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PubMed1968

Efficiency of nitrous acid as an inactivating and mutagenic agent of intact tobