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PubMed1995

The Nir1 locus in barley is tightly linked to the nitrite reductase apoprotein gene Nii.

pBNiR1, a cDNA clone encoding part of the barley nitrite reductase apoprotein, was isolated from a barley (cv. Maris Mink) leaf cDNA library using the 1.85 kb insert of the maize nitrite reductase cDNA clone pCIB808 as a heterologous probe. The cDNA insert of pBNiR1 is 503 bp in length. The nucleotide coding sequence could be aligned with the 3' end of other higher plant nitrite reductase apoprotein cDNA sequences but diverges in the 3' untranslated region. The whole-plant barley mutant STA3999, previously isolated from the cultivar Tweed, accumulates nitrite after nitrate treatment in the light, has very much lowered levels of nitrite reductase activity and lacks detectable nitrite reductase cross-reacting material due to a recessive mutation in a single nuclear gene which we have designated Nir1. STA3999 has the characteristics expected of a nitrite reductase apoprotein gene mutant. Here we have used pB-NiR1 in RFLP analysis to determine whether the mutation carried by STA3999 is linked to the nitrite reductase apoprotein gene locus Nii. An RFLP was identified between the wild-type barley cultivars Tweed (major hybridising band of 11.5 kb) and Golden Promise (major hybridising band of 7.5 kb) when DraI-digested DNA was probed with the insert from the partial barley nitrite reductase cDNA clone, pBNiR1. DraI-digested DNA from the mutant STA3999 also exhibited a major hybridising band of 11.5 kb after hybridisation with the insert from pBNiR1.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗

PubMed2003

Nitrite as an energy-conserving electron sink for the acetogenic bacterium Moorella thermoacetica.

Nitrite served as an energy-conserving electron acceptor for the acetogenic bacterium Moorella thermoacetica. Growth occurred in an undefined (0.1% yeast extract) medium containing 20 m M glyoxylate and 5 m M nitrite and was essentially equivalent to that observed in the absence of nitrite. In the presence of nitrite, acetate (the normal product of glyoxylate-derived acetogenesis) was not detected during growth. Instead, growth was coupled to nitrite dissimilation to ammonium, and acetogenesis was limited to the stationary phase. Furthermore, membranes from glyoxylate-grown cells under nitrite-dissimilating conditions were deficient in the b-type cytochrome that is typically found in the membranes of acetogenic cells. Unlike glyoxylate, other acetogenic substrates (fructose, oxalate, glycolate, vanillin, and hydrogen) were not growth supportive in the undefined medium containing nitrite, and glyoxylate-dependent growth did not occur in a nitrite-supplemented, basal (without yeast extract) medium. Glyoxylate-dependent growth by Moorella thermoautotrophica was not observed in the undefined medium containing nitrite.

Acetates↗

PubMed1983

Mutagenicity of methyl nitrite in Salmonella typhimurium.

Methyl nitrite was tested for mutagenicity in Salmonella typhimurium TA1535. In the first set of experiments, plated bacteria were exposed to methyl nitrite in desiccators both in the absence and presence of a metabolizing system (S9 from Aroclor-pretreated Sprague-Dawley rats). Initial concentrations from 125 to 500 ppm were tested. In all experiments an increased initial concentration gave an increased mutagenic response. The mutagenic effect in the presence of S9 was similar to that in the absence of S9. Owing to difficulties in dose determinations in this type of experiment it could not be decided, unequivocally, whether the mutagenic effect was caused by methyl nitrite or its hydrolysis products. Experiments were therefore carried out in suspension, and the concentrations of methyl nitrite and inorganic nitrite were determined. Treatments with inorganic nitrite were also carried out under similar conditions. From the results of these experiments we concluded that methyl nitrite is mutagenic. Possible mechanisms of action of methyl nitrite are discussed, and it is suggested that mutagenicity may be a general property of alkyl nitrites.

Animals↗

PubMed2004

Oxidative stress and inhibition of oxidative phosphorylation induced by peroxynitrite and nitrite in rat brain subcellular fractions.

Nitrite and nitrate, two endogenous oxides of nitrogen, are toxic in vivo. Furthermore, the reaction of superoxide (produced by all aerobic cells) with nitric oxide (NO) generates peroxynitrite, a potent oxidizing agent, that can cause biological oxidative stress. Using subcellular fractions from rat brain hemispheres we studied oxidative stress induced by these nitrogen compounds with special emphasis on nitrite. The consumption of Vitamin C (ascorbate) and Vitamin E (alpha tocopherol), two of the important nutritional antioxidants, was followed in synaptosomes (nerve-ending particles) and mitochondria along with changes in parameters of mitochondrial oxidative phosphorylation. Nitrite, but not nitrate, oxidized ascorbate without oxidizing alpha tocopherol in both synaptosomes and mitochondria whereas peroxynitrite oxidized both ascorbate and alpha tocopherol. Functionally, both nitrite and peroxynitrite inhibited mitochondrial oxidative phosphorylation. Nitrite was less potent than peroxynitrite when the effects of equal concentrations of the two were compared. However, since nitrite is much more stable than peroxynitrite the impact of nitrite as an oxidant in vivo could be as much or even more significant than peroxynitrite. Nitrate would not have similar action unless it is reduced to nitrite. It is possible that nitrite may impair oxidative phosphorylation through modulating levels of nitric oxide, changing the activity of heme proteins or a mild uncoupling of mitochondria.

Animals↗

PubMed2006

The effects of topical treatment with acidified nitrite on wound healing in normal and diabetic mice.

The effects of the application of a nitric oxide generating acidified nitrite cream comprising sodium nitrite and citric acid, on the healing of incisional wounds in mice, has been investigated. The effects of acidified nitrite on wound healing were critically dependent on the time of application after wounding. Application of acidified nitrite starting on the day of wounding and on consecutive days thereafter significantly inhibited both half time to closure and extent of wound closure. Conversely, application starting on days 1-4 after wounding and on consecutive days thereafter significantly augmented the rate and extent of wound healing. Optimal effects on improving wound healing were observed with cream concentrations of 3.0% (w/v) sodium nitrite and 4.5% (w/v) citric acid. Starting application on day 5 after wounding had no effect on the rate or extent of wound healing. In diabetic Lepr db/db mice, starting treatment at day 2 after wounding, acidified nitrite at 3.0% (w/v) sodium nitrite and 4.5% (w/v) citric acid significantly increased the rate and extent of wound healing. This suggests that acidified nitrite is effective in improving wound healing against a diabetic background. The present data shows that acidified nitrite cream, a clinically effective means of topically delivering nitric oxide, augments the wound healing process and may be of clinical benefit.

Acids↗

PubMed1998

Ion chromatographic determination of nitrate and nitrite in meat products.

Nitrate and nitrite are usually added to processed meat products to provide protection against microorganisms that cause food poisoning. Nitrite may react with secondary amines to form nitrosoamines, a class of carcinogens. Nitrate, although it is more stable than nitrite, can act as a reservoir for nitrite. Thus, both nitrate and nitrite need to be monitored to ensure the quality and safety of meat products. In this paper, an accurate and sensitive method is described by which nitrate and nitrite are extracted from food samples, then analyzed by ion chromatography (IC). Commercial samples of ham and salami were analyzed by IC with UV absorbance detection. UV absorbance was specific for nitrate and nitrite, eliminating interference from other ions present at much higher concentrations. Recoveries of nitrate and nitrite were greater than 90%. The method was linear (r2 > 0.999) over the working range, and detection limits for nitrate and nitrite were 50 micrograms/l and 30 micrograms/l, respectively.

Animals↗

PubMed2001

The time-course change of nitrogenous excretion in the Kuruma shrimp Penaeus japonicus following nitrite exposure.

