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PubMed2005

Corrosion risk associated with microbial souring control using nitrate or nitrite.

Souring, the production of hydrogen sulfide by sulfate-reducing bacteria (SRB) in oil reservoirs, can be controlled through nitrate or nitrite addition. To assess the effects of this containment approach on corrosion, metal coupons were installed in up-flow packed-bed bioreactors fed with medium containing 8 mM sulfate and 25 mM lactate. Following inoculation with produced water to establish biogenic H(2)S production, some bioreactors were treated with 17.5 mM nitrate or up to 20 mM nitrite, eliminating souring. Corrosion rates were highest near the outlet of untreated bioreactors (up to 0.4 mm year(-1)). Nitrate (17.5 mM) eliminated sulfide but gave pitting corrosion near the inlet of the bioreactor, whereas a high nitrite dose (20 mM) completely eliminated microbial activity and associated corrosion. More gradual, step-wise addition of nitrite up to 20 mM resulted in the retention of microbial activity and localized pitting corrosion, especially near the bioreactor inlet. We conclude that: (1) SRB control by nitrate or nitrite reduction shifts the corrosion risk from the bioreactor outlet to the inlet (i.e. from production to injection wells) and (2) souring treatment by continuous addition of a high inhibitory nitrite dose is preferable from a corrosion-prevention point of view.

Bacteria↗

PubMed2006

Optimization of free ammonia concentration for nitrite accumulation in shortcut biological nitrogen removal process.

A shortcut biological nitrogen removal (SBNR) utilizes the concept of a direct conversion of ammonium to nitrite and then to nitrogen gas. A successful SBNR requires accumulation of nitrite in the system and inhibition of the activity of nitrite oxidizers. A high concentration of free ammonia (FA) inhibits nitrite oxidizers, but unfortunately decreases the ammonium removal rate as well. Therefore, the optimal range of FA concentration is necessary not only to stabilize nitrite accumulation but also to achieve maximum ammonium removal. In order to derive such optimal FA concentrations, the specific substrate utilization rates of ammonium and nitrite oxidizers were measured. The optimal FA concentration range appeared to be 5-10 mg/L for the adapted sludge. The simulated results from the modified inhibition model expressed by FA and ammonium/nitrite concentrations were shown very similar to the experimental results.

Ammonia↗

PubMed2005

Therapeutic efficacy of decreased nitrite production by bezafibrate in patients with primary biliary cirrhosis.

BACKGROUND: The therapeutic efficacy of bezafibrate, a hypolipidemic drug, has been shown in patients with primary biliary cirrhosis (PBC) in some pilot studies; however, little is known regarding the mechanism of action of bezafibrate in PBC. This study was conducted to evaluate the therapeutic efficacy, as well as to gain insight about the possible mechanism of action, of bezafibrate in PBC. METHODS: Sixteen patients with PBC were administered with bezafibrate (400 mg/day) either with (n = 10) or without ursodeoxycholic acid (UDCA; n = 6). The peripheral blood of these patients was collected before and at different times after therapy commencement, and antigen-presenting dendritic cells (DCs) were then cultured. The DCs were enriched and cultured with Staphylococcus aureus Cowan strain-1 for 48 h to evaluate their capacity to produce nitrite. RESULTS: One month after the start of bezafibrate therapy, the serum levels of alkaline phosphatase (P = 0.0005), gamma-glutamyl transpeptidase (P = 0.0006), total cholesterol (P = 0.0072), and immunoglobulin M (P = 0.0281) were decreased significantly compared to those before patients started bezafibrate therapy. The levels of nitrite produced by DCs decreased in all patients with PBC within 1 month of commencement of bezafibrate therapy. Moreover, decreased nitrite production by DCs was also seen when nitrite production was evaluated 1 year after the start of bezafibrate therapy. CONCLUSIONS: This study reconfirms the therapeutic efficacy of bezafibrate in patients with PBC, including those with UDCA-resistant PBC. Downregulation of nitrite production by DCs may have some relationship with the therapeutic efficacy of bezafibrate; however, further study will be needed to clarify whether or not the antiinflammatory activity of bezafibrate is mediated through nitrite production.

