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PubMed2000

Anion uptake and acid-base and ionic effects during isolated and combined exposure to hypercapnia and nitrite in the freshwater crayfish, Astacus astacus.

Nitrite influx into crayfish showed saturation kinetics, supporting a carrier-mediated uptake. Addition of 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS: at 10(-5), 10(-4) and 10(-3) M) and bumetanide (at 10(-5) M and 10(-4) M) to the ambient water did not significantly affect nitrite influx. Rather than suggesting that neither Cl-/HCO3- exchange nor K+/Na+/2Cl- cotransport were involved in the transport, this may reflect that the gill cuticle has a low permeability to the pharmacological agents, or that the sensitivity of the transport mechanism to the inhibitors is low. Nitrite accumulation in the haemolymph was significantly decreased during hypercapnic conditions compared to normocapnic conditions. This supports the idea that an acid-base regulatory decrease in Cl-(influx)/HCO3- (efflux) induced by hypercapnia should decrease NO2- uptake if NO2- and Cl- share this uptake route. The respiratory acidosis caused by exposure to hypercapnia alone was partially compensated by HCO3- accumulation in the haemolymph. Combined exposure to hypercapnia and nitrite improved pH recovery, mainly by augmenting the [HCO3-] increase, but also by decreasing haemolymph PCO2. Exposure to nitrite in normocapnic water induced an initial increase in haemolymph [HCO3-] and later also a decrease in PCO2. Thus, the improved acid-base compensation during combined hypercapnia and nitrite exposure was an amplification of this nitrite-induced response. Haemolymph base excess rose much more than haemolymph [Ca], suggesting that transfer of acid-base equivalents between animal and water was more important than H+ buffering by exoskeletal CaCO3 in mediating the increase in haemolymph [HCO3-].

Acid-Base Equilibrium↗

PubMed1975

Studies on the in vitro inactivation of the Neurospora crassa assimilatory nitrite reductase in the presence of reduced pyridine nucleotides plus flavin.

In vitro inactivation of Neurospora crassa nitrite reductase (NAD(P)H: nitrite oxidoreductase, EC 1.6.6.4) can be obtained by preincubation of the enzyme with reduced pyridine nucleotide plus FAD. The presence of nitrite or hydroxylamine, electron acceptors for the N. crassa nitrite reductase, or cyanide, sulfite or arsenite, competitive inhibitors with respect to nitrite of this enzyme, protects the enzyme against this inactivation. Anaerobic experiments reveal that oxygen is required in order to obtain complete inactivation of nitrite reductase by preincubation with reduced pyridine nucleotide plus FAD. Also, inactivation is prevented if catalase is included in the preincubation mixture. The presence of hydrogen peroxide in the preincubation mixture increases the sensitivity of nitrite reductase to the in vitro FAD-dependent NAD(P)H inactivation. Neither electron acceptors, competitive inhibitors nor catalase, agents which protect the enzyme against the FAD-dependent NAD(P)H inactivation, can reverse this process once it has occurred.

Anaerobiosis↗

PubMed1984

Differences in the nitrite ion formation and the toxicological findings between isosorbide dinitrate and isosorbide-5-mononitrate.

In the metabolism of isosorbide dinitrate (ISDN), fast denitration with the formation of nitrite ions and a mononitrate plays an important role. In contrast, the denitration of isosorbide-5-mononitrate (IS-5-MN) to isosorbide is very slow. Accordingly po administration of high doses of ISDN (92.5 and 236 mg/kg) in conscious dogs led to maximum nitrite concentrations in the blood of 0.9 and 3.3 mg/liter, respectively. In contrast, with equimolar doses of IS-5-MN (75 and 191 mg/kg) we were able to detect nitrite ions reliably only at the higher dose and this gave a maximum blood concentration of 0.4 mg/liter. The rise in nitrite ion concentration is followed by the formation of methemoglobin. As is known from the literature, there is a rise in the activity of alkaline phosphatase in the serum of rabbits in addition to methemoglobin formation following repeated administration of sodium nitrite. So we have specifically investigated whether this is also the case following ISDN and IS-5-MN administration. On po administration of 236 mg/kg ISDN/day to dogs, there was a continuous rise in alkaline phosphatase from about the 20th day onward which we did not observe after the equimolar dose of IS-5-MN (191 mg/kg). NaNO2, 35 mg/kg po, led to a comparable maximal rise in methemoglobin to that obtained with 236 mg/kg ISDN. Repeated po administration of 35 mg/kg NaNO2/day also caused a rise in alkaline phosphatase. It is concluded that the formation of nitrite ions from ISDN is the reason for the rise in methemoglobin and alkaline phosphatase. The lower formation of nitrite ions from IS-5-MN can also be of clinical importance, at least in certain cases.

Alkaline Phosphatase↗

PubMed1986

Relation of nitrite concentration to mutagen formation in soy sauce.

When soy sauce was mixed with nitrite solutions at pH 1.0 and 3.0, only mixtures containing nitrite concentrations above 250 ppm were mutagenic in the Salmonella/mammalian microsome test. In buffered aqueous solution (pH 3) the mutagen precursor, (-)-(1S,3S)-1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid [(1S,3S)-MTCA] and its stereoisomer ( - )-(1R,3S)-MTCA reacted with 10 ppm or more of sodium nitrite; but at least 250 ppm nitrite was required for them to react in soy sauce (pH 3). Similarly, another mutagen precursor, tyramine, did not react even with 2300 ppm nitrite in soy sauce (pH 1), although pure tyramine in aqueous solution (pH 1) reacted with as little as 50 ppm nitrite. Nitrite concentration in human saliva and gastric juice does not generally exceed 50 ppm. Therefore, the most probable source of mutagens--nitrosation of MTCAs and tyramine--is likely to be very restricted in vivo and soy sauce is unlikely to be significantly mutagenic.

Animals↗

PubMedDate not supplied

Formation of mutagenic N-nitroso compounds in vegetable extracts upon nitrite treatment: a comparison with the glucosinolate content.

More than 30 vegetables were screened for their potential to form biologically active N-nitroso compounds upon treatment with nitrite under acidic conditions. The total N-nitroso content was determined in the nitrite-treated and untreated extracts of the vegetables according to a modified method of Walters et al. (Analyst, Lond. 1978, 103, 1127). All treated extracts contained N-nitroso compounds at levels ranging from 23 to 789 nmol/25 mg dry matter. In the same samples the mutagenic activity was determined using the Salmonella typhimurium assay. About half of the vegetables were found to be mutagenic upon nitrite treatment. (Nitrite-treated extracts were considered to be mutagenic if the number of induced revertants was at least twice as high as that induced by the corresponding untreated extract). The content of different glucosinolates in the dry matter of the vegetables was also determined. Glucosinolates could be detected only in cruciferous vegetables, at levels ranging from 1.8 to 26.0 mumol/g dry matter. Although the nitrite-treated extracts of brassica species contained more N-nitroso compounds and induced more revertants than did other vegetables, there was no significant correlation between these parameters. However, the amounts of N-nitroso compounds formed upon nitrite treatment (expressed per fresh weight) did correlate significantly (P less than 0.01) with the amounts of glucosinolates (r = 0.95). When the glucosinolates were divided into aryl/alkyl- and indolyl-glucosinolates, the significant correlation was maintained for both subgroups (r = 0.93 and 0.95, respectively). From this it can be concluded that glucosinolates are probably involved in the formation of N-nitroso compounds in certain nitrite-treated vegetables.

Glucosinolates↗

PubMed1995

Effect of ethanol on nitrite oxidation in the perfused rat liver.

The effect of ethanol on nitrite oxidation was investigated in the perfused rat liver. Real-time spectral changes in catalase were obtained using a reflectance scanning spectrophotometer in rat liver perfused with Krebs-Henseleit bicarbonate buffer in a non-recirculating system. The nitrite oxidation rate and nitrate production rate were calculated from the differences in concentrations between the influx and efflux perfusates and from the flow rate/g liver weight. Nitrite infusion caused an increase in absorbance difference delta A (640-660 nm), indicating decomposition of catalase compound I to the free form. Administration of ethanol during the nitrite infusion caused a further increase in delta A (640-660 nm) and significant decreases in both the nitrite oxidation rate and the nitrate production rate. Both the nitrite oxidation rate and nitrate production rate decreased, depending on the concentration of ethanol administered. At 10 mM ethanol, they reached about half the rates before the ethanol infusion. In conclusion, ethanol inhibits nitrite oxidation by catalase in the perfused rat liver at relatively low concentrations that can be realized in blood by daily alcohol consumption.

Animals↗

PubMed2007

Is there a link between hyperbilirubinemia and elevated urine nitrite.