Penaeus japonicus (12.83 +/- 1.24 g) which were exposed individually to 0.002 (control), 0.076, 0.362, 0.719 and 1.433 mM nitrite at 30 ppt of salinity were examined for hemolymph ammonia, urea and nitrite, and nitrogenous excretion after 3, 6, 12, 24 and 48 h, respectively. Hemolymph nitrite and hemolymph urea increased directly with ambient nitrite and exposure time, whereas hemolymph ammonia was inversely related to ambient nitrite and exposure time. Specific excretions of total-N (total nitrogen), ammonia-N, urea-N and organic-N (organic nitrogen) increased directly with ambient nitrite and exposure time. The contribution of ammonia-N excretion and urea-N excretion in the total-N excreted by the control shrimp was 41.7-90.8 and 2.8-10.5%, respectively. The contribution of ammonia-N in the total-N excreted by P. japonicus decreased to 10.0 and 3.8%, when they were exposed for 24 h to 0.076 and 1.433 mM nitrite, respectively. The contribution of urea-N excretion increased to 58.7 and 21.4%, and the organic-N excretion increased to 31.3 and 74.8% in the total-N excreted by the shrimp following 24 h exposure to 0.076 and 1.433 mM nitrite, respectively. It was concluded that P. japonicus following 24 h exposure to nitrite as low as 0.076 mM increased its ammonia-N excretion by a factor of 1.9, its urea-N excretion by 200, and its organic-N excretion by 37, as compared to those in the control solution.

Ammonia↗

PubMedDate not supplied

Effects of nitrite and nitrate on the growth and acidogenicity of Streptococcus mutans.

UNLABELLED: It is hypothesised that exogenous nitrite acidified by metabolic products of acidogenic bacteria in the mouth will be converted to products which inhibit growth of the bacteria in question which contribute to dental caries. OBJECTIVES: The aims of this study were (1) to test the activity of both sodium nitrate and sodium nitrite at differing concentrations on the ability of Streptococcus mutans to lower the pH of its surroundings and hence (2) to determine whether either nitrate or nitrite might be bactericidal or bacteriostatic against S. mutans. METHODS: S. mutans NCTC 10449(T) was cultured in a liquid medium to which either sodium nitrate or sodium nitrite was added to a final concentration of 0.0, 0.2, 2.0, 20 or 200 mM, of which the first acted as a test substance negative control. After 24 h, the cultures were streaked onto agar to test for growth and the remaining culture used for pH measurement. The Mann-Whitney U-Test was used for statistical comparison of pH values. RESULTS: Nitrite at concentrations of 20 and 200 mM had a highly significant inhibitory effect (p < 0.001) on the ability of S. mutans NCTC 10449(T) to lower pH. Moreover, bacteria that had been subjected to these levels of nitrite were unable to recover on solid medium. Nitrate had no such effect on either the growth of the bacteria or on their ability to lower pH. CONCLUSIONS: It is concluded that nitrite, at final concentrations of either 20 or 200 mM, is both bactericidal and anti-acidogenic with respect to S. mutans, while lower concentrations of nitrite and all concentrations of nitrate are ineffective. Nitrite might be worthy of consideration as a mouth-rinse constituent.

Actinomyces↗

PubMed2003

Plasma nitrite reflects constitutive nitric oxide synthase activity in mammals.

Changes in plasma nitrite concentration in the human forearm circulation have recently been shown to reflect acute changes in endothelial nitric oxide synthase (eNOS)-activity. Whether basal plasma nitrite is a general marker of constitutive NOS-activity in vivo is yet unclear. Due to the rapid metabolism of nitrite in blood and the difficulties in its analytical determination literature data on levels of nitrite in mammals are largely inconsistent. We hypothesized that constitutive NOS-activity in the circulatory system is relatively uniform throughout the mammalian kingdom. If true, this should result in comparable systemic plasma nitrite levels in different species. Using three different analytical approaches we determined plasma nitrite concentration to be in a nanomolar range in a variety of species: humans (305 +/- 23 nmol/l), monkeys (367 +/- 62 nmol/l), minipigs (319 +/- 24 nmol/l), dogs (305 +/- 50 nmol/l), rabbits (502 +/- 21 nmol/l), guinea pigs (412 +/- 44 nmol/l), rats (191 +/- 43 nmol/l), and mice (457 +/- 51 nmol/l). Application of different NOS-inhibitors in humans, minipigs, and dogs decreased NOS-activity and thereby increased vascular resistance. This was accompanied by a significant, up to 80%, decrease in plasma nitrite concentration. A comparison of plasma nitrite concentrations between eNOS(-/-) and NOS-inhibited wild-type mice revealed that 70 +/- 5% of plasma nitrite is derived from eNOS. These results provide evidence for a uniform constitutive vascular NOS-activity across mammalian species.