Adult↗

PubMed2006

Dynamics of corrosion rates associated with nitrite or nitrate mediated control of souring under biological conditions simulating an oil reservoir.

Representative microbial cultures from an oil reservoir and electrochemical techniques including potentiodynamic scan and linear polarization were used to investigate the time dependent corrosion rate associated with control of biogenic sulphide production through addition of nitrite, nitrate and a combination of nitrate-reducing, sulphide-oxidizing bacteria (NR-SOB) and nitrate. The addition of nitrate alone did not prevent the biogenic production of sulphide but the produced sulphide was eventually oxidized and removed from the system. The addition of nitrate and NR-SOB had a similar effect on oxidation and removal of sulphide present in the system. However, as the addition of nitrate and NR-SOB was performed towards the end of sulphide production phase, the assessment of immediate impact was not possible. The addition of nitrite inhibited the biogenic production of sulphide immediately and led to removal of sulphide through nitrite mediated chemical oxidation of sulphide. The real time corrosion rate measurement revealed that in all three cases an acceleration in the corrosion rate occurred during the oxidation and removal of sulphide. Amendments of nitrate and NR-SOB or nitrate alone both gave rise to localized corrosion in the form of pits, with the maximum observed corrosion rates of 0.72 and 1.4 mm year(-1), respectively. The addition of nitrite also accelerated the corrosion rate but the maximum corrosion rate observed following nitrite addition was 0.3 mm year(-1). Furthermore, in the presence of nitrite the extent of pitting was not as high as those observed with other control methods.

Corrosion↗

PubMed2005

Proposed mechanism of nitrite-induced methemoglobinemia.

A scheme of development of nitrite-induced oxyhemoglobin oxidation in erythrocytes based on the analysis of experimental data is proposed. It was found that, contrary to widespread opinion, direct oxidative-reductive interaction between hemoglobin and nitrite is absent or negligible under physiological conditions. The driving stage of this process is methemoglobin-catalyzed peroxidase oxidation of nitrite. The product of the oxidation (presumably NO2*) directly oxidizes oxyhemoglobin to methemoglobin-peroxide complex without hydrogen peroxide release into the environment. The oxidant itself is reduced to nitrite or oxidized to nitrate as a result of interaction with another NO2* molecule. Thus, the stoichiometry of the process depends on the ratio of rates of these two reactions. Substances that are able to compete with nitrite for peroxidase and therefore to prevent the nitrite oxidation effectively protect hemoglobin from oxidation. Catalase is not able to destroy methemoglobin-peroxide complexes, but it can prevent their production in the course of interaction of methemoglobin and free peroxide by destroying the latter.

Animals↗

PubMed2005

Effects of honey on the urinary total nitrite and prostaglandins concentration.