OBJECTIVE: The aim of this study was to determine whether hyperbilirubinemia affects the association between a positive urine nitrite test and a positive urine culture. METHODS: We conducted an institutional review board-approved, retrospective review of 12 months of patient data, compiling information for patients having urinalysis, urine culture, and total serum bilirubin. Patients were divided into 3 groups according to total serum bilirubin: less than 1.5 mg/dL, 1.5 to 3.0 mg/dL, and greater than 3.0 mg/dL. The point estimates and 95% confidence intervals of the sensitivity, specificity, false-positive proportion (proportion of false positive to all positive tests), and other test characteristics of urine nitrite as an indicator of urinary tract infection were calculated and tested for trend as a function of the 3 total serum bilirubin ranges. RESULTS: Three thousand one hundred seventy-four patients met our study criteria. Specificity of the nitrite test decreased as a function of increasing total serum bilirubin (0.974, 0.966, and 0.855 for the 3 total bilirubin levels, respectively) with a significant trend (P < .0001). There was no significant trend in comparable sensitivity values (0.380, 0.417, and 0.241, respectively) with P = .55. The false-positive proportion also increased as a function of total serum bilirubin (17.5%, 17.3%, and 72.0%) with P < .0001. Thus, if a patient's total serum bilirubin was elevated to the point of jaundice (>3.0 mg/dL), it was approximately 4 times more likely that a positive urine nitrite test would be a "false positive" (ie, nitrite-positive/culture-negative) compared with those with normal serum bilirubin levels. CONCLUSIONS: Specificity of the urine nitrite test for urinary tract infection decreases as a function of increasing serum bilirubin. Most patients with hyperbilirubinemia and a positive nitrite test in our sample did not have an associated urinary tract infection.

Humans↗

PubMedDate not supplied

Emerging role of nitrite in human biology.

Nitric oxide (NO) plays a fundamental role in maintaining normal vascular function. NO is produced by endothelial cells and diffuses both into smooth muscle causing vasodilation and into the vessel lumen where the majority of this highly potent gas is rapidly inactivated by dioxygenation reaction with oxyhemoglobin to form nitrate. Diffusional barriers for NO around the erythrocyte and along the endothelium in laminar flowing blood reduce the inactivation reaction of NO by hemoglobin, allowing sufficient NO to escape for vasodilation and also to react in plasma and tissues to form nitrite anions (NO(2)(-)) and NO-modified peptides and proteins (RX-NO). Several recent studies have highlighted the importance of the nitrite anion in human biology. These studies have shown that measurement of plasma nitrite is a sensitive index of constitutive NO synthesis, suggesting that it may be useful as a marker of endothelial function. Additionally, recent evidence suggests that nitrite represents a circulating storage pool of NO and may selectively donate NO to hypoxic vascular beds. The conversion of nitrite to NO requires a reaction with a deoxygenated heme protein, suggesting a novel function of hemoglobin as a deoxygenation-dependent nitrite reductase. This review focuses on the role of nitrite as a circulating NO donor, its potential as an index of NO synthase (NOS) activity and endothelial function, and discusses potential diagnostic and therapeutic applications.

Cardiovascular System↗

PubMed2005

Nitrification-denitrification via nitrite accumulation for nitrogen removal from wastewaters.

The biological nitrification-denitrification process is used extensively for removal of ammonia nitrogen from wastewaters. Saves in aeration, organic matter (for denitrification) and surplus sludge are achievable if nitrite accumulation is possible in the nitrification step. In this paper, operational parameters were studied for each process for maximum nitrite accumulation in the nitrification step and nitrite adaptation in the denitrification step. Nitrite accumulation during nitrification can be controlled by the dissolved oxygen (DO) concentration, presenting a maximum of 65% at around 0.7 mg DO/L. Denitrification can be adapted to nitrite and the process is stable if nitrite in the reactor is keep low. The performance of a continuous stirred tank reactor (CSTR) and an up flow sludge blanket reactor (USB) were compared. Once the operational parameters were established, a CSTR for nitrification and an USB reactor for denitrification were operated in series for 25 days. The process was stable and a steady state was maintained for 20 days, and 93.5% of overall nitrogen removal was achieved in the nitrification-denitrification via the nitrite process.

Ammonia↗

PubMed2006

Effects of flavonoids extracted from Scutellaria baicalensis Georgi on hemin-nitrite-H2O2 induced liver injury.

