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PubMed1997

Case-control study on influence of methionine, nitrite, and salt on gastric carcinogenesis in northern Italy.

A new mutagen, 2-chloro-4-methylthiobutanoic acid, has recently been identified from a nitrite-treated Japanese salted fish. Its structure suggests that it derives from methionine in the presence of salt and nitrite. We thus considered the interaction between intake of methionine, salt, and nitrites on gastric cancer risk using data from a case-control study conducted in Northern Italy on 746 cases of incident histologically confirmed gastric cancer and 2,053 controls in hospital for acute nonneoplastic nondigestive tract disorders. Compared with subjects reporting low-methionine and low-salt intake, the odds ratios (ORs) were 2.4 [95% confidence interval (CI) = 1.5 - 4.0] for those reporting low-salt and high-methionine, 1.5 (95% CI = 1.0 - 2.2) for those with high-salt and low-methionine, and 2.8 (95% CI = 1.9 - 4.2) for those with high-salt and high-methionine intake. Likewise, with reference to nitrites, compared with subjects with low-methionine and low-nitrite intake, the ORs were 1.9 (95% CI = 1.3 - 2.6) in the high-methionine and low-nitrite stratum, 1.5 (95% CI = 1.0 - 2.1) in the low-methionine and high-nitrite stratum, and 2.5 (95% CI = 1.9 - 3.2) in the high-methionine and high-nitrite stratum. All these estimates were statistically significant. Thus the present findings from a large case-control study conducted in a relatively high-incidence area for gastric cancer suggest that a diet rich in methionine, salt, and nitrite is associated with increased gastric cancer risk.

Adult↗

PubMed2005

Nitrite enhances neutrophil-induced DNA strand breakage in pulmonary epithelial cells by inhibition of myeloperoxidase.

Chronic inhalation of environmental particles is associated with pulmonary carcinogenesis. Although the mechanism has not yet been fully elucidated, influx of inflammatory cells, including neutrophils, is suggested to play a major role in this process. Typically, in the particle-exposed lung, influx of neutrophils is accompanied by an accumulation of nitrite. Previous studies indicated that nitrite may affect the toxicity of neutrophils, involving an interaction with neutrophil-derived myeloperoxidase (MPO). To evaluate the possible consequences of this interaction for inflammation-mediated genotoxicity, we investigated the effect of nitrite on neutrophil-induced DNA damage in pulmonary target cells. Therefore, activated neutrophils were co-cultured with alveolar type II epithelial cells (RLE), and DNA strand breakage was evaluated using single-cell gel electrophoresis (comet assay). In this system, addition of nitrite caused an increase in neutrophil-induced DNA strand breakage in RLE cells, which was associated with an inhibition of MPO activity. Similar results were obtained by co-culturing RLE cells with neutrophils in the presence of the specific MPO inhibitor 4-aminobenzoic acid hydrazide (4-ABAH). To further investigate the mechanism underlying these observations, in vitro experiments were performed using mixtures of nitrite, MPO and its substrate H2O2. DNA strand breakage by reagent H2O2 was inhibited when it was allowed to react with MPO before addition to the RLE cells. However, when MPO and H2O2 were pre-mixed in the presence of nitrite or 4-ABAH, the inhibitory effect of MPO on resultant DNA damage was reversed. Further studies using catalase indicated that DNA strand breakage by the pre-mixtures of MPO, H2O2 and nitrite was H2O2-specific, suggesting that nitrite prevents consumption of H2O2 by MPO. Collectively, our results show that nitrite enhances neutrophil-induced DNA strand breakage in pulmonary epithelial cells. This effect is probably due to an inhibition of MPO activity, which increases the availability of its DNA strand breaking substrate H2O2.

Animals↗

PubMed2006

Electron transfer to nitrite reductase of Rhodobacter sphaeroides 2.4.3: examination of cytochromes c2 and cY.

The role of cytochrome c(2), encoded by cycA, and cytochrome c(Y), encoded by cycY, in electron transfer to the nitrite reductase of Rhodobacter sphaeroides 2.4.3 was investigated using both in vivo and in vitro approaches. Both cycA and cycY were isolated, sequenced and insertionally inactivated in strain 2.4.3. Deletion of either gene alone had no apparent effect on the ability of R. sphaeroides to reduce nitrite. In a cycA-cycY double mutant, nitrite reduction was largely inhibited. However, the expression of the nitrite reductase gene nirK from a heterologous promoter substantially restored nitrite reductase activity in the double mutant. Using purified protein, a turnover number of 5 s(-1) was observed for the oxidation of cytochrome c(2) by nitrite reductase. In contrast, oxidation of c(Y) only resulted in a turnover of approximately 0.1 s(-1). The turnover experiments indicate that c(2) is a major electron donor to nitrite reductase but c(Y) is probably not. Taken together, these results suggest that there is likely an unidentified electron donor, in addition to c(2), that transfers electrons to nitrite reductase, and that the decreased nitrite reductase activity observed in the cycA-cycY double mutant probably results from a change in nirK expression.

Amino Acid Sequence↗

PubMed1996

Characterization of the gene encoding nitrite reductase and the physiological consequences of its expression in the nondenitrifying Rhizobium "hedysari" strain HCNT1.

Rhizobium "hedysari" HCNT1 is an unclassified rhizobium which contains a nitric oxide-producing nitrite reductase but is apparently incapable of coupling the reduction of nitrite to energy conservation. The gene encoding the nitrite reductase, nirK, has been cloned and sequenced and was found to encode a protein closely related to the copper-containing family of nitrite reductases. Unlike other members of this family, nirK expression in HCNT1 is not dependent on the presence of nitrogen oxides, being dependent only on oxygen concentration. Oxygen respiration of microaerobically grown Nir-deficient cells is not affected by concentrations of nitrite that completely inhibit oxygen respiration in wild-type cells. This loss of sensitivity suggests that the product of nitrite reductase, nitric oxide, is responsible for inhibition of oxygen respiration. By using a newly developed chemically modified electrode to detect nitric oxide, it was found that nitrite reduction by HCNT1 produces significantly higher nitric oxide concentrations than are observed in true denitrifiers. This indicates that nitrite reductase is the only nitrogen oxide reductase active in HCNT1. The capacity to generate such large concentrations of freely diffusible nitric oxide as a consequence of nitrite respiration makes HCNT1 unique among bacteria.

Amino Acid Sequence↗

PubMed1973

Effect of sodium nitrite and sodium nitrate on botulinal toxin production and nitrosamine formation in wieners.

Wieners were formulated and processed approximating commercial conditions as closely as possible. Twenty-four batches of product were made with the addition of six levels of sodium nitrite (0, 50, 100, 150, 200, and 300 mug/g), four levels of sodium nitrate (0, 50, 150, and 450 mug/g), and two levels of Clostridium botulinum (0 and 620 spores/g). After formulation, processing, and vacuum packaging, portions of each batch were incubated at 27 C or held for 21 days at 7 C followed by incubation at 27 C for 56 days. The latter storage condition approximated distribution of product through commercial channels and potential temperature abuse at the consumer level. Samples were analyzed for botulinal toxin, nitrite, and nitrate levels after 3, 7, 14, 21, 28, and 56 days of incubation. When nitrite was not added, toxic samples were detected after 14 days of incubation at 27 C. At the lowest level of nitrite added (50 mug/g), no toxic samples were observed until 56 days of incubation. Higher levels of nitrite completely inhibited toxin production throughout the incubation period. Nine uninoculated samples, representing various levels and combinations of nitrite and nitrate, were evaluated organoleptically. The flavor quality of wieners made with nitrite was judged significantly higher (P = 0.05) than of wieners made without nitrite. The nine samples were negative for 14 volatile nitrosamines at a sensitivity level of 10 ng/g. The results indicated that nitrite effectively inhibited botulinal toxin formation at commercially employed levels in wieners and that detectable quantities of nitrosamines were not produced during preparation and processing of the product for consumption.

Botulinum Toxins↗

PubMed1997

Nitrite reductase from Pseudomonas aeruginosa induces inflammatory cytokines in cultured respiratory cells.

