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 325 records · Page 18Linked to original sources

Preparation and some properties of homogeneous Neurospora crassa assimilatory NADPH-nitrite reductase.

The Neurospora crassa assimilatory NADPH-nitrite reductase (NAD(P)H: nitrite oxidoreductase, EC 1.6.6.4), which catalyzes the NADPH-dependent formation of ammonia from nitrite, has been purified to homogeneity as judged by polyacrylamide gel electrophoresis. The specific activity of the purified enzyme is 26.9 mumol nitrite reduced/min per mg protein, which corresponds to a turnover number of 7800 min(-1). The enzyme also has associated NADH-nitrite reductase, NADPH-hydroxylamine reductase and NADH-hydroxylamine reductase activities. The stoichiometry of 3 mol NADPH oxidized per mol nitrite reduced and ammonia formed has been confirmed. The visible absorption spectrum of the nitrite reductase reveals maxima at 280,390 (Soret) and 580 (alpha) nm. The latter bands are indicative of the occurrence of siroheme as a prosthetic group. The A280nm/A390nm ratio of 7.0 and the Soret/alpha ratio of 3.8 are compatible with values reported for other purified siroheme-containing enzymes. These results are discussed in terms of the comparative biochemistry of various enzymes involved in nitrite, hydroxylamine and sulfite metabolism in Neurospora crassa and other organisms.

Hydroxylamines↗

Direct demonstration of NO formation in vivo from organic nitrites and nitrates, and correlation to effects on blood pressure and to in vitro effects.

Previous studies, utilizing nitric oxide synthase inhibitors and nitric oxide application, indicate that nitric oxide has the capacity to modulate contractile responses in pulmonary vessels. In the present study, in vitro effects of organic nitrates/nitrites were compared with their in vivo ability to generate nitric oxide and their effects on blood pressure. Glyceryl trinitrate, ethyl nitrite, isobutyl nitrate, isobutyl nitrite, isoamyl nitrite and butyl nitrite inhibited contractions in response to nerve stimulation in guinea pig pulmonary artery and vas deferens. Glyceryl trinitrate (also known as nitroglycerin) was the most potent and isobutyl nitrate the least potent substance with this action (IC50 4.5 +/- 0.2 x 10(-10) and 1.1 +/- 0.1 x 10(-5) M, respectively). Contractile responses to noradrenaline were inhibited, whereas noradrenaline release was unaffected by organonitrates/nitrites, indicating a post-junctional inhibitory effect. When infused intravenously to anaesthetized rabbits glyceryl trinitrate, ethyl nitrite and isobutyl nitrate generated dose-dependent increments of nitric oxide in exhaled air and dose-dependent decrements in systemic blood pressure. Significant correlations were obtained between in vivo NO generation and effects on blood pressure, as well as between NO generation in vivo and the in vitro activity of the organic nitrites and organic nitrates. In conclusion, organic nitrites and organic nitrates can modulate adrenergic neuroeffector transmission in guinea pig pulmonary artery and vas deferens, and produce detectable concentrations of nitric oxide in exhaled air in vivo, in the rabbit. The observations give direct in vivo evidence that organic nitrites and nitrates generate NO, and strongly support them exerting their action via NO formation.

Animals↗

Urinary nitrite in Japanese patients with urinary tract infections.

Urinary nitrite, a precursor of carcinogenic nitrosamines, and nitrate were measured in 73 Japanese patients with urinary tract infections (UTI) and in two control groups. Nitrite was detected in 12% of patients with uncomplicated UTI (226 +/- 161 mumol/l) and in 42% of those with complicated UTI (375 +/- 297 mumol/l). None of the subjects in the control groups excreted detectable amounts of nitrite. The excretion of nitrite in four out of five nitrite excretors continued for at least 14-55 days. The concentrations of urinary nitrite were significantly correlated with those of nitrate- plus nitrite-nitrogen, which reflect dietary nitrate ingestion. The results suggest the importance of close monitoring of nitrite excretor group in UTI patients, to clarify the mechanism of the association between UTI and bladder cancer.

Diet↗

Mutagenicity of soy sauce treated with nitrite in the presence of ethanol or alcoholic beverages.

The mutagenicity induced by soy sauce after reaction with 50 mM nitrite at pH 3, 37 degrees C, for 60 min in the presence of 1.25-10% ethanol was reduced in proportion to the ethanol concentration. The mutagenicity of soy sauce treated with nitrite was also reduced in the presence of commercial alcoholic beverages, Japanese sake, wine, 'shochu', whiskey and brandy, but not beer, in proportion to the concentration. The mutagenicity of nitrite-treated tyramine, which is a major precursor of a mutagen in soy sauce treated with nitrite, was strongly reduced in the presence of ethanol, n-propanol or isopropanol and more strongly reduced in the presence of methanol, but was increased twofold in the presence of the sugars glucose or sucrose. The reduction of the mutagenicity of nitrite-treated tyramine required simultaneous treatment of tyramine with ethanol and nitrite. The mutagenicity of tyramine treated with nitrite was clearly reduced in the presence of shochu and whiskey, similarly to ethanol. Analysis by high-performance liquid chromatography revealed that the reduction of the mutagenicity of nitrite-treated tyramine in the presence of ethanol resulted from the reduced production of mutagenic 3-diazotyramine from tyramine.

1-Propanol↗

Production of nitrite by primary rat astrocytes in response to pneumococci.

Recent studies using a rat model of pneumococcal meningitis have shown that nitric oxide synthase (NOS) inhibitors greatly attenuated microvascular changes and brain edema formation. The site of NO production during bacterial meningitis is unknown. In this study we tested whether primary astrocyte cultures from neonatal rat cortex can be induced to release NO upon stimulation with pneumococci. NO production was assessed by measuring nitrite in the cell culture supernatant using the Griess reaction. Stimulation with heat-killed unencapsulated pneumococci (HKP) increased nitrite concentrations in astrocyte culture supernatants in a dose-dependent fashion. Administration of N-nitro-L-arginine (L-NA), aminoguanidine, L-canavanine, cycloheximide, and dexamethasone prevented the increase in nitrite concentrations. Addition of L-arginine, but not of D-arginine, partially reversed the inhibitory effect of L-NA. Administration of SOD increased nitrite accumulation. Moreover, at 72 h after stimulation with heat-killed pneumococci (10(7) cfu/ml) astrocytes showed an inducible NOS-like immunoreactivity. Accumulation of nitrite was also observed when rat cerebellar neurons and microglia were stimulated with HKP, whereas there was only a slight increase of nitrite in media of rat C6 glioma cells, but no increase of nitrite when the human glioblastoma cell line LN-229 was stimulated with HKP. There was a stronger increase in nitrite levels when astrocytes from Lewis rats were used compared to that from Wistar rats. In conclusion, our study indicates that astrocytes, neurons and microglia are inducible for NO production upon stimulation with pneumococci.

Animals↗

Exposure to inhaled isobutyl nitrite reduces T cell blastogenesis and antibody responsiveness.

Isobutyl nitrite is a drug of abuse popular among male homosexuals and among adolescents. In order to approximate the nitrite exposures of inhalant abusers, mice were treated with 900 ppm isobutyl nitrite in an inhalation chamber for 45 min per day for 14 days. After 14 consecutive days of exposure to isobutyl nitrite, mice weighed an average of 4% less than mice exposed to air. The spleens of nitrite-exposed mice weighed 15% less and had 24% fewer cells per spleen than those of controls. Adjusted for equal cell numbers, T cell mitogenic and allogeneic proliferative responses were significantly reduced by 33 and 47%, respectively. The frequency of T-dependent plaque-forming cells (PFC) was inhibited by 63% and the total number of PFC per spleen was reduced by 72% in nitrite-exposed mice. In contrast, B cell proliferative responses to LPS were unaltered, suggesting that the toxicity of isobutyl nitrite did not affect all lymphoid cells equally. The data suggest that habitual inhalation of isobutyl nitrite could impair immune competence and that toxicity appeared to be directed toward T cell functions.

Administration, Inhalation↗

Proteins and amino acids as scavengers of nitrite: inhibitory effect on the formation of nitrosodimethylamine and diazoquinone.

Protein and its components in high concentrations similar to those found in the digestive tract effectively scavenged nitrite and thus inhibited the formation of mutagens from nitrite. Various amino acids at 100 mM, bovine serum albumin (BSA) and trypsinized casein at 100 mg/ml effectively decreased the nitrite level of 50 mM-nitrite solution at pH 3 and 37 degrees C. Most, but not all, amino acids can convert nitrite into nitrogen gas; Pro can be converted into non-mutagenic nitrosoproline, CySH to S-nitrosocysteine, Trp to weakly mutagenic nitrosotryptophan and Tyr to non-mutagenic diazotyrosine. BSA was cross-linked, probably owing to the reaction of Tyr and Lys residues. Most amino acids inhibited more than 50% of nitrosodimethylamine formation in the reaction between 200 mM-dimethylamine and 50 mM-nitrite at pH 3 and 37 degrees C; BSA inhibited 50% of nitrosodimethylamine formation, and trypsinized casein, 100%. Most amino acids inhibited more than 50% of p-diazoquinone formation in the reaction between 25 mM-phenol and 100 mM-nitrite at pH 3 and 37 degrees C; BSA inhibited 80%, and trypsinized casein, 95% of such formation. Trypsinized casein effectively inhibited the development of the mutagenic effects attributable to the formation of diazobamethan from bamethan and nitrite.

Amino Acids↗

Nitrite biotransformation by mitochondria from the earthworm Eisenia foetida (Savigny).

1. Nitrite oxidase and cytochrome-c oxidase activity catalysed by cytochrome-aa3 were assayed in earthworms and rats. 2. Cytochrome-aa3 and intact mitochondria from the two species were anaerobically incubated in the presence of nitrite; the occurrence of mitochondria-induced nitrite biotransformations was evaluated by monitoring nitrite recovery in incubation medium. Possible nitric oxide production was also tested. 3. The ratio nitrite oxidase/cytochrome-c oxidase activity was much higher in earthworms than in rats. 4. Under anaerobic conditions and in the presence of respiratory substrates, earthworm mitochondria produced a time-dependent loss of nitrite in the incubation medium. On the contrary, rat mitochondria are unable to decrease environmental nitrite concentration. 5. Results support the notion that metabolic properties of earthworm mitochondria can be considered as an adaptation to chronic nitrite exposure, this toxicant being typically present in natural habitats of these worms.

Adaptation, Physiological↗

Increased reproductive toxicity of landfill leachate after degradation was caused by nitrite.

Leachate from the landfill Lindbodarna was suspected to cause reproductive effects on fish in a Swedish lake, called Molnbyggen. The acute toxicity of this landfill leachate is caused by ammonia. In the present study the acute and chronic toxicity of the leachate from the landfill was tested with Ceriodaphnia dubia before and after treatment, either with (inoculated) or without addition of microorganisms from activated sludge, in both 2000 and 2001. On both occasions, the acute toxicity decreased after treatment, more rapidly with inoculum than without, and the cause of the decrease was mainly explained by decreasing concentrations of ammonia. However, the chronic toxicity decreased after treatment with inoculum but increased after treatment without inoculum. Therefore, we performed a series of acute and reproductive tests with ammonia, nitrite and nitrate on C. dubia, and the 24-h EC50s were 1.0, 2.7 and 59 mM, respectively, which are consistent with literature data. However, the chronic toxicity of these compounds gave quite a different picture with 8-day EC50s for reproduction of 3.0 mM for ammonia, 0.016 mM for nitrite and 1.5 mM for nitrate. Thus, the acute-chronic ratios for these compounds were 0.33 for ammonia, 170 for nitrite and 39 for nitrate. These findings show that reproduction is more sensitive than survival for both nitrite and nitrate, and that nitrite is the more hazardous of the two. This implies that the chronic and reproductive toxicity of nitrite and nitrate on zooplankton may in fact increase effects of eutrophication. In this study the toxicity of the fresh leachate was dominated by ammonia, but after treatment the contribution of nitrite increased, and especially the chronic toxicity of the treated landfill leachate was dominated by nitrite toxicity.

Ammonia↗

Haematological responses of acute nitrite exposure in walleye (Sander vitreus).