Hemin-nitrite-H2O2 system may play a role in liver oxidative injury in some pathological events. In this paper, the effects of the three active components of the root of Scutellaria baicalensis Georgi, i.e. baicalin, baicalein and wogonin, on hemin-nitrite-H2O2 induced liver injury were studied in liver homogenate, liver microsome and human hepatoblastoma cell line HepG2 cells. It was found that hemin-nitrite-H2O2 could induce liver homogenate protein nitration, lipid peroxidation and liver microsome protein oxidation; it also caused a decrease of HepG2 cells viability. Baicalein, baicalin and wogonin could inhibit protein nitration and lipid peroxidation in liver homogenate as well as in HepG2 cells in a dose-dependent manner, the inhibition order was baicalein>baicalin>>wogonin. These three flavonoids also inhibited the oxidation of protein in liver microsome, the decrease of cell viability and the content of GSH in HepG2 cells, among which baicalin represented the most inhibitory effect. Besides, hemin-H2O2 induced cell injury could be augmented with the existence of nitrite, indicating protein nitration involved in hemin-nitrite-H2O2 induced liver injury. These results demonstrated hemin-nitrite-H2O2 could induce liver injury through oxidizing or nitrating different biomolecules. Baicalein, baicalin and wogonin could inhibit hemin-nitrite-H2O2 induced liver injury in dose-dependent manners by inhibiting oxidation and nitration.

Animals↗

PubMed2005

Use of nitrite inhalants ("poppers") among American youth.

PURPOSE: We examined the patterns and correlates of nitrite inhalant use among adolescents aged 12 to 17 years. METHODS: Study data were drawn from the 2000 and 2001 National Household Surveys on Drug Abuse. Logistic regression was used to identify the characteristics associated with nitrite inhalant use. RESULTS: Among adolescents aged 12 to 17 years, 1.5% reported any lifetime use of nitrite inhalants. The prevalence of lifetime nitrite inhalant use increased to 12% and 14% among adolescents who were dependent on alcohol and any drug in the past year, respectively. Many nitrite inhalant users used at least three other types of inhalants (68%) and also met the criteria for alcohol (33%) and drug (35%) abuse or dependence. Increased odds of nitrite inhalant use were associated with residing in nonmetropolitan areas, recent utilization of mental health services, delinquent behaviors, past year alcohol and drug abuse and dependence, and multi-drug use. CONCLUSIONS: Adolescents who had used nitrite inhalants at least once in their lifetime tend to engage in delinquent activities and report co-occurring multiple drug abuse and mental health problems in the past year.

Administration, Inhalation↗

PubMed2005

Effects of repeated in vivo inhalant nitrite exposure on gene expression in mouse liver and lungs.

Exposure to inhalant organic nitrites (drugs of abuse commonly known as "poppers") has been reported to enhance tumor growth in mice, but the mechanism is not fully defined. This study examined the effect of repeated in vivo nitrite exposures on gene expression in the mouse liver and lungs using a gene array panel of 94 cancer- and angiogenesis-related genes. Using 2-fold change as a threshold criterion, repeated nitrite exposure was found to alter the expression of 65 and 23 genes in the liver and lungs, respectively. Six genes were significantly upregulated (p<or=0.05), viz., those encoding VEGF, VEGFD (vascular endothelial growth factor A and D, respectively) in the lungs and FGF1, FGF4 (fibroblast growth factor 1 and 4, respectively), Hsp70 (heat shock 70kDa protein 4), and PF4 (platelet factor 4) in the liver. mRNA encoding HO-1 (heme oxygenase-1) and Smad7 were marginally (p=0.057) stimulated in the liver. Follow-up studies in the liver revealed significant nitrite-induced expression of VEGF protein and mRNA. Immuno-staining of liver slices revealed that the increased hepatic VEGF expression resided mainly in hepatocytes. Stimulation of hepatic VEGF expression by ISBN was not different in endothelial nitric oxide synthase (eNOS) knockout vs. wild-type mice. In conclusion, multiple exposures to inhalant nitrite appeared to cause alteration in the expression of a number of genes relating to cancer and angiogenesis, including VEGF. eNOS presence did not appear to be essential for nitrite-induced VEGF expression. These studies demonstrate that in vivo exposure to inhalant nitrites results in changes in the angiogenesis cascade.

Administration, Inhalation↗

PubMed1999

Serum nitrite sensitively reflects endothelial NO formation in human forearm vasculature: evidence for biochemical assessment of the endothelial L-arginine-NO pathway.