Animals↗

PubMed2003

Characterization of the magnitude and kinetics of xanthine oxidase-catalyzed nitrate reduction: evaluation of its role in nitrite and nitric oxide generation in anoxic tissues.

In addition to nitric oxide (NO) generation from specific NO synthases, NO is also formed during anoxia from nitrite reduction, and xanthine oxidase (XO) catalyzes this process. While in tissues and blood high nitrate levels are present, questions remain regarding whether nitrate is also a source of NO and if XO-mediated nitrate reduction can be an important source of NO in biological systems. To characterize the kinetics, magnitude, and mechanism of XO-mediated nitrate reduction under anaerobic conditions, EPR, chemiluminescence NO-analyzer, and NO-electrode studies were performed. Typical XO reducing substrates, xanthine, NADH, and 2,3-dihydroxybenz-aldehyde, triggered nitrate reduction to nitrite and NO. The rate of nitrite production followed Michaelis-Menten kinetics, while NO generation rates increased linearly following the accumulation of nitrite, suggesting stepwise-reduction of nitrate to nitrite then to NO. The molybdenum-binding XO inhibitor, oxypurinol, inhibited both nitrite and NO production, indicating that nitrate reduction occurs at the molybdenum site. At higher xanthine concentrations, partial inhibition was seen, suggesting formation of a substrate-bound reduced enzyme complex with xanthine blocking the molybdenum site. The pH dependence of nitrite and NO formation indicate that XO-mediated nitrate reduction occurs via an acid-catalyzed mechanism. With conditions occurring during ischemia, myocardial xanthine oxidoreductase and nitrate levels were determined to generate up to 20 microM nitrite within 10-20 min that can be further reduced to NO with rates comparable to those of maximally activated NOS. Thus, XOR catalyzed nitrate reduction to nitrite and NO occurs and can be an important source of NO production in ischemic tissues.

Animals↗

PubMed2004

Mechanisms of ferriheme reduction by nitric oxide: nitrite and general base catalysis.

The reductive nitrosylation (Fe(III)(P) + 2NO + H(2)O = Fe(II)(P)(NO) + NO(2)(-) + 2H(+)) of the ferriheme model Fe(III)(TPPS) (TPPS = tetra(4-sulfonatophenyl)porphyrinato) has been investigated in moderately acidic solution. In the absence of added or adventitious nitrite, this reaction displays general base catalysis with several buffers in aqueous solutions. It was also found that the nitrite ion, NO(2)(-), is a catalyst for this reaction. Similar nitrite catalysis was demonstrated for another ferriheme model system Fe(III)(TMPy) (TMPy = meso-tetrakis(N-methyl-4-pyridyl)porphyrinato), and for ferriheme proteins met-hemoglobin (metHb) and met-myoglobin (metMb) in aqueous buffer solutions. Thus, it appears that such catalysis is a general mechanistic route to the reductive nitrosylation products. Two nitrite catalysis mechanisms are proposed. In the first, NO(2)(-) is visualized as operating via nucleophilic addition to the Fe(III)-coordinated NO in a manner similar to the reactions proposed for Fe(III) reduction promoted by other nucleophiles. This would give a labile N(2)O(3) ligand that hydrolyzes to nitrous acid, regenerating the original nitrite. The other proposal is that Fe(III) reduction is effected by direct outer-sphere electron transfer from NO(2)(-) to Fe(III)(P)(NO) to give nitrogen dioxide plus the ferrous nitrosyl complex Fe(II)(P)(NO). The NO(2) thus generated would be trapped by excess NO to give N(2)O(3) and, subsequently, nitrite. It is found that the nitrite catalysis rates are markedly sensitive to the respective Fe(III)(P)(NO) reduction potentials, which is consistent with the behavior expected for an outer-sphere electron-transfer mechanism. Nitrite is the product of NO autoxidation in aqueous solution and is a ubiquitous impurity in experiments where aqueous NO is added to an aerobic system to study biological effects. The present results demonstrate that such an impurity should not be assumed to be innocuous, especially in the context of recent reports that endogenous nitrite may play physiological roles relevant to the interactions of NO and ferriheme proteins.