OBJECTIVES: To evaluate effects of natural and artificial honey solutions on urinary nitrite content, prostaglandin excretion and urinary variables in healthy individuals. METHODS: The study comprised 12 individuals, nine males and three females; age range 25-45 years. Urinary total nitrite, prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha) and thromboxane B2 (TXB2) were assessed in spot morning sample and 1, 2, and 3 hours after ingestion of 80 g of natural honey dissolved in 250 ml water. Honey solution was given at night; urine volume, urinary osmolality and electrolytes, and serum osmolality and electrolytes, were assayed 10 hours after drinking honey. Same procedure was repeated after drinking artificial honey (30 g glucose plus 38 g fructose) and compared with control (drinking 250 ml of water). RESULTS: The mean (SD) of total urinary nitrite excretion was 103 +/- 43.5 micromol/l which was increased by 40%, 55% and 74% at 1, 2, and 3 hours after drinking honey solution respectively. The mean urinary PGE2 was 1.323 +/- 0.8 ng/ml that was decreased by 31% 3 hours after honey ingestion. The mean urinary PGF2 alpha was 1.554 +/- 1.2 ng/ml and that of TXB2 was 0.35 +/- 0.4 ng/ml. Forty-four percent reductions in urinary PGF2 alpha and 67% reduction in TXB2 were obtained 3 hours after drinking honey. Honey increased insignificantly free water clearance, filtered sodium and creatinine clearance. It decreased insignificantly urinary osmolality, urinary calcium, urinary sodium, and fasting blood sugar (FBS). Little changes were obtained in urine volume and urinary urea, glucose and creatinine concentration. Artificial honey decreased urinary nitrite and increased urinary prostaglandins concentration. It increased insignificantly free water clearance, filtered sodium, urinary urea, urinary creatinine and creatinine clearance. It decreased insignificantly urinary osmolality, urinary calcium, urinary sodium, and fractional excretion of sodium (FENa). Artificial honey increased FBS by 14% and urinary glucose by 76.5%, and decreased serum sodium and plasma osmolality. CONCLUSION: Honey solution decreased urinary prostaglandins concentration and increased total urinary nitrite content whilst artificial honey decreased urinary nitrite and increased urinary prostaglandins.

Administration, Oral↗

PubMed1992

Possible mechanism of inhibition of nitrite-induced oxidation of oxyhemoglobin by ergothioneine and uric acid.

The time course of oxyhemoglobin oxidation by nitrite consisted of a kinetic lag followed by a transition phase which progressed into a rapid autocatalytic phase. The imidazolthione and imidazolone derivatives, ergothioneine and uric acid, respectively, caused an increase in the duration of the lag phase in a concentration-dependent manner, without affecting the onset and rate of the autocatalytic phase. Neither compound reacted with H2O2 or nitrite, oxidizing species required in the initiation steps of oxyhemoglobin oxidation. On the other hand, both compounds reduced effectively and at comparable rates the high oxidation state of hemoglobin, i.e., ferrylhemoglobin, which is an intermediate species occurring in the autocatalytic phase. In addition, the rate of ergothioneine oxidation, upon its reaction with ferrylmyoglobin, was accelerated by nitrite, thus suggesting a reaction between the thione and nitrogen dioxide. Nitrogen oxide and ferrylhemoglobin are key species in the free radical chain propagation leading to oxyhemoglobin oxidation by nitrite. These data support the view that ergothioneine and urate delay oxyhemoglobin oxidation by nitrite upon the temporary removal of the propagating species, i.e., nitrogen dioxide and, secondarily, ferrylhemoglobin, and within a mechanism encompassing alterations of the nitrite in equilibrium with nitrogen dioxide and ferrylhemoglobin in equilibrium with methemoglobin redox transitions.

Adult↗

PubMed1985

The effect of nitrite on cytochrome oxidase.

Nitrite inhibits the oxygen uptake by the system ferrocytochrome c-cytochrome oxidase with Ki = 1.5 mM. In the absence of ferrocytochrome c the oxygen uptake by cytochrome oxidase in the presence of nitrite was observed indicating that the enzyme has some nitrite oxidase activity. Nitrite induces changes in optical difference spectra of cytochrome oxidase and, in particular, the formation of the transient band at 607 nm. The reciprocal relation was observed between the intensity of this band and the rate of the oxygen uptake by cytochrome oxidase. This means that the form of the enzyme with this band does not involved in the nitrite oxidase activity. It is suggested that the nitrite oxidase activity relates to the oxygen binding site rather than the cytochrome c binding site of the enzyme.

Animals↗

PubMed1994

Human glutathione transferase catalysis of the formation of S-nitrosoglutathione from organic nitrites plus glutathione.

The kinetics of spontaneous and human glutathione transferase catalysed formation of S-nitrosoglutathione (GSNO) from glutathione (GSH) and n-butyl- or amyl nitrite have been studied. At physiological pH and temperature, k2 values of 22.3 and 21.0 M-1.min-1 were obtained for n-butyl- and amyl nitrites, respectively. Rate enhancements, (kcat/Km x k2) x 10(-4), due to purified human GSH transferases A1-1, A2-2 and M1a-1a were, respectively, 7.00, 2.94 and 10.6 for n-butyl nitrite and 121, 3.92 and 34.5 for amyl nitrite. GSH transferase P1-1 showed no detectable catalysis of the formation of GSNO. The data suggest that the presence of GSTs A1-1, A2-2 or M1-1 contribute substantially to intracellular metabolism of alkyl nitrites to GSNO. The results may be significant with regard to the immunotoxicity of alkyl nitrites.

Catalysis↗

PubMed1994

Exogenous NG-hydroxyl-L-arginine causes nitrite production in vascular smooth muscle cells in the absence of nitric oxide synthase activity.

Nitric oxide (NO) production from exogenous NG-hydroxy-L-arginine (OH-L-Arg) was investigated in rat aortic smooth muscle cells in culture by measuring nitrite accumulation in the culture medium. As well, the interaction between OH-L-Arg and L-arginine uptake via the y+ cationic amino acid transporter was studied. In cells without NO-synthase activity, OH-L-Arg (1-1000 microM) induced a dose-dependent nitrite production with a half-maximal effective concentration (EC50) of 18.0 +/- 1.5 microM (n = 4-7). This nitrite accumulation was not inhibited by the NO-synthase inhibitor NG-nitro-L-arginine methyl ester, L-NAME (300 microM). In contrast, it was abolished by miconazole (100 microM), an inhibitor of cytochrome P450. Incubation of vascular smooth muscle cells with LPS (10 micrograms/ml) induced an L-NAME inhibited nitrite accumulation, but did not enhance the OH-L-Arg induced nitrite production. OH-L-Arg and other cationic amino acids, L-lysine and L-ornithine, competitively inhibited [3H]-L-arginine uptake in rat aortic smooth muscle cells, with inhibition constants of 195 +/- 23 microM (n = 12), 260 +/- 40 microM (n = 5) and 330 +/- 10 microM (n = 5), respectively. These results show that OH-L-Arg is recognized by the cationic L-amino acid carrier present in vascular smooth muscle cells can be oxidized to NO and nitrite in these cells in the absence of NO-synthase, probably by cytochrome P450 or by a reaction involving a cytochrome P450 by-product.

Amino Acid Oxidoreductases↗

PubMed1982

The role of dietary nitrate and nitrite in the reductive deamination of sulfadiazine by the rat, guinea pig, and neonatal calf.

Previous metabolic depletion studies of 14C-sulfadiazine (SDZ) in the neonatal calf led to identification of two novel metabolites, 2-benzenesulfonamidopyrimidine (desNH2SDZ) and 2-benzenesulfonamido-4-hydroxypyrimidine. The novelty of the biotransformation prompted examination of mechanisms for the reductive deamination of SDZ in vivo. In subsequent work, it was found that neonatal calves did not consistently convert SDZ to desNH2SDZ; however, calves that were treated simultaneously with nitrite did. Further, when SDZ was given orally to guinea pigs, whose diet is high in nitrate and who demonstrate the capacity to reduce nitrate to nitrite in the oral cavity, SDZ was transformed to desNH2SDZ. Rats did not reductively deaminate SDZ even if they consumed a diet high in nitrate for two weeks prior to treatment with SDZ. However, they did so when nitrite was added to their diet. These observations strongly suggest that reductive deamination of sulfonamides is dependent on the ingestion of nitrite or the reduction of dietary nitrate to nitrite. This reduction of nitrate to nitrite proceeds in the oral cavity, presumably via microflora residing there.

Animal Feed↗

PubMed1991

Induction of nitrite production in mouse spleen cells by immunization.