Persistent infection with Pseudomonas aeruginosa increases interleukin-8 (IL-8) levels and causes dense neutrophil infiltrations in the airway of patients with chronic airway diseases. To investigate the role of P. aeruginosa infection in IL-8 production in the airway of these patients, we examined whether cell lysates of P. aeruginosa could cause IL-8 production from human bronchial epithelial cells. Diluted sonicated supernatants of P. aeruginosa (SSPA) with a mucoid or nonmucoid phenotype stimulated human bronchial epithelial (BET-1A) cells to produce IL-8. In this study, we have purified a 59-kDa heat-stable protein with IL-8-inducing activity from the SSPA by sequential ion-exchange chromatography. The N-terminal sequence of this purified protein completely matched a sequence at the N-terminal part of the mature protein of nitrite reductase from P. aeruginosa. In addition, immunoblotting with a polyclonal immunoglobulin G (IgG) against recombinant Pseudomonas nitrite reductase demonstrated a specific binding to the purified protein. Furthermore, the immunoprecipitates of the SSPA with a polyclonal IgG against recombinant nitrite reductase induced a twofold-higher IL-8 production in the BET-1A cell culture than did the immunoprecipitates of the SSPA with a control IgG. These lines of evidence confirmed that Pseudomonas nitrite reductase was responsible for IL-8 production in the BET-1A cells. The purified nitrite reductase induced maximal expression of IL-8 mRNA in the BET-1A cells at 1 to 3 h after stimulation, and the IL-8 mRNA expression declined by 8 h after stimulation. New protein translation was not required for nitrite reductase-mediated IL-8 mRNA expression in the BET-1A cells. Nitrite reductase stimulated the BET-1A cells, as well as human alveolar macrophages, pulmonary fibroblasts, and neutrophils, to produce IL-8. In contrast, nitrite reductase induced significant levels of tumor necrosis factor alpha and IL-1beta protein only in human alveolar macrophages. These data support the notion that nitrite reductase from P. aeruginosa induces the production of inflammatory cytokines by respiratory cells and may contribute to the pathogenesis of chronic airway diseases and persistent P. aeruginosa infection.

Bronchi↗

PubMed1998

Regulation of ntcA expression and nitrite uptake in the marine Synechococcus sp. strain WH 7803.

NtcA is a transcriptional activator involved in global nitrogen control in cyanobacteria. In the absence of ammonium it regulates the transcription of a series of genes encoding proteins required for the uptake and assimilation of alternative nitrogen sources (I. Luque, E. Flores, and A. Herrero, EMBO J. 13:2862-2869, 1994). ntcA, present in a single copy in the marine Synechococcus sp. strain WH 7803, was cloned and sequenced. The putative amino acid sequence shows a high degree of identity to NtcA from freshwater cyanobacteria in two functional domains. The expression of ntcA was negatively regulated by ammonium from a putative transcription start point located downstream of an NtcA consensus recognition sequence. Addition of either rifampin or ammonium led to a rapid decline in ntcA transcript levels with half-lives of less than 2 min in both cases. Nitrate-grown cells showed high ntcA transcript levels, as well as the capacity for active nitrite uptake. However, ammonium-grown cells showed low levels of the ntcA transcript and did not utilize nitrite. The addition of ammonium to nitrite uptake-active cells resulted in a gradual decline in the rate of uptake over a 24-h period. Active nitrite uptake was not induced in cells transferred to medium lacking a nitrogen source despite evidence of elevated expression of ntcA, indicating that ntcA expression is not sufficient for uptake capacity to develop. Nitrate and nitrite addition led to the development of nitrite uptake, whereas the addition of leucine did not. Furthermore, nitrite addition triggered the de novo protein synthesis required for uptake capacity to develop. These data suggest that nitrite and nitrate act as specific inducers for the synthesis of proteins required for nitrite uptake.

Amino Acid Sequence↗

PubMed2002

Serum nitrate and nitrite levels in patients with rheumatoid arthritis, ankylosing spondylitis, and osteoarthritis.

OBJECTIVE: To assess and compare serum nitrate and nitrite levels in patients with ankylosing spondylitis (AS), rheumatoid arthritis (RA), and osteoarthritis (OA). METHODS: Thirty five patients with RA, 32 patients with AS, and 36 patients with OA were entered into this study. In addition, 30 healthy volunteers acted as a control group. Concentrations of nitrate and nitrite in serum were determined by direct and indirect Griess reactions. C reactive protein and erythrocyte sedimentation rate levels were determined as markers of systemic activity of disease (SAD) in RA and AS groups. RESULTS: Serum nitrate and nitrite levels were found to be higher in patients with AS and RA than in the OA group (p<0.01). In addition, serum nitrate and nitrite levels were higher in all three groups than in the control group (p<0.01). Moreover, serum nitrate and nitrite levels were higher in patients who had SAD than in those who had not in the RA and AS groups (p<0.01 and p<0.05, respectively), and there was a correlation between serum nitrate and nitrite concentrations and SAD variables in patients with RA (Spearman's r(s)=0.414, p<0.05 and r(s)=0.408, p<0.05, respectively) and AS (r(s)=0.421, p<0.05 and r(s)=0.412, p<0.05, respectively). CONCLUSION: The findings suggest that nitrate and nitrite production is enhanced in patients with inflammatory arthritis compared with OA. In addition, serum nitrate and nitrite levels are enhanced in patients with RA, AS, and OA compared with healthy subjects. Furthermore, there is a correlation between the SAD variables and serum nitrate and nitrite levels in patients with RA and AS.

Arthritis, Rheumatoid↗

PubMed1986

Detectable colonic nitrite levels in inflammatory bowel disease--mucosal or bacterial malfunction?

In the healthy colon, sodium nitrite stimulates mucosal metabolism of short-chain fatty acids and absorption of ions, both functions that are impaired in the mucosa of patients with ulcerative colitis (UC). To assess the role of nitrite in colonic inflammatory disease, sodium nitrite was measured in rectal dialysate of 49 subjects (18 controls, 23 UC and 8 other colitis). None of the control or quiescent UC patients had measurable levels of nitrite while 78% of patients with acute UC and 38% of patients with other colitis had measurable nitrite levels (acute UC vs. other colitis chi 2 = 5.555, p less than 0.02). Functional activity of the colonic mucosa, judged by bicarbonate output, was impaired in all subjects with measurable nitrite levels in UC. Detection of nitrite in acute colitis suggests impaired oxidation of nitrite to nitrate in the colonic mucosa or impaired luminal reduction of nitrite to NH4 by bacteria.

Ammonia↗

PubMed2004

Malfunction of vascular control in lifestyle-related diseases: formation of systemic hemoglobin-nitric oxide complex (HbNO) from dietary nitrite.

Nitric oxide (NO) has many physiological functions. It is believed to be produced from L-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are waste forms of it. By the way, nitrate and nitrite are abundant in vegetables and fruits, especially leafy vegetables and pickled vegetables. Orally-ingested nitrate is changed to nitrite by micro-organelles living in the hypopharynx area, and nitrite is expected to change to NO in the stomach due to its low pH. Indeed, some researchers reported that NO is produced in the gastric cavity, although few reports mentioned the physiological meanings of this NO formation. Therefore, we investigated whether the nitrite-derived NO can shift to the circulation and acts like NOS-derived NO does in tissues. We adopted a stable isotope of nitrite (15NO2-) in order to distinguish between the endogenous nitrite and the exogenously administered one and measured nitrosyl hemoglobin (HbNO) as an index of circulating NO using electron paramagnetic resonance spectroscopy. It appeared that the oral administration of 15N-nitrite formed the Hb15NO in rat blood and decreased the blood pressure of chronic L-NAME treated rats. Our findings suggest that the intake of nitrite (or nitrate)-rich foods such as vegetables and fruits would alter the systemic HbNO dynamism, resulting in the improvement of cardiovascular diseases.

Animals↗

PubMed1998

Plasma nitrate+nitrite levels are regulated by ovarian steroids but do not correlate with trabecular bone mineral density in rats.