Catalysis↗

PubMed2006

Effects of nitrite and nitrate on DNA damage induced by ultraviolet light.

UV light is a major cause of human skin cancers. Nitrite and nitrate are well-known potential risk factors for gastric cancer. Little attention has been paid to the relationship between UV light and nitrite or nitrate on cancer. We examined the effects of nitrite and nitrate on the damage to nucleosides and DNA induced by UV light from a mercury lamp and by sunlight at neutral pH. A biologically relevant dose of nitrite and nitrate increased the generation of nucleobases and malondialdehyde on the reaction of nucleosides and DNA with UV light. The efficiency of nitrite enhancing the reaction was higher than that of nitrate at low doses. The contribution of the hydroxyl radical as the reactive species was suggested from the results of the inhibitory effects of hydroxyl radical scavengers. Nitrite and nitrate also enhanced the formation of nucleobases and malondialdehyde from DNA induced by sunlight. In the presence of 5 muM nitrite, the concentration in human skin cells, the product yields by sunlight were 5-10-fold greater than those in the absence of nitrite. The addition of 80 muM NO(3)(-), a concentration in human skin cells, also increased the yields significantly. Nitrite and nitrate may play a role in enhancing the genotoxic effects of UV light in humans.

Animals↗

PubMed2006

Thiocyanate cannot inhibit the formation of reactive nitrogen species in the human oral cavity in the presence of high concentrations of nitrite: detection of reactive nitrogen species with 4,5-diaminofluorescein.

In the human oral cavity, nitrite is reduced to nitric oxide (NO) by certain bacteria. 4,5-Diaminofluorescein (DAF-2) was transformed to a fluorescent component triazolfluorescein (DAF-2T) in a bacterial fraction of saliva in the presence of nitrite. No detectable consumption of DAF-2 and formation of DAF-2T were observed in bacterial fraction in the absence of nitrite. The nitrite-dependent transformation of DAF-2 to DAF-2T was inhibited by catalase, SCN(-), and CN(-) suggesting the participation of peroxidases in saliva in the transformation. The formation of DAF-2T, which was observed by the addition of an NO generating reagent (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (NOR 3) to bacterial fraction, was also inhibited by catalase, SCN(-), and CN(-). The degree of the inhibition by SCN(-) decreased as the concentration of nitrite or NOR 3 was increased. Superoxide dismutase (SOD) enhanced nitrite- and NOR 3-induced fluorescence increase in the bacterial fraction, and the degree of the enhancement decreased as the concentrations of nitrite and NOR 3 were increased. In whole saliva filtrate, the inhibitory effects of SCN(-) on the fluorescence increase decreased as the concentration of nitrite was increased, but the enhancement by SOD was not significantly affected by the increase in the concentration of nitrite. As salivary bacteria produce O(2)(-), H(2)O(2), and NO and as peroxidase/H(2)O(2)/nitrite systems in saliva produce NO(2), the effects of SCN(-) are discussed taking SCN(-)-dependent inhibition of NO(2) formation by peroxidases in saliva into consideration and the effects of SOD are discussed taking O(2)(-)-dependent consumption of NO into consideration. It is concluded that when the rate of the formation of NO is high, SCN(-) is not effective enough to inhibit the formation of N(2)O(3) in the oral cavity.

Chromatography, High Pressure Liquid↗

PubMed1996

Plasma nitrate plus nitrite changes during continuous intravenous infusion interleukin 2.