Changes of nitrite production in mouse spleen cells of in vitro secondary antibody response were investigated. Mouse spleen cells immunized with gamma globulin fraction of rat serum produced nitrite 3 days after in vitro challenging with the same antigen. Nitrite production of rabbit IgG-challenged spleen cells was found to be about 2.9-times higher than that of spleen cells primed with the gamma globulin fraction of rat serum. Nitrite production in this system was completely suppressed by T cell depletion (99.7% inhibition). Furthermore, nitrite production in these cells significantly decreased by addition of anti-interferon gamma antibody (62.9% inhibition). These data indicate that nitrite production in antigen-immunized spleen cells is affected with the immunogenicity of an antigen and regulated by T cells, especially interferon (IFN) gamma.

Animals↗

PubMed1994

Growth of Listeria monocytogenes on vacuum-packed cooked meats: effects of pH, aw, nitrite and ascorbate.

Slices of cooked meats were inoculated with Listeria monocytogenes strain Murray B, vacuum-packed and stored at either 0 or 5 degrees C. Decreases in pH (6.9-5.9) and aw (0.993-0.960; adjusted with sodium chloride) of the cooked meats increased the lag time and reduced the growth rate at 5 degrees C. The type of meat (beef, pork, chicken or turkey) had no effect on the growth of the organism after allowance was made for pH. Sodium tripolyphosphate (0.3%) increased growth by increasing the pH of the cooked meat. Sodium nitrite reduced the growth rate and increased the lag time. Three microM of residual undissociated nitrite doubled the time taken for a 3 log increase in numbers of L. monocytogenes. The effectiveness of nitrite was significantly increased by sodium ascorbate (0.042%). In the absence of nitrite, ascorbate had no detectable effect on growth. The extent of growth at 0 degree C was similarly influenced by the interaction of pH, aw, nitrite and ascorbate, and was considerably less than at 5 degrees C. Quadratic equations were developed to describe some of the combined effects of pH, aw and residual nitrite on lag, growth rate and time for a 3 log increase in numbers of L. monocytogenes.

Animals↗

PubMed1989

Disruption of auditory function by acute administration of a "room odorizer" containing butyl nitrite in rats.

Butyl nitrite is the predominant and presumed active ingredient in a variety of commercial preparations sold as "room odorizers." These compounds have significant abuse potential, giving the user the sensation of a "rush", which may be related to their intense cardiovascular effects. The pharmacological properties of butyl nitrites are similar to those of amyl nitrite which is also abused for its psychological effects, but whose availability is limited by prescription for treatment of angina. A significant body of literature suggests that the inner ear is vulnerable to acute hypoxic exposure. Since butyl nitrite induces high levels of methemoglobin and also reduces blood pressure due to peripheral vasodilation, we hypothesized that this compound might produce auditory dysfunction. We studied the effect of acute exposure to a butyl nitrite "room odorizer" on 10- and 40-kHz auditory function in rats. A loss in auditory sensitivity was found at both frequencies on the day following administration of the compound. Auditory dysfunction tended to subside over the next several days at 40 kHz, although a significant loss of sensitivity for tones of 10 kHz was observed over a 6-day period after administration of the agent. Methemoglobin levels measured in rats of the same age were elevated significantly 30 and 60 min after butyl nitrite to levels of 30-45%. Methemoglobin levels were found to be normal 18 hr after administration when the first audiometric tests were conducted. The data suggest that auditory function in the middle of the rats' auditory range, 10 kHz, was disrupted for a longer period than was high-frequency (40 kHz) auditory function.

Air Pollutants↗

PubMed1986

Mutagen formation in the reaction of Maillard browning products, 2-acetylpyrrole and its analogues, with nitrite.