Nitric oxide (NO) is a mediator of bone metabolism and its production is under the control of gender hormones in several cell types or tissues. Changes in endogenous NO production, measured as plasma nitrate+nitrite levels, may therefore contribute to ovariectomy (OVX)-induced bone loss. We studied plasma nitrate+nitrite levels and trabecular bone mineral density (TBMD) 4 weeks after sham-operation or OVX in rats receiving various hormonal treatments. OVX decreased plasma nitrate+nitrite levels significantly and this was accompanied by a significant decrease in TBMD. Treatment with oral ethinyl oestradiol (EE) and subcutaneous 17beta-oestradiol dose-dependently prevented the decrease in plasma nitrate+nitrite levels after OVX, but treatment with oral 17beta-oestradiol did not. Oestrogen treatment, 17beta-oestradiol (s. c. or orally) or EE (orally), prevented the OVX-induced decrease in TBMD. Treatment of sham-operated rats with the anti-oestrogen ICI164, 384 induced a significant decrease in TBMD that corresponded to 54% of the decrease observed after OVX, but did not affect plasma nitrate+nitrite levels. Treatment of ovariectomized rats with Org 2058, a pure progestagen, did not prevent bone loss, but prevented the decrease in plasma nitrate+nitrite levels dose-dependently. Treatment with tibolone, a synthetic steroid with combined weak oestrogenic, progestagenic, and androgenic properties, or with progestagen in combination with EE completely prevented bone loss after OVX. These treatments, however, only partly prevented the OVX-induced decrease in plasma nitrate+nitrite levels. In conclusion, OVX decreased both TBMD and plasma nitrate+nitrite levels. Although plasma nitrate+nitrite levels were under the control of both oestrogen and progesterone, TBMD was affected by oestrogen only. Decreased systemic production of NO is, therefore, not involved in OVX-induced bone loss in rats.

Anabolic Agents↗

PubMed2004

Effect of nitrite on immune response of Taiwan abalone Haliotis diversicolor supertexta and its susceptibility to Vibrio parahaemolyticus.

Taiwan abalones Haliotis diversicolor supertexta held in 30% per thousand seawater and 26 degrees C were injected with tryptic soy broth (TSB)-grown Vibrioparahaemolyticus (1.6 x 10(5) CFU [colony-forming units] abalone(-1)), and then placed in water containing different concentrations of nitrite-N (nitrite as nitrogen): 0.01 mg l(-1) (control), 1.05, 3.04, 5.10 and 10.06 mg l(-1). Mortality of the abalones increased in direct parallel to ambient nitrite-N concentration. Over 12 to 48 h, the mortality of V. parahaemolyticus-injected abalones held in 3.04 mg l(-1) nitrite-N was significantly higher than that of abalones in the control solution. Abalones that had been exposed to control, 0.96, 2.95, 5.03 and 10.16 mg l(-1) nitrite-N for 24, 72 and 120 h were examined for THC (total hemocyte count), phenoloxidase activity, respiratory bursts (release of superoxide anion), phagocytic activity, and clearance efficiency of V. parahaemolyticus. The THC increased in abalone after 72 h exposure to 0.96 and 2.95 mg l(-1) nitrite-N, but decreased in abalones after 24 h exposure to 5.03 and 10.16 mg l(-1) nitrite-N. Phenoloxidase activity and respiratory bursts increased, while phagocytic activity and clearance efficiency decreased in abalones exposed to > or = 0.96 mg l(-1) nitrite-N for 24 h. It is concluded that nitrite-N in water at concentrations as low as 0.96 mg l(-1) weakens the immune response and increases mortality of H. diversicolor supertexta infected with V. parahaemolyticus.

Animals↗

PubMed2002

Circulating nitrite anions are a directly acting vasodilator and are donors for nitric oxide.

Inhaled nitric oxide (NO) is a pulmonary vasodilator, but also acts systemically, causing negative cardiac inotropic effects and a fall in systemic vascular resistance. Circulating metabolites of NO are presumed to be responsible. We questioned the role of nitrite anions and the manner in which they might contribute to these effects. Nitrite and nitrate anions coexist in blood, while circulating levels of dissolved NO are very low. Nitrate anions are not biologically active, but nitrite anions may have a biological role through the release of NO. In vitro, at 37 degrees C and in aerated Krebs bicarbonate solution, the steady-state concentration of dissolved NO was proportional to the concentration of NO in the gas. Nanomolar concentrations of dissolved NO coexisted with micromolar concentrations of nitrite anions. The idea of an equilibrium between the two in solution was also supported by the observed release of NO from nitrite anions in the absence of gas. With rings of precontracted pig pulmonary arteries (prostaglandin F(2alpha); 10 micromol/l), the steady-state concentration of dissolved NO causing 50% relaxation (EC(50)) was 0.84+/-0.25 nmol/l, corresponding to a gaseous concentration of 2.2 p.p.m. The EC(50) of nitrite was 4.5+/-0.7 micromol/l, a concentration normally found in plasma. The estimated concentration of dissolved NO derived from this nitrite was 4.5 pmol/l, some 100 times lower than would be needed to cause relaxation. The rate of exhalation of NO was increased and pulmonary vascular resistance was reduced by the addition of nitrite solution to the perfusate of isolated perfused and ventilated pig lungs, but only when millimolar concentrations were achieved. Thus circulating nitrite anions are a direct vasodilator, only being a carrier of effective amounts of "free" NO at higher than physiological concentrations.

Analog-Digital Conversion↗

PubMed2001

[Research on the dynamic variation and elimination of nitrite content in sauerkraut during pickling].

To investigate the dynamic variation and elimination of nitrite content in pickles and sauerkraut during pickling, green tuber growing in Fuling was selected to make semi-manufactured mustard according to the process technology. Green tuber, cabbage and cauliflower were selected as raw materials to make sauerkraut in family way. The nitrite content in pickles and sauerkraut was determined by spectrophotometry with 1-Amino-2-(a-naphthy lamine) ethoine dihydrochloride. The nitrite content in mustard was 258.8 mg/kg when 6% salt was used and pickling for 8 days; the nitrite content was 235.9 mg/kg when 15% salt was used and pickling for 15 days. There was no nitrite in mustard when pickling for 35 days. The nitrite content in the sauerkraut was 258.7 mg/kg when pickling for 6 days and no nitrite was found after 20 days. The higher nitrite content in pickle and sauerkraut could be eliminated by water. The elimination ratio was 91% for leafy sauerkraut and semi-manufactured cut mustard and only 72% for whole mustard. It was concluded that pickles and sauerkraut that pickled for enough time (for leafy vegetable more than 20 days, for tuber more than 35 days) had no harm for people to eat, The higher nitrite content in pickles and sauerkrauts could be reduced by 91% with water for several times.

Food Preservation↗

PubMed2004

The stability of nitrite nitrification with strong nitrogenous wastewater: effects of organic concentration and microbial diversity.

A stable achievement of nitritation with strong nitrogenous wastewaters is considered as a difficult task in practice, probably due to the fate of interaction between dominating heterotrophs and nitrifier species. An experimental study was carried out to examine the organic effects in lab-scale biofilm nitritation reactors. The control unit without organic addition showed a stable nitritation performance for more than 220 days of operating period. The nitritation activity gradually failed at the reactors with an organic addition, but the nitritation activity eventually recovered with a prolonged aeration. It was not possible to explain the nitritation recovery with neither free ammonia inhibition concept nor DO competition hypothesis in these cases. The results suggest that the nitritation with organic requires a long start-up period for acclimation. In addition, the results of quinone profile analysis were in agreement with nitritation activity in reactors. The diversity of microbial community in the nitritation reactors could be described by the quinone profiles.

Biofilms↗

PubMed2004

Simultaneous determination of nitrate and nitrite in biological fluids by capillary electrophoresis and preliminary study on their determination by microchip capillary electrophoresis.

In order to develop a highly sensitive and high-throughput screening method for nitrogen monoxide metabolites in biological fluids, we have investigated the simultaneous determination of nitrite and nitrate, using capillary electrophoresis and microchip capillary electrophoresis. In capillary zone electrophoresis, a running buffer based on human serum components with high ionic strength has been developed for the determination of nitrite and nitrate in human serum and human saliva. We obtained successful separation of nitrite and nitrate in the serum and the saliva within 7 min under optimum analytical conditions. Linear calibration curves for nitrite and nitrate for both peak height and area were obtained by a standard addition method. The limits of detection obtained at a signal-to-noise ratio (S/N) of 3 for nitrite and nitrate in the serum were 2.6 and 1.5 microM, respectively. The values of the relative standard deviation of peak height for the serum with 9.2 microM nitrite and 20.9 microM nitrate were 5.7 and 4.1%, respectively. For on-site analysis with high-throughput screening, a microchip capillary electrophoresis method using a microchip made of quartz with a UV detector was developed. In this high-throughput format, using a running buffer with an electroosmotic flow modifier, the peaks of nitrite and nitrate in an artificial serum sample were obtained within 8 s. In high-resolution mode, using the buffer without electroosmotic flow modifier, the separation of nitrite and nitrate was obtained within 15 s. In high-resolution mode, using an artificial serum sample with 50 microM NO2- and 50 microM NO3-, the limits of detection (S/N = 3) of 41 microM for NO2- and 26 microM for NO3- were obtained. The method was applied to human serum and saliva. We obtained peaks due to nitrite and nitrate in 10-fold diluted saliva.