Nitrite (NO2-) is a toxic intermediary of the bacterial oxidation of nitrogenous wastes (e.g. ammonia) in an aquatic environment. It becomes most lethal when oxygen becomes limited due to high fish densities or in the presence of high bacterial activity due to waste build-up-both situations commonly found in intensive aquaculture. To date however, little is known about how this toxin affects the physiology of walleye, an intended culture species, particularly in intensive re-circulating systems. This study aims to define threshold concentrations of nitrite that affect haemoglobin-oxygen affinity and carrying capacity in walleye. During in vivo tests, fish (N=20) were subjected to a medium effective concentration (EC50) of nitrite (0.9 mmol L(-1)) for 48 h while the effects of nitrite accumulation on blood properties were measured. The effects of oxygenation state on red blood cell (RBC) nitrite uptake and metHb formation was further investigated by in vitro tonometry. In vitro nitrite exposure to 3 mmol L(-1) resulted in a significantly higher methaemoglobin formation in 50% air saturated than 100% air saturated RBCs. Both cell water content and haematocrit decreased with time in 50% air saturated treatments, whereas total Hb remained constant, suggesting a reduction in RBC volume. Similar effects were observed during 48 h in vivo and in vitro nitrite exposure tests, indicating the reduction in RBC volume likely was not the result of a catecholamine response. Walleye were found to be tolerant to an accumulation of blood-NO2- levels similar to common carp, a highly Mean Cellular Volume (MCV) tolerant species, before succumbing to methaemoglobinemia. The elevated tolerance to nitrite of walleye is a beneficial characteristic for successful rearing in a culture setting, where reduced oxygen and elevated MCV levels are prevalent. The findings from this study may be used in developing guidelines for species-specific management of nitrogenous wastes in aquaculture.

Animals↗

A novel microperoxidase activity: methyl viologen-linked nitrite reducing activity of microperoxidase.

To investigate the nitrite reducing activity of microperoxidases (mps) in the presence of methyl viologen and dithionite, the fragments C14-K22 (mp9), V11-L32 (mp22), and G1-M65 (mp65) containing heme were prepared by enzymatic hydrolysis of commercially equine heart cytochrome c (Cyt c), in which His is axially coordinated to heme iron, and acts as its fifth ligand. The nitrite reducing activity of mps was measured under anaerobic condition, and the nitrite reducing activity of mps increased with the cutting of the peptide chain. The activity of the shortest nonapeptide mp9 was approximately 120-fold that of Cyt c (104 amino acid residues) and 3.2-fold that of nitrite reductase (EC 1.7.7.1) from Escherichia coli. In the nitrite reduction by mp, nitrite was completely reduced to ammonia. We presumed that ferrous mps reduced NO2- to NO by donating one electron, the NO was completely reduced to NH4+ under anaerobic condition via ferrous-NO complexes as a reaction intermediate using visible spectra and ESR spectra, and this overall reaction was a 6-electron and 8-proton reduction. Sepharose-immobilized mp9 had a nitrite reducing activity similar to that of mp9 in solution, and the resin retained the activity after five uses and even 1-year storage. The mp will be able to use as a substitute for nitrite reductase.

Acrylamide↗

Plasma nitrite reserve and endothelial function in the human forearm circulation.

Attenuation of endothelium-derived nitric oxide (NO) synthesis is a hallmark of endothelial dysfunction. Early detection of this disorder may have therapeutic and prognostic implications. Plasma nitrite mirrors acute and chronic changes in endothelial NO-synthase activity. We hypothesized that local plasma nitrite concentration increases during reactive hyperemia of the forearm, reflecting endothelial function. In healthy subjects (n = 11) plasma nitrite and nitrate were determined at baseline and during reactive hyperemia of the forearm using reductive gas-phase chemiluminescence and flow-injection analysis, respectively. Endothelium-dependent dilation of the brachial artery was measured as flow-mediated dilation (FMD) using high-resolution ultrasound. Results were compared to patients with endothelial dysfunction as defined by reduced FMD (n = 11). Reactive hyperemia of the forearm increased local plasma nitrite concentration from 68 +/- 5 to 126 +/- 13 nmol/L (p < 0.01), whereas in endothelial dysfunction nitrite remained unaffected (116 +/- 12 to 104 +/- 10 nmol/L; n.s.), corresponding to nitrite reserves of 94 +/- 21 and -8 +/- 4%. This was accompanied by a significantly greater increase in brachial artery diameter (FMD: 8.5 +/- 0.4% vs 2.9 +/- 0.5%, for healthy subjects and endothelial dysfunction, respectively; p < 0.001). This observation suggests that nitrite changes reflect endothelial function. Assessment of local plasma nitrite during reactive hyperemia may open new avenues in the diagnosis of vascular function.

Adult↗

Changes in the mutagenic and estrogenic activities of bisphenol A upon treatment with nitrite.

