. In continuous cultures where steady-state concentrations of nitrate and nitrite were varied, T. pseudonana produced nitrite at rates which increased with increasing concentrations of nitrate. Again, the rates of nitrite production were uncoupled from rates of nitrate assimilation. The study was used to derive a mathematical description of nitrate and nitrite metabolism by T. pseudonana.The validity of this model was supported by the results of a study in which (15)N-labeled nitrite was introduced into the continuous culture, and the model was used to examine patterns in distribution of nitrite in the Antarctic Ocean and the Sargasso Sea.

Journal Article↗