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PubMed2003

Expression of a fully functional cd1 nitrite reductase from Pseudomonas aeruginosa in Pseudomonas stutzeri.

Nitrite reductases are redox enzymes catalysing the one electron reduction of nitrite to nitrogen monoxide (NO) within the bacterial denitrification process. We have cloned the gene for cd(1) nitrite reductase (Pa-nirS) from Pseudomonas aeruginosa into the NiRS(-) strain MK202 of Pseudomonas stutzeri and expressed the enzyme under denitrifying conditions. In the MK202 strain, denitrification is abolished by the disruption of the endogenous nitrite reductase gene; thus, cells can be grown only in the presence of oxygen. After complementation with Pa-nirS gene, cells supplemented with nitrate can be grown in the absence of oxygen. The presence of nitrite reductase was proven in vivo by the demonstration of NO production, showing that the enzyme was expressed in the active form, containing both heme c and d(1). A purification procedure for the recombinant PaNir has been developed, based on the P. aeruginosa purification protocol; spectroscopic analysis of the purified protein fully confirms the presence of the d(1) heme cofactor. Moreover, the functional characterisation of the recombinant NiR has been carried out by monitoring the production of NO by the purified NiR enzyme in the presence of nitrite by an NO electrode. The full recovery of the denitrification properties in the P. stutzeri MK202 strain by genetic complementation with Pa-NiR underlines the high homology between enzymes of nitrogen oxianion respiration. Our work provides an expression system for cd(1) nitrite reductase and its site-directed mutants in a non-pathogenic strain and is a starting point for the in vivo study of recombinant enzyme variants.

Cloning, Molecular↗

PubMed2006

Quantitative analysis of nitrate and nitrite contents in vegetables commonly consumed in Delta State, Nigeria.

Plasma thiocyanate has been reported to be high among cassava-eating populations such as that in Nigeria because of the cyanide content of cassava. Thiocyanate, which is secreted into the stomach contents of animals, has been demonstrated to catalyse the formation of nitrosamines (potent carcinogens) in the stomach from secondary amines and nitrite. The main source of the nitrite precursor in this environment is vegetables, primarily eaten as the chief supplier of proteins. The present study attempts to analyse the levels of nitrate and nitrite in vegetables commonly grown and consumed in Delta State, Nigeria. The nitrate and nitrite contents in green vegetable (Amaranthus spp.), bitter leaf (Vernonia amygdalina), pumpkin (Telfaria occidentalis) and water leaf (Talinum triangulare) grown in different localities of the state were determined by standard analytical procedures. The results show that those vegetables grown in the industrialised urban centres of the state had higher nitrate (223 (SD 71) mg/kg dry weight; P<0.05) and nitrite (12.6 (SD 1.7) mg/kg dry weight; P>0.05) levels when compared with the same species (188 (SD 77) mg nitrate/kg dry weight and 10.9 (SD 1.1) mg nitrite/kg dry weight) cultivated in less industrialised suburbs. We conclude that frequent consumption of such vegetables whose nitrate and nitrite contents are high by cassava-eating individuals might put them at risk of developing stomach cancer and other possible results of nitrate and/or nitrite toxicity. In order to avoid an outbreak in our communities, appropriate agencies should monitor and regulate the release of chemicals into the environment. In the meantime, the cultivation and consumption of vegetables grown in industrialised areas of the state should be discouraged.

Amaranthus↗

PubMed1995

Aqueous nitrite ion determination by selective reduction and gas phase nitric oxide chemiluminescence.