Bisphenol A (4,4'isopropylidenediphenol: BPA), an endocrine-disrupting chemical, is contained in food-packaging and can-coating agents as well as in dental sealants. Nitrite is present in vegetables, fish and tap water as an ingredient or contaminant, and also in human saliva. Here, we explored the possible generation of genotoxicity from the reactions of BPA and nitrite under acidic conditions, a situation simulating the stomach. We determined the changes in the mutagenic and estrogenic activities of BPA before and after nitrite treatment. Untreated BPA did not exhibit any mutagenicity. However, the mixture of BPA and sodium nitrite after incubation at pH 3.0 showed strong mutagenic activity toward Salmonella typhimurium strains TA 100 and TA 98 either with or without a metabolic activation system (S9 mix). The clastogenic properties of nitrite-treated and untreated BPA were analyzed by a micronucleus test with male ICR mice. A single gastric intubation of nitrite-treated BPA induced a significantly higher frequency of micronucleated reticulocytes (MNRETs) in mice. The results of analysis of electron spin resonance (ESR) suggest that the expression of the mutagenic activity of nitrite-treated BPA is related to the generation of radicals in the reaction mixture. By applying 1H and 13C NMR, AB-MS and APCI/LC/MS, we identified two compounds 3-nitrobisphenol A and 3,3'-dinitro-bisphenol A. These compounds were synthesized by the reaction of BPA with nitric acid. 3,3'-Dinitro-bisphenol induced a significantly greater frequency of MNRETs in male ICR mice. By applying a green fluorescent protein (GFP)-reporter expression system and an estrogen R(alpha) competitor screening kit, we found that nitrite-treated BPA and 3,3'-dinitro-bisphenol A showed weak estrogenic activity compared to that of untreated BPA.

Animals↗

Vibrational analysis of n-butyl, isobutyl, sec-butyl and tert-butyl nitrite.

Raman and infrared spectra of n-butyl, isobutyl, sec-butyl and tert-butyl nitrite are reported. Density functional theory and Møeller-Plesset calculations with 6-31G* and 6-311G* basis sets were used to determine ground state molecular geometries and vibrational frequencies of these compounds. Calculations and spectral data of these molecules were used to perform partial vibrational mode assignments for the observed transitions. In agreement with previous investigations of alkyl nitrites, cis and trans rotational conformers of n-butyl, isobutyl and sec-butyl nitrite were observed in the gas phase infrared spectra and the condensed phase Raman and infrared spectra. Among the several predicted geometries of these compounds, the cis-trans geometry (cis with respect to the C-O-N=O dihedral angle and trans with respect to the C-C-O-N dihedral) was calculated to be the most stable conformer of n-butyl and isobutyl nitrite, while the cis-gauche conformer was found to be the most stable geometry of sec-butyl nitrite. The cis-type structures of these three molecules are favored due to formation of a pseudo hydrogen bond between the nitrite group and the alpha-carbon hydrogen atoms. Hindrance with the alkyl moiety, however, causes the trans conformer (trans with respect to the C-O-N=O dihedral) of tert-butyl nitrite to lie lower than its cis conformer, a result that was supported by our spectroscopic measurements. The characteristic N=O stretch frequency for the trans conformers of all the compounds examined was observed to decrease with increasing branching at the alpha-carbon, while the same mode for the cis conformers shows no change among the primary and secondary nitrites. Evidence is also provided that suggests that the relative number of cis conformers to trans conformers decreases as the alpha-carbon branching increases.

Models, Molecular↗

Sodium nitrite-induced cytotoxicity in cultured human gastric epithelial cells.

To investigate the effect of sodium nitrite on the viability of the human gastric adenocarcinoma epithelial cell line, AGS, cultured AGS cells were exposed to various concentrations of sodium nitrite for 24, 48 or 72 h. The cytotoxic response was assessed using a cell proliferation assay, and the extent of the response was evaluated on the basis of intracellular and extracellular levels of interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), interleukin 8 (IL-8) and tumor necrosis factor (TNF-alpha). Both mRNA and protein levels were measured for each cytokine. Sodium nitrite had a significant effect on AGS cell proliferation after a 72-h exposure. At low sodium nitrite concentrations (up to 6.25 mM), cell proliferation increased in a dose-dependent manner; however, exposure to higher concentrations resulted in a dose-dependent decrease in cell proliferation. Sodium nitrite at a low concentration (6.25 mM) increased IL-8 release, whereas IL-1 beta, IL-6, and TNF-alpha release increased only after exposure to high sodium nitrite concentration (25 mM). Our data demonstrate that sodium nitrite can induce the release of these inflammatory cytokines and that high concentrations of sodium nitrite decrease AGS cell proliferation.