OBJECTIVE: A reduced bioactivity of endothelial nitric oxide (NO) has been implicated in the pathogenesis of atherosclerosis. In humans, the endothelial L-arginine-NO pathway has been indirectly assessed via the flow response to endothelium-dependent vasodilators locally administered into the coronary, pulmonary or forearm circulation. However, biochemical quantification of endothelial NO formation in these organ circulations has been hampered so far because of the rapid metabolism of NO. Therefore, we aimed to work out a reliable biochemical index to assess endothelial NO formation in human circulation. METHODS: In 33 healthy volunteers, forearm blood flow (FBF) was measured by standard techniques of venous occlusion plethysmography at rest, after local application of the endothelium-dependent vasodilator acetylcholine (ACH), the endothelium-independent vasodilator papaverine (PAP), the stereospecific inhibitor of endothelial NO synthase (eNOS) L-NMMA, and L-arginine (ARG), the natural substrate of eNOS. In parallel, nitrite and nitrate concentrations in blood samples taken from the antecubital vein were measured by HPLC using anion-exchange chromatography in combination with electrochemical and ultraviolet detection following a specific sample preparation method. RESULTS: ACH dose-dependently increased resting FBF (from 3.0 +/- 0.3 to 10.4 +/- 0.9 ml/min per 100 ml tissue) and serum nitrite concentration (from 402 +/- 59 to 977 +/- 82 nmol/l, both p < 0.05, n = 12). A significant correlation was observed between the changes in FBF and the serum nitrite concentration (r = 0.61, p < 0.0001). L-NMMA reduced resting FBF and endothelium-dependent vasodilation by 30% and this was paralleled by a significant reduction in serum nitrite concentration at the highest dose of ACH (n = 9, p < 0.001). PAP increased FBF more than fourfold, but did not affect serum nitrite concentration (n = 11), whereas ARG significantly increased both FBF and nitrite. Basal serum nitrate amounted to 25 +/- 4 mumol/l and remained constant during the application of ACH, PAP and L-NMMA. CONCLUSIONS: The concentration of serum nitrite sensitively reflects changes in endothelial NO formation in human forearm circulation. This biochemical measure may help to characterize the L-arginine-NO pathway in disease states associated with endothelial dysfunction and to further elucidate its pathophysiological significance for the development of atherosclerosis in humans.

Acetylcholine↗

PubMed2003

Reduction of nitrite production by endothelin-1 in isolated porcine ciliary processes.

It has been postulated that endothelin-1 and nitric oxide (NO) could participate in the modulation of aqueous humor dynamic in the eye. This study investigates whether endothelin-1 can reduce the production of nitrite (a stable metabolite of NO) in isolated porcine ciliary processes. Nitrite production was measured (Griess reaction) in the medium surrounding isolated ciliary processes before and after exposure to different drugs. Results are expressed in percent of basal nitrite production. In a concentration-dependent manner (0.1 nM to 1 microM), endothelin-1 significantly decreased basal nitrite production (1 microM: 81.7+/-3.5%; P<0.001). This effect was prevented by the endothelin type A (ETA)-receptor antagonist BQ123 (1 microM: 95.6+/-4.3%; P<0.05), but not by the endothelin type B (ETB)-receptor antagonist BQ788 (1 microM: 83.3+/-4.4%; P=0.86) or by the prostaglandin F2alpha analog unoprostone (30 microM: 86.7+/-3.7%; P=0.74). The adenylcyclase activator forskolin significantly increased basal nitrite production (1 microM: 143.4+/-3.9%, P<0.001). This effect was prevented both by endothelin-1 (0.1 microM; 113.9+/-6.7%: P<0.01) or the nitric oxide synthase inhibitor L-NAME (0.5 mM: 103.3+/-8.4%: P<0.001). The inhibitory effect of endothelin-1 on forskolin-induced nitrite production was significantly reversed by BQ123 (1 microM: 132.4+/-5.1%; P<0.01), but not by BQ788 (1 microM: 112.7+/-4.1%; P=0.64) or unoprostone (30 microM: 109.3+/-4.8%; P=0.98). These results suggest that endothelin-1, through an ETA receptor activation, can reduce both basal and forskolin-induced nitrite production in isolated porcine ciliary processes.

Animals↗

PubMed2001

Comparison of three post-column reaction methods for the analysis of bromate and nitrite in drinking water.