Nitric oxide (NO), a biologically active mediator generated in many cell types by the enzyme NO synthase, may play an important role in cardiovascular toxicity that is frequently observed in cancer patients during intravenous (i.v.) interleukin 2 (IL-2) therapy. The induction of NO synthase and the production of NO seem to be involved in the pathogenesis of the vascular leakage syndrome, as well as in the regulation of myocardial contractility. In the present study, we evaluated the pattern of plasmatic NO changes during multiple cycles of continuous i.v. infusion (CIVI) of IL-2 in ten advanced cancer patients (five males, five females, median age 59 years, range 33-67 years; eight affected by renal cell cancer and two affected by malignant melanoma). The patients received IL-2 at 18 MIU m-2 day-1 (14 cycles) or 9 MIU m-2 day-1 (seven cycles) for 96 h, repeated every 3 weeks. Interferon alpha (IFN alpha) was also administered subcutaneously (s.c) during the 3 week interval between IL-2 cycles. For each cycle, plasma samples were collected before treatment (t0), 24 h (t1), 48 h (t2), 72 h (t3) and 96 h (t4) after the start of IL-2 infusion, and 24 h after the end of the cycle. NO concentration was determined spectrophotometrically by measuring the accumulation of both nitrite and nitrate (after reduction to nitrite). The following observations may be drawn from data analysis: (1) plasma nitrate + nitrite significantly raised during treatment (P = 0.0226 for t0 vs t3), but statistical significance was retained only when cycles administered with IL-2 18 MIU m-2 day-1 are considered (P = 0.0329 for t0 vs t3; P = 0.0354 for t0 vs t2 vs t4) (dose-dependent pattern); (2) during subsequent cycles a significant trend toward a progressive increase of plasma nitrate + nitrite levels, with increasing cumulative dose of IL-2, was observed (linear regression coefficient r = 0.62, P = 0.0141 for t0; r = 0.80, P = 0.0003 for t1; r = 0.62, P = 0.013 for t2; r = 0.69, P = 0.045 for t3); (3) plasma nitrate + nitrite levels peaked earlier in subsequent cycles than in the first cycle; (4) all patients experienced hypotension. The mean of the systolic blood pressure values was significantly lower at the time of plasma nitrate + nitrite peak than at t0 (P = 0.0004); (5) the two cases of grade III hypotension occurred in patients with the higher mean and peak plasma nitrate + nitrite values. We conclude that determination of plasma nitrate + nitrite levels during CIVI IL-2 can usefully estimate, in a dose-dependent pattern, the degree of peripheral vascular relaxation and capillary leakage associated with cytokine action, clinically manifested as hypotension. However, isolated cardiac toxicity that continues to represent a relevant problem during IL-2 therapy, does not appear to correlate with plasma nitrate + nitrite levels; therefore, further studies are required to understand adequately the mechanisms underlying IL-2-induced cardiac toxicity.

Adult↗

PubMed2006

Ceruloplasmin is a NO oxidase and nitrite synthase that determines endocrine NO homeostasis.

Nitrite represents a bioactive reservoir of nitric oxide (NO) that may modulate vasodilation, respiration and cytoprotection after ischemia-reperfusion injury. Although nitrite formation is thought to occur via reaction of NO with oxygen, this third-order reaction cannot compete kinetically with the reaction of NO with hemoglobin to form nitrate. Indeed, the formation of nitrite from NO in the blood is limited when plasma is substituted with physiological buffers, which suggests that plasma contains metal-based enzymatic pathways for nitrite synthesis. We therefore hypothesized that the multicopper oxidase, ceruloplasmin, could oxidize NO to NO+, with subsequent hydration to nitrite. Accordingly, plasma NO oxidase activity was decreased after ceruloplasmin immunodepletion, in ceruloplasmin knockout mice and in people with congenital aceruloplasminemia. Compared to controls, plasma nitrite concentrations were substantially reduced in ceruloplasmin knockout mice, which were more susceptible to liver infarction after ischemia and reperfusion. The extent of hepatocellular infarction normalized after nitrite repletion. These data suggest new functions for the multicopper oxidases in endocrine NO homeostasis and nitrite synthesis, and they support the hypothesis that physiological concentrations of nitrite contribute to hypoxic signaling and cytoprotection.

Animals↗

PubMed2005

Nitrate and nitrite transport in Escherichia coli.