Electrochemistry↗

PubMed2005

The effects of nitric oxide synthase--versus lipoxygenase inhibition on coronary flow and nitrite outflow in isolated rat heart.

The aim of this study was to assess the changes of coronary flow (CF) and nitrite outflow under inhibition of nitric oxide synthase (NOS) by Nomega-nitro-L-arginine monomethyl ester (L-NAME) or lipoxygenase (LOX) induced by nordihydroguaiaretic acid (NDGA) in isolated rat heart. The hearts of male Wistar albino rats (n=18, age 8 weeks, body mass 180-200 g) were retrograde perfused according to the Langendorff's technique at gradually increased constant coronary perfusion pressure (CPP) conditions (40-120 cm H2O) which induced flow-dependent nitric oxide (NO) release (nitrite outflow). The experiments were performed during control conditions, in the presence of NO synthesis inhibitor L-NAME (30 micromol/l) or nonspecific LOX inhibitor (NDGA, 0.1 mmol/l) which were administered separately or in combination. CF varied in autoregulatory range from 4.12+/-0.26 ml/min/g wt at 50 cm H2O to 5.22+/-0.26 ml/min/g wt at 90 cm H2O. In autoregulatory range, nitrite outflow varied from 2.05+/-0.17 nmol/min/g wt at 50 cm H2O to 2.52+/-0.21 nmol/min/g wt at 90 cm H2O and was strictly parallel with CPP/CF curve. The autoregulatory range of CF was significantly extended (40-100 cm H2O, 2.22+/-0.12 ml/min/g wt and 2.90+/-0.25 ml/min/g wt, respectively) under the influence of L-NAME. Hemodynamic effects were accompanied by significant decrease in nitrite outflow after L-NAME administration (0.56+/-0.11 nmol/min/g wt at 40 cm H2O to 1.45+/-0.14 nmol/min/g wt at 100 cm H2O). NDGA affected CF in the range of CPP 40-70 cm H2O only (from 42% at 50 cm H2O to 12% at 90 cm H2O, respectively) with no significant changes in nitrite outflow. When L-NAME was applied in combination with NDGA vs. NDGA only, CF was significantly reduced (from 34% at 50 cm H2O to 50% at 90 cm H2O, respectively) with parallel changes in nitrite outflow (from 40% at 50 cm H2O to 51% at 90 cm H2O, respectively). The results showed that CF and nitrite outflow could be decreased under L-NAME administration. Nonselective LOX inhibitor (NDGA) decreased control values of CF only at lower values of CPP but did not change nitrite outflow indicating antioxidant properties of NDGA. In addition, L-NAME decreased the effects induced by NDGA on CF and nitrite outflow indicating the role of NO.

Animals↗

PubMed2006

[Effect of nitrite on aerobic phosphate uptake by phosphate accumulating organisms].

Effect of nitrite at various concentration levels on aerobic phosphate uptake was investigated through a series of batch experiments. Furthermore, the effect of nitrite accumulated in the process of nitrification on aerobic phosphate uptake was studied in saline wastewater treatment. The results show that NO2(-) -N concentration of 4 mg/L inhibits aerobic phosphate uptake by phosphate uptake by phosphate accumulating organisms (PAO) and phosphate uptake rate decreases 8%. Exposure to higher nitrite concentration levels inhibits aerobic phosphate uptake severely. At NO2(-) -N concentration of 15 mg/L, phosphate uptake rate decreases 61%. The toxic effect of nitrite is presumed to be linked with free nitrous acid (FNA). Significant inhibition on aerobic phosphate uptake appeared at 0.000 2 mg/L of FNA concentration. The inhibiting effect of nitrite is found to occur only when nitrite is present. The ability of accumulating phosphate resumes afternitrite is no longer present. During the process of nitrification of nitrification of saline wastewater, the inhibition of nitrite on aerobic phosphate uptake is slight at the initial 1 - 2 h due to low nitrite accumulation. With the build-up of NO2(-) -N(up to about 8 to 9 mg/L), the inhibiting effect of nitrite increases gradually. It is found that higher ammonium concentration causes lower pH value and higher FNA concentration, which could decrease the amount of phosphate uptake.

Bacteria, Aerobic↗