An improved method of flow injection analysis for aqueous nitrite ion exploits the sensitivity and selectivity of the nitric oxide (NO) chemilluminescence detector. Trace analysis of nitrite ion in a small sample (5-160 microL) is accomplished by conversion of nitrite ion to NO by aqueous iodide in acid. The resulting NO is transported to the gas phase through a semipermeable membrane and subsequently detected by monitoring the photoemission of the reaction between NO and ozone (O3). Chemiluminescence detection is selective for measurement of NO, and, since the detection occurs in the gas-phase, neither sample coloration nor turbidity interfere. The detection limit for a 100-microL sample is 0.04 ppb of nitrite ion. The precision at the 10 ppb level is 2% relative standard deviation, and 60-180 samples can be analyzed per hour. Samples of human saliva and food extracts were analyzed; the results from a standard colorimetric measurement are compared with those from the new chemiluminescence method in order to further validate the latter method. A high degree of selectivity is obtained due to the three discriminating steps in the process: (1) the nitrite ion to NO conversion conditions are virtually specific for nitrite ion, (2) only volatile products of the conversion will be swept to the gas phase (avoiding turbidity or color in spectrophotometric methods), and (3) the NO chemiluminescence detector selectively detects the emission from the NO + O3 reaction. The method is free of interferences, offers detection limits of low parts per billion of nitrite ion, and allows the analysis of up to 180 microL-sized samples per hour, with little sample preparation and no chromatographic separation. Much smaller samples can be analyzed by this method than in previously reported batch analysis methods, which typically require 5 mL or more of sample and often need chromatographic separations as well.

Colorimetry↗

PubMed1998

Electronic structural information from Q-band ENDOR on the type 1 and type 2 copper liganding environment in wild-type and mutant forms of copper-containing nitrite reductase.

Q-band ENDOR elucidated proton and nitrogen hyperfine features to provide spin density information at ligands of blue-green Type 1 and catalytic Type 2 copper centers in nitrite reductase. The blue-green Type 1 center of nitrite reductase has a redox, electron-transfer role, and compared to the blue center of plastocyanin, it has the following structural differences: a shortened Cu-Smet bond length, a longer Cu-Scys bond length, and altered ligand-copper-ligand bond angles (Adman, E. T., Godden, J. W., and Turley, S. (1995) J. Biol. Chem. 270, 27458-27474). The hyperfine couplings of the two Type 1 histidine (N delta) ligands showed a larger percentage difference from each other in electron spin density than previously reported for other blue Type 1 proteins, while the cysteine beta-proton hyperfine couplings, a measure of unpaired p pi spin density on the liganding cysteine sulfur, showed a smaller electron spin density. A mutation of the Type 1 center, M182T, having the copper-liganding Met182 transformed to Thr182, caused the center to revert to an optically "blue" center, raised its redox potential by approximately 100 mV, and led to the loss of activity (prior paper). Surprisingly, in M182T there was no change from native Type 1 copper either in the histidine or cysteine hyperfine couplings or in g values and Cu nuclear hyperfine couplings. The conclusion is that the optical and redox alterations due to changed Type 1 methionine ligation need not be concurrent with electron spin delocalization changes in the HOMO as reported from its essential cysteine and histidines. A detailed picture of the nitrogen couplings from the three histidine (N epsilon) ligands of the Type 2 center indicated a substantial ( approximately 200%) electronic hyperfine inequivalence of one of the histidine nitrogens from the other two within the Type 2 HOMO and thus provided evidence for electronic distortion of the Type 2 site. In the presence of the nitrite substrate, hyperfine couplings of all histidines diminished. We suggest that this nitrite-induced decreased covalency would correlate with an increased Type 2 redox potential to assist electron transfer to the Type 2 center. Dipole-coupled, angle-selected exchangeable proton features, observed over a range of g values, predicted a ligand-water proton distance of 2.80 A from copper, and these water protons were eliminated by nitrite. His287 is not a Type 2 ligand but is positioned to perturb an axial water or a nitrite of Type 2 copper. In the presence of nitrite the mutant H287E showed no evidence for the loss of water protons and no diminished ligand histidine covalency. H287E has vastly diminished activity (prior paper), and the ENDOR information is that NO2- does not bind to Type 2 copper of H287E. In summary, the electronic information from this study of native and suitably chosen mutants provided a test of the highest occupied molecular orbital (HOMO) wave function at Type 1 and Type 2 coppers and an intimate electronic insight into functional enzymatic properties.

Copper↗

PubMedDate not supplied

Containment of biogenic sulfide production in continuous up-flow packed-bed bioreactors with nitrate or nitrite.

Produced water from the Coleville oil field in Saskatchewan, Canada was used to inoculate continuous up-flow packed-bed bioreactors. When 7.8 mM sulfate and 25 mM lactate were present in the in-flowing medium, H(2)S production (souring) by sulfate-reducing bacteria (SRB) was prevented by addition of 17.5 mM nitrate or 20 mM nitrite. Changing the sulfate or lactate concentration of the in-flowing medium indicated that the concentrations of nitrate or nitrite required for containment of souring decreased proportionally with a lowered concentration of the electron donor lactate, while the sulfate concentration of the medium had no effect. Microbial communities were dominated by SRB. Nitrate addition did not give rise to changes in community composition, indicating that lactate oxidation and H(2)S removal were caused by the combined action of SRB and nitrate-reducing, sulfide-oxidizing bacteria (NR-SOB). Apparently the nitrite concentrations formed by these NR-SOB did not inhibit the SRB sufficiently to cause community shifts. In contrast, significant community shifts were observed upon direct addition of high concentrations (20 mM) of nitrite. Strains NO3A and NO2B, two newly isolated, nitrate-reducing bacteria (NRB) emerged as major community members. These were found to belong to the epsilon-division of the Proteobacteria, to be most closely related to Campylobacter lari, and to oxidize lactate with nitrate or nitrite as the electron acceptor. Thus the mechanism of microbial H(2)S removal in up-flow packed-bed bioreactors depended on whether nitrate (SRB/NR-SOB) or nitrite (SRB/NR-SOB as well as NRB) was used. However, the amount of nitrate or nitrite needed to completely remove H(2)S was dictated by the electron donor (lactate) concentration, irrespective of mechanism.

Biodegradation, Environmental↗

PubMed2002

Kinetics of nitrate, nitrite, and Cr(VI) reduction by iron metal.

The kinetics of nitrate, nitrite, and Cr(VI) reduction by three types of iron metal (Fe0) were studied in batch reactors for a range of Fe0 surface area concentrations and solution pH values (5.5-9.0). At pH 7.0, there was only a modest difference (2-4x) in first-order rate coefficients (k(obs)) for each contaminant among the three Fe0 types investigated (Fisher, Peerless, and Connelly). The k(obs) values at pH 7.0 for both nitrite and Cr(VI) reduction were first-order with respect to Fe0 surface area concentration, and average surface area normalized rate coefficients (kSA) of 9.0 x 10(-3) and 2.2 x 10(-1) L m(-2) h(-1) were determined for nitrite and Cr(VI), respectively. Unlike nitrite and Cr(VI), Fe0 surface area concentration had little effect on rates of nitrate reduction (with the exception of Connelly Fe0, which reduced nitrate at slower rates at higher Fe0 surface areas). The rates of nitrate, nitrite, and Cr(VI) reduction by Fisher Fe0 decreased with increasing pH with apparent reaction orders of 0.49 +/- 0.04 for nitrate, 0.61 +/- 0.02 for nitrite, and 0.72 +/- 0.07 for Cr(VI). Buffer type had minimal effects on reduction rates, indicating that pH was primarily responsible for the differences in rate. At high pH values, Cr(VI) reduction ceased after a short time period, and negligible nitrite reduction was observed over 48 h.

Carcinogens, Environmental↗

PubMed2006

Mechanistic studies on the nitrite-catalyzed reductive nitrosylation of highly charged anionic and cationic Fe(III) porphyrin complexes.

The nitrosyl complexes formed during the binding of NO to the (Pn)FeIII(H2O)2 (n = 8+ and 8-) complexes, viz., (P8-)FeII(H2O)(NO+) and (P8+)FeII(H2O)(NO+), undergo subsequent reductive nitrosylation reactions that were found to be catalyzed by nitrite, which was also produced during the reaction. The effect of the nitrite concentration, pH, temperature, and pressure on the nitrite-catalyzed reductive nitrosylation process was studied in detail for (P8-)FeIII(H2O)2, (P8+)FeIII(H2O)2, and (P8+)FeIII(OH)(H2O), from which rate and activation parameters were obtained. On the basis of these data, we propose mechanistic pathways for the studied reactions. The available results favor the operation of an innersphere electron-transfer process between nitrite and coordinated NO(+). By way of comparison, the cationic porphyrin complex (P8+)FeIII(L)2 (L = H2O or OH-) was found to react with NO2(-) to yield the nitrite adduct (P8+)FeIII(L)(NO2)(-)). A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2 according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O) at higher pH follows an associative mechanism, similar to that reported for the binding of NO to these complexes.

Anions↗

PubMed1999

Antimicrobial effect of acidified nitrite on cariogenic bacteria.

The antimicrobial agent nitric oxide (NO) is formed in the mouth and its concentration is directly related to salivary nitrite, which in turn is related to dietary nitrate intake. The aim of this study was to determine whether nitrite under acidic conditions will have an inhibitory effect, possibly occurring through NO production, on Streptococcus mutans, Lactobacillus casei and Actinomyces naeslundii. Whereas the growth of S. mutans was inhibited by a more acid pH, the addition of nitrite caused a marked, further dose-dependent reduction in bacterial numbers after 24 h of exposure. Similar effects were observed with A. naeslundii and L. casei. The ability of these bacteria to recover from nitrite exposure was also markedly affected by nitrite concentration. At acidity levels below pH 7, low concentrations of nitrite (0.2 mM) caused effective complete killing of S. mutans, with similar effects on the other organisms tested. These results demonstrate the possibility that nitrite in saliva has an effect on the growth and survival of cariogenic bacteria.

Actinomyces↗

PubMed2001

Control of biogenic H(2)S production with nitrite and molybdate.

The effects of the metabolic inhibitors, sodium nitrite and ammonium molybdate, on production of H(2)S by a pure culture of the sulfate-reducing bacterium (SRB) Desulfovibrio sp. strain Lac6 and a consortium of SRB, enriched from produced water of a Canadian oil field, were investigated. Addition of 0.1 mM nitrite or 0.024 mM molybdate at the start of growth prevented the production of H(2)S by strain Lac6. With exponentially growing cultures, higher levels of inhibitors, 0.25 mM nitrite or 0.095 mM molybdate, were required to suppress the production of H(2)S. Simultaneous addition of nitrite and molybdate had a synergistic effect: at time 0, 0.05 mM nitrite and 0.01 mM molybdate, whereas during the exponential phase, 0.1 mM nitrite and 0.047 mM molybdate were sufficient to stop H(2)S production. With an exponentially growing consortium of SRB, enriched from produced water of the Coleville oil field, much higher levels of inhibitors, 4 mM nitrite or 0.47 mM molybdate, were needed to stop the production of H(2)S. The addition of these inhibitors had no effect on the composition of the microbial community, as shown by reverse sample genome probing. The results indicate that the efficiency of inhibitors in containment of SRB depends on the composition and metabolic state of the microbial community.

Desulfovibrio↗

PubMed2004

Electrospray ionization-ion mobility spectrometry: a rapid analytical method for aqueous nitrate and nitrite analysis.

This paper reports the first example of electrospray ionization (ESI) for the separation and detection of anions in aqueous solutions by ion mobility spectrometry (IMS). Standard solutions of arsenate, phosphate, sulfate, nitrate, nitrite, chloride, formate, and acetate were analyzed using ESI-IMS and distinct peak patterns and reduced mobility constants (K(0)) were observed for respective anions. Real world water samples were analyzed for nitrate and nitrite to determine the feasibility of using ESI-IMS as a rapid analytical method for monitoring nitrate and nitrite in water systems. The data showed satisfactory correlation between the measured value ([similar]0.16 ppm) and the reported maximum nitrate-nitrogen concentration (0.2 ppm) found in a local drinking water system. For on-site measurement applications, direct sample introduction and air as an alternate drift gas to nitrogen were evaluated. The identities of the nitrite and nitrate mobility peaks were verified by comparison of reduced mobility constants with mass identified nitrate and nitrite ions reported in literature. In the mixing ratio, a linear dynamic range of 3 orders of magnitude and instrument detection limits of 10 ppb for nitrate and 40 ppb for nitrite were obtained. The calibration curves showed r(2) value of 0.98 and slope of 0.06 for nitrate and r(2) value of 0.99 and slope of 0.11 for nitrite.

Environmental Monitoring↗

PubMed2001

Suicide inactivation of xanthine oxidoreductase during reduction of inorganic nitrite to nitric oxide.