Two polytopic membrane proteins, NarK and NarU, are involved in nitrate and nitrite uptake and nitrite extrusion by Escherichia coli. A third polytopic membrane protein, NirC, functions only in nitrite transport. During exponential growth, the quantity of NarU in membrane fractions was <0.01% of the quantity of NarK. During the stationary phase of growth, the ratio of NarU to NarK increased to 0.1%. However, in the exponential phase of growth, the strain expressing only NarK transports and reduces nitrate and nitrite at a rate only slightly higher than that of the strain expressing only NarU, indicating that, in a NarK(+) strain, the rate of nitrate reduction is not limited by the rate of nitrate transport. By measuring nitrate and nitrite transport abilities of strains expressing only narK or expressing both narK and nirC, we hypothesized that NarK might function as a primary nitrate-nitrite antiporter. After nitrate is imported by NarK and reduced to nitrite, some nitrite is expelled from the cell and then reimported for reduction to ammonia. Two highly conserved positively charged residues, Arg-87 and Arg-303 of NarU, were shown by site-directed mutagenesis to play a key role in anion transport. This result indicates that NarU might form a single channel for nitrate and nitrite transport.

Bacterial Proteins↗

PubMed2001

Antimicrobial effect of acidified nitrite on dermatophyte fungi, Candida and bacterial skin pathogens.

AIMS: Nitric oxide is generated from sweat nitrite in the acidic environment of the skin surface and is thought to contribute to protection against infection. This study examined the sensitivity of Trichophyton mentagrophytes, T. rubrum, Candida albicans, Streptococcus pyogenes, Staphylococcus aureus and Propionibacterium acnes to acidified nitrite. METHODS AND RESULTS: Organisms were cultured in varying concentrations of nitrite and pH for different lengths of time, before being transferred to recovery medium. With the exception of Strep. pyogenes, addition of nitrite increased the antimicrobial activity of acid solutions against all organisms tested. The rank order of sensitivity was: C. albicans < T. rubrum < T. mentagrophytes < Staph. aureus < P. acnes, with P. acnes being most sensitive. CONCLUSION: This work has shown that acidified nitrite is microbiocidal to common cutaneous pathogens. The concentrations of nitrite required to kill pathogenic fungi and bacteria in in vitro assays were higher than the concentrations of nitrite measured in sweat. However, additional co-factors in vivo and in sweat may potentiate the effect of acidified nitrite. SIGNIFICANCE AND IMPACT OF THE STUDY: Pharmacological preparations of acidified nitrite are novel antimicrobial agents. These data suggest skin organisms which may be sensitive to this treatment.

Acids↗

PubMed1989

Nitrite and nitrate levels in ileostomy effluent: effect of dietary change.

1. Nitrite and nitrate levels were measured in samples from ileostomy bags or stomal samples of thirty-one ileostomists (twenty-two ulcerative colitis, nine Crohn's disease), 14-16 h after ingestion of a conventional meal or a meal containing a high content of nitrite and nitrate. 2. Ileostomy samples were decolourized with barium chloride, sodium sulphate and charcoal. Nitrite was determined spectrophotometrically by the Griess reaction and nitrate determined as nitrite after reduction with nitrate reductase (EC 1.7.99.4) in the presence of sodium formate. The mean percentage recovery from twenty-six spiked samples was 101.9 (SE 3.5)% for nitrite and 82.9 (SE 3.3)% for nitrate. 3. Ileostomy bag samples were obtained in twenty-nine cases of which ten had measurable nitrite (median 0, range 0-20.7 nmol/g) on a conventional meal compared with twenty-three cases (median 7.2, range 0-31.1 nmol/g) on the test meal (P less than 0.01). Nitrate levels were measurable in sixteen (median 6.7, range 0-48.2 nmol/g) after a conventional meal compared with twenty-one (median 20.5, range 0-53.2 nmol/g) after the test meal (P less than 0.01). 4. Stomal fresh-catch samples were obtained in twenty-four cases: combined nitrate and nitrite was higher in eighteen, lower in four and unchanged in two subjects after the test meal (P less than 0.05). 5. The type of foodstuff ingested can significantly alter measurable levels of nitrite-nitrate in the distal ileum and is one factor determining nitrite-nitrate input into the proximal colon.

Diet↗