Three 2-substituted pyrroles (2-acetylpyrrole, pyrrole-2-carboxaldehyde and pyrrole-2-carboxylic acid), which are products of the Maillard browning reaction, were reacted with nitrite in buffer solution (pH 3) at 50 degrees C for 24 hr. The reaction mixtures were extracted with methylene chloride and the extracts were tested for mutagenicity using Salmonella typhimurium strains TA97, TA98, TA100, TA102 and TA104, with and without S-9 metabolic activation. The methylene chloride extract of the 2-acetylpyrrole-nitrite reaction mixture showed strong mutagenicity to all the tester strains, both in the presence and absence of S-9 mix. The reaction product of pyrrole-2-carboxaldehyde with nitrite only gave a weak mutagenic response with strain TA100, while the pyrrole-2-carboxylic acid-nitrite reaction product did not produce a mutagenic response in any of the tester strains. Two mutagenically active fractions, separated by thin-layer chromatography, were found in the reaction of 2-acetylpyrrole with nitrite. The formation of mutagenic products in the latter reaction was found to vary with reaction pH, time and temperature, with nitrite level and with 2-acetylpyrrole concentration.

Animals↗

PubMed1987

Estimation of dietary intake of nitrate and nitrite in Great Britain.

A survey was conducted of the dietary intake of nitrate and nitrite of 747 people aged 15-74 yr living in four regions in Britain. The mean intakes from food were estimated to be about 95 mg nitrate and 1.4 mg nitrite. Vegetables contributed over 90% of the nitrate intake and cured meats 65% of the nitrite intake. The contribution from drinking-water was estimated to add a further 13.5 mg, about 12% of total intake, but varied greatly depending upon water nitrate concentration. Residents of Oxford and the South-east had a higher intake of dietary nitrate, due to a greater vegetable consumption, whereas those from North Wales and the North-east had a higher nitrite intake due mainly to a greater consumption of bacon. The consumption of relatively low ascorbic acid/high nitrate vegetables was significantly greater in Oxford and the South-east. Smoking appeared to inhibit the uptake of circulating nitrate into the saliva, especially at higher levels of dietary nitrate intake. The efficiency of reduction of nitrate to nitrite in vivo and the effect of differing rates of this conversion on the relative importance of different dietary items as potential sources of nitrite are discussed.

Adolescent↗

PubMed1988

A possible role of the dietary fibre product, wheat bran, as a nitrite scavenger.

We found that wheat bran acted as a nitrite scavenger under conditions similar to those that exist in the stomach. Wheat flour and cellulose did not act as nitrite scavengers. Wheat bran, at a concentration equivalent to that in the stomach after ingestion of about two pieces of whole-wheat bread, reduces the nitrite concentration from 20 microM to about 10 microM in 60 min at pH 3.5 and 37 degrees C. At pH 2.5 and 1.5, most of the nitrite had disappeared in 10 min. At pH less than or equal to 2.5 the nitrite scavenging effect of bran was as efficient as that of ascorbic acid. Ferulic acid, a component of bran, reacted rapidly with 20 microM-nitrite both at pH 3.5 and 1.5, whereas phenolic lignin model compounds only reacted at pH 1.5.

Ascorbic Acid↗

PubMed1988

Reduction of benzo[a]pyrene-induced forestomach neoplasms in mice given nitrite and dietary soy sauce.

This study was conducted to determine the effects of nitrite (0.05% in drinking-water) and soy sauce (20% in a refined diet) on the initiation and promotion of benzo[a]pyrene-induced forestomach neoplasia in ICR mice. In two experiments nitrite and soy sauce together significantly reduced the number of neoplasms per animal. Soy sauce (without nitrite) produced a smaller apparent (non-significant) reduction whereas nitrite (without soy sauce) had no effect. Evidence suggested that soy sauce might contain factors that reduce calorie absorption or utilization, but this observation was independent of the inclusion of nitrite in the drinking-water and therefore could not by itself explain the significant reduction in neoplasms in mice given soy sauce plus nitrite. Protection appeared to primarily involve the tumour promotion stage.

Animals↗