Three post-column ion chromatographic methods (i.e., a sodium bromide-sodium nitrite method, an o-dianisidine method, and a potassium iodide-ammonium heptamolybdate method) were compared for bromate and nitrite analysis. Also, the effect of direct mixing of the reagents without ion suppressors for the sodium bromide-sodium nitrite method and the potassium iodide-ammonium heptamolybdate method was investigated. For the analysis of bromate, the three methods showed similar method detection limits (0.17-0.24 microg/l) with pneumatic reagent delivery systems. Direct reagent mixing achieved comparable detection limits to the suppressor configuration. The three methods are also compatible with conductivity detection. When used in combination with conductivity detection, this compatibility allows simultaneous analysis of bromate, nitrite, and other common ions in drinking water, such as bromide. It was found that the o-dianisidine method achieves microg/l-level detection of nitrite and bromate with a simpler configuration than the potassium iodide-ammonium heptamolybdate method, while the sodium bromide-sodium nitrite method was not sufficiently sensitive for nitrite analysis at the microg/l level.

Bromates↗

PubMed2001

Effect of pH on the reduction of nitrite in water by metallic iron.

Chemical reduction is an alternative technique to remove nitrogen oxides from contaminated groundwater and closed-surface water body. Metallic iron was employed as a reductant for the reduction of nitrite in water in this study. The effect of pH on the rate and products of nitrite reduction was investigated with a fixed dosage of metallic iron powder (12 mol-Fe/mol-N, size of the powder: 80 mesh). The reduction of nitrite by metallic iron was a pseudo-zero-order reaction under the experimental conditions. The reduction rate of nitrite was increased with decreasing the pH of reaction solution, and the pseudo-zero-order reaction rate constants were 180, 130, 60, 15, 10, and 1 mM/h at pH = 2, 3, 4, 5, 6, and 7, respectively. The reduction products of nitrite were nitrogen gas and ammonium. The yields of nitrogen gas from nitrite reduction were 0.63, 0.74, 0.81, 0.87, 0.92, and 0.98 as molar ratios of nitrogen atom at pH =2, 3, 4, 5, 6, and 7, respectively. Neutral condition enhanced the formation of nitrogen gas from nitrite reduction.

Aerobiosis↗

PubMed2000

Bacterial cytochrome c nitrite reductase: new structural and functional aspects.

Cytochrome c nitrite reductase catalyzes the six-electron reduction of nitrite to ammonia as a key step within the biological nitrogen cycle. Most recently, the crystal structure of the soluble enzyme from Sulfurospirillum deleyianum could be solved to 1.9 A resolution. This set the basis for new experiments on structural and functional aspects of the pentaheme protein which carries a Ca(2+) ion close to the active site heme. In the crystal, the protein was a homodimer with ten hemes in very close packing. The strong interaction between the nitrite reductase monomers also occurred in solution according to the dependence of the activity on the protein concentration. Addition of Ca(2+) to the enzyme as isolated had a stimulating effect on the activity. Ca(2+) could be removed from the enzyme by treatment with chelating agents such as EGTA or EDTA which led to a decrease in activity. In addition to nitrite, the enzyme converted NO, hydroxylamine and O-methyl hydroxylamine to ammonia at considerable rates. With N2O the activity was much lower; most likely dinitrogen was the product in this case. Cytochrome c nitrite reductase exhibited a remarkably high sulfite reductase activity, with hydrogen sulfide as the product. A paramagnetic Fe(II)-NO, S = 1/2 adduct was identified by rapid freeze EPR spectroscopy under turnover conditions with nitrite. This potential reaction intermediate of the reduction of nitrite to ammonia was also observed with PAPA NONOate and Spermine NONOate.

Binding Sites↗

PubMed2001

Effect of repeated addition of nitrite to semi-continuous activated sludge reactors.

To a semi-continuous lab-scale activated sludge system (SCAS), nitrite was dosed discontinuously, i.e. together with the feed. The nitrite was added at a concentration (50 mg N/l) which had been found earlier not to cause acute inhibition of the general running of the reactors. Repeated nitrite addition, however, exerted an inhibitory effect which was reflected in decreased removal efficiencies and was also expressed in decreases in total respiratory and nitrifying activity of 20% and 40%, respectively. The inhibition by nitrite was reversible as removal efficiencies improved after ceasing nitrite addition. The two consecutive test runs revealed that addition of nitrite gave rise to high amounts of dispersed cells and free-swimming protozoa. Moreover, DGGE patterns confirmed a shift in microbial community structure upon application of nitrite.

Bioreactors↗