Cell Line, Tumor↗

Influence of oxygen, temperature and carbon dioxide on nitric oxide formation from nitrite as measured in expired gas from in situ perfused rabbit lungs.

In biological systems, nitric oxide (NO) may be generated non-enzymatically from nitrite (nitrite-derived NO), in addition to nitric oxide synthase-catalyzed (NOS-derived) L-arginine-dependent formation. Through recordings of expired NO, we studied the influence of temperature on NOS- and nitrite-derived NO in the perfused lung. We also studied the impact of other influencing factors (O(2), CO(2), and pH) on nitrite-derived NO in the same system. Both NO-generating systems exhibited biphasic temperature dependence with a positive correlation between temperature and NO generation that peaked between 42 and 44 degrees C. The nitrite-derived NO generation was enhanced by hypoxia alone (>20 x after 5 min) and further by concomitant increase in CO(2). The CO(2) effect could not be explained by changes in extracellular pH and was unaltered by acetazolamide. We conclude that the temperature dependence in the known enzyme-catalyzed NOS-derived NO and especially in the nitrite-derived NO strengthens the hypothesis that an enzyme could be involved in nitrite-derived NO formation. The enhancement of nitrite-derived NO by increases in CO(2) suggests that this system could be of importance to improve perfusion in ischemic tissues.

Animals↗

Volatile fatty acid impacts on nitrite oxidation and carbon dioxide fixation in activated sludge.

Batch test were performed to assess nitrite removal, nitrate formation, CO2 fixation, gaseous nitrogen production and microbial density in activated sludge exposed to volatile fatty acid (VFA) mixtures. Nitrite removal and nitrate formation were both affected by the presence of VFAs, but to different degrees. Nitrate formation rates were reduced to a greater extent (79%) than nitrite removal rates (36%) resulting in an apparent unbalanced nitrite oxidation reaction. Since the total bacterial density and the nitrite oxidizing bacteria (NOB, Nitrospira) concentration remained essentially constant under all test conditions, the reduction in rates was not due to heterotrophic uptake of nitrogen or to a decrease in the NOB population. In contrast to the nitrogen results, VFAs were not found to impact CO2 fixation efficiency. It appeared that nitrite oxidation occurred when VFAs were present since the oxidation of nitrite provides energy for CO2 fixation. However, nitrate produced from the oxidation of nitrite was reduced to gaseous nitrogen products. N2O gas was detected in the presence of VFAs which was a clear indication that VFAs stimulated an alternative pathway, such as aerobic denitrification, during biotransformation of nitrogen in activated sludge.

Bacteria↗

Automated simultaneous monitoring of nitrate and nitrite in surface water by sequential injection analysis.

A fully automated procedure based on Sequential Injection Analysis (SIA) methodology for simultaneous monitoring of nitrate and nitrite in surface water samples is described. Nitrite was determined directly using the Griess diazo-coupling reaction and the formed azo dye was measured at 540 nm in the flow cell of the fibre-optic spectrophotometer. Nitrate zone was passed through a reducing mini-column containing copperised-cadmium. After the reduction of nitrate into nitrite the sample was aspirated by flow reversal to the holding coil, treated with the reagent and finally passed through the flow cell. The calibration curve was linear over the range 0.05-1.00 mg N l(-1) of nitrite and 0.50-50.00 mg N l(-1) of nitrate; correlation coefficients were 0.9993 and 0.9988 for nitrite and nitrate, respectively. Detection limits were 0.015 and 0.10 mg N l(-1) for nitrite and nitrate, respectively. The relative standard deviation (RSD) values (n = 3) were 1.10% and 1.32% for nitrite and nitrate, respectively. The total time of one measuring cycle was 250 s, thus the sample throughput was about 14 h(-1). Nitrate and nitrite were determined in the real samples of surface water, and the results have been compared with those obtained by two other flow methods; flow injection analysis based on the same reactions and isotachophoretic determination used in a routine environmental control laboratory.

Automation↗