Xanthine oxidoreductase (XOR) is progressively inactivated while catalysing the reduction of inorganic nitrite to NO by xanthine. Inactivation results from conversion of the enzyme into its desulpho-form. The rate of inactivation increases with nitrite concentration. Similar behaviour was shown when NADH replaced xanthine as reducing substrate. A kinetic model is proposed incorporating a 'suicide' inactivation involving an enzyme-substrate (product) complex, rather than inactivation by free NO. The model provides a good fit to progress curves of the reaction of xanthine or NADH with nitrite in the presence of the oxidase or dehydrogenase forms of the enzyme. Inorganic nitrate, like nitrite, was shown to be reduced at the molybdenum site of XOR. With xanthine as reducing substrate, nitrite was produced in essentially a 1:1 stoichiometric ratio with respect to urate. Unlike the case of nitrite, the enzyme was not significantly inactivated, implying that inactivation during nitrite reduction depends on the presence of nascent NO in its enzyme complex.

Animals↗

PubMed2001

Alterations in intragastric nitrite and vitamin C levels during acid inhibitory therapy.

Most nitrite entering the healthy acid-secreting stomach is derived from dietary nitrate. The latter is absorbed from the small intestine, 25% then being secreted by the salivary glands into the mouth. Buccal organisms subsequently convert 20% of this nitrate to nitrite. When this nitrite is swallowed, the ascorbic acid in the acidic gastric juice reduces it to nitric oxide, which is absorbed by the mucosa. In the process, the ascorbic acid is oxidized to dehydroascorbic acid. When the intragastric pH is elevated by powerful anti-secretory agents, this gastric chemistry is profoundly modified. At a neutral pH, the swallowed nitrite does not react with ascorbic acid but accumulates in the stomach. The level of nitrite in the gastric juice during treatment with anti-secretory medication is particularly high after a nitrate-containing meal. Powerful anti-secretory medication also lowers the intragastric concentration of ascorbic acid and total vitamin C, probably because of the relative instability of the vitamin at a higher pH. These changes in the intragastric concentrations of nitrite and ascorbic acid are most marked in Helicobacter pylori -infected subjects on proton pump inhibitor therapy. It is recognized that an elevated nitrite-to-ascorbic acid ratio predisposes to the formation of potentially carcinogenic N -nitroso compounds. It is, however, unclear at present whether such compounds are formed within the human stomach.

Anti-Ulcer Agents↗

PubMed2002

The effects of calcium channel antagonists on coronary nitrite outflow in isolated rat heart.

The aim of the study was to compare the effects of Ca2+ channel antagonists on coronary endothelial L-arginine/NO system in isolated rat heart. The hearts of male Wistar albino rats (n = 36, age 8 weeks, body mass 180-200 g) were perfused according to Langendorff technique at gradually increased coronary perfusion pressure (CPP) which induced flow-dependent NO release (nitrite outflow). The experiments were performed during control condition or in the presence of different Ca2+ channel antagonists: nifedipine (CAS 21829-25-4, 30 nmol/l), diltiazem (CAS 42399-41-7, 3 mumol/l), verapamil (CAS 52-53-9, 0.4 mumol/l) or amlodipine (CAS 88150-42-9, 100 nmol/l) were administered separately. Also, nifedipine or amlodipine were administered in combination with an inhibitor of nitric oxide synthase (NOS), L-NAME (NG-nitro-L-arginine-methylester, 30 mumol/l). Coronary flow (CF) varied in autoregulatory range from 3.93 +/- 0.25 ml/min/g wt at 50 cmH2O to 4.49 +/- 0.31 ml/min/g wt at 90 cmH2O. In autoregulatory range nitrite outflow varied from 1.80 +/- 0.22 nmol/min/g wt at 50 cmH2O to 2.21 +/- 0.25 nmol/min/g wt at 90 cmH2O and was strictly parallel with the CPP-CF (coronary perfusion pressure/coronary flow) curve. The autoregulatory range of CF was significantly extended (40-100 cmH2O) under the influence of nifedipine. Hemodynamic effects were accompanied by significant changes in nitrite outflow in all groups except for the verapamil group. Nifedipine and diltiazem induced statistically significant increases of nitrite outflow in coronary venous effluent, strictly parallel with the CPP-CF curve, from 58% at 120 cmH2O to 190% at 40 cmH2O and from 74% at 120 cmH2O to 166% at 40 cmH2O, respectively. On the contrary, amlodipine induced significant reduction of nitrite outflow which was stronger at the lower value of CPP (44-46% at 40-80 cmH2O), compared to the higher value of CPP (32-37% at 100-120 cmH2O). When L-NAME was applied in combination with nifedipine or amlodipine, CF was significantly reduced with parallel changes in nitrite outflow. The results show that Ca2+ channel antagonists (verapamil, diltiazem, nifedipine and amlodipine) strongly influence the coronary endothelial L-arginine/NO system in isolated rat heart leading to the difference in nitrite outflow.

Animals↗

PubMed1992

Amyl nitrite: use as a smooth muscle relaxant in difficult preterm cesarean section.

Amyl nitrite is a smooth muscle relaxant that has been used clinically to facilitate uterine relaxation in difficult deliveries. In this retrospective study, we evaluate the safety of amyl nitrite use during preterm cesarean deliveries, and we assess possible advantageous effects on surgical incision choice. Women who received amyl nitrite cesarean section were compared to a control group matched for gestational age, fetal presentation, and mode of delivery who did not receive amyl nitrite. There were no statistical differences between the groups in the independent variables (maternal age, parity, medical or obstetric history, type of anesthesia, anesthesia or obstetric attending physician, antepartum hematocrit, or neonatal weight). Outcome (dependent) variables (estimated blood loss, Apgar scores, postpartum hematocrit, cord gases, or postpartum complications) were assessed, and there were no significant differences between the groups. Low transverse cesarean section was performed more frequently in the amyl nitrite group (58 of 64) than in the comparison group (48 of 64) (p less than 0.03). Considering the 128 women with and without amyl nitrite together, the decrease in hematocrit observed postpartum was greater after classic section (7%) than after low transverse section (4%) (p less than 0.002). We conclude that the use of amyl nitrite during preterm cesarean section poses no threat to mother or fetus and may facilitate delivery by allowing the performance of a low transverse rather than a classic cesarean section without maternal or neonatal complications.

Amyl Nitrite↗

PubMed2000

Reduction of nitrite to nitric oxide catalyzed by xanthine oxidoreductase.

Xanthine oxidase (XO) was shown to catalyze the reduction of nitrite to nitric oxide (NO), under anaerobic conditions, in the presence of either NADH or xanthine as reducing substrate. NO production was directly demonstrated by ozone chemiluminescence and showed stoichiometry of approximately 2:1 versus NADH depletion. With xanthine as reducing substrate, the kinetics of NO production were complicated by enzyme inactivation, resulting from NO-induced conversion of XO to its relatively inactive desulfo-form. Steady-state kinetic parameters were determined spectrophotometrically for urate production and NADH oxidation catalyzed by XO and xanthine dehydrogenase in the presence of nitrite under anaerobic conditions. pH optima for anaerobic NO production catalyzed by XO in the presence of nitrite were 7.0 for NADH and </=6.0 for xanthine. Involvement of the molybdenum site of XO in nitrite reduction was shown by the fact that alloxanthine inhibits xanthine oxidation competitively with nitrite. Strong preference for Mo=S over Mo=O was shown by the relatively very low NADH-nitrite reductase activity shown by desulfo-enzyme. The FAD site of XO was shown not to influence nitrite reduction in the presence of xanthine, although it was clearly involved when NADH was the reducing substrate. Apparent production of NO decreased with increasing oxygen tensions, consistent with reaction of NO with XO-generated superoxide. It is proposed that XO-derived NO fulfills a bactericidal role in the digestive tract.

Anaerobiosis↗

PubMed2000

The nitric oxide congener nitrite inhibits myeloperoxidase/H2O2/ Cl- -mediated modification of low density lipoprotein.

Nitric oxide, a pivotal molecule in vascular homeostasis, is converted under aerobic conditions to nitrite. Recent studies have shown that myeloperoxidase (MPO), an abundant heme protein released by activated leukocytes, can oxidize nitrite (NO(2-)) to a radical species, most likely nitrogen dioxide. Furthermore, hypochlorous acid (HOCl), the major strong oxidant generated by MPO in the presence of physiological concentrations of chloride ions, can also react with nitrite, forming the reactive intermediate nitryl chloride. Since MPO and MPO-derived HOCl, as well as reactive nitrogen species, have been implicated in the pathogenesis of atherosclerosis through oxidative modification of low density lipoprotein (LDL), we investigated the effects of physiological concentrations of nitrite (12.5-200 microm) on MPO-mediated modification of LDL in the absence and presence of physiological chloride concentrations. Interestingly, nitrite concentrations as low as 12.5 and 25 microm significantly decreased MPO/H2O2)/Cl- -induced modification of apoB lysine residues, formation of N-chloramines, and increases in the relative electrophoretic mobility of LDL. In contrast, none of these markers of LDL atherogenic modification were affected by the MPO/H2O2/NO2-) system. Furthermore, experiments using ascorbate (12.5-200 microm) and the tyrosine analogue 4-hydroxyphenylacetic acid (12.5-200 microm), which are both substrates of MPO, indicated that nitrite inhibits MPO-mediated LDL modifications by trapping the enzyme in its inactive compound II form. These data offer a novel mechanism for a potential antiatherogenic effect of the nitric oxide congener nitrite.

Chlorides↗

PubMed2006

Coordinated regulation of the Neisseria gonorrhoeae-truncated denitrification pathway by the nitric oxide-sensitive repressor, NsrR, and nitrite-insensitive NarQ-NarP.

Neisseria gonorrhoeae survives anaerobically by reducing nitrite to nitrous oxide catalyzed by the nitrite and nitric oxide reductases, AniA and NorB. P(aniA) is activated by FNR (regulator of fumarate and nitrate reduction), the two-component regulatory system NarQ-NarP, and induced by nitrite; P(norB) is induced by NO independently of FNR by an uncharacterized mechanism. We report the results of microarray analysis, bioinformatic analysis, and chromatin immunoprecipitation, which revealed that only five genes with readily identified NarP-binding sites are differentially expressed in narP(+) and narP strains. These include three genes implicated in the truncated gonococcal denitrification pathway: aniA, norB, and narQ. We also report that (i) nitrite induces aniA transcription in a narP mutant; (ii) nitrite induction involves indirect inactivation by nitric oxide of a gonococcal repressor, NsrR, identified from a multigenome bioinformatic study; (iii) in an nsrR mutant, aniA, norB, and dnrN (encoding a putative reactive nitrogen species response protein) were expressed constitutively in the absence of nitrite, suggesting that NsrR is the only NO-sensing transcription factor in N. gonorrhoeae; and (iv) NO rather than nitrite is the ligand to which NsrR responds. When expressed in Escherichia coli, gonococcal NarQ and chimaeras of E. coli and gonococcal NarQ are ligand-insensitive and constitutively active: a "locked-on" phenotype. We conclude that genes involved in the truncated denitrification pathway of N. gonorrhoeae are key components of the small NarQP regulon, that NarP indirectly regulates P(norB) by stimulating NO production by AniA, and that NsrR plays a critical role in enabling gonococci to evade NO generated as a host defense mechanism.

Antigens, Bacterial↗

PubMed2003

Studies of nitric oxide generation from salivary nitrite in human gastric juice.

BACKGROUND: Saliva contains substantial concentrations of nitrite derived from the enterosalivary recirculation of dietary nitrate. METHODS: We have investigated factors in gastric juice influencing the fate of nitrite in swallowed saliva. When nitrite (100 microM) is added to human gastric juice pH 1.5 or pH 2.5 at 37 degrees C containing physiological concentrations of thiocyanate (1 mM) and ascorbic acid (200 microM), it is converted to nitric oxide within a few seconds. RESULTS: The reduction of nitrite to nitric oxide is slower at pH 3.5 and very little is generated at pH 4.5. The rate of nitric oxide generation at acid pH increases with increasing thiocyanate concentration. The concentration of nitric oxide generated in the above way is maintained until the ascorbic acid is depleted by the recycling of nitric oxide to nitrite. In gastric juice depleted of ascorbic acid, very little nitrite is reduced to nitric oxide at any pH. CONCLUSION: These studies indicate that in the healthy acid-secreting stomach most salivary nitrite will be reduced to nitric oxide at the gastro-oesophageal junction and gastric cardia where it first encounters gastric juice.

Ascorbic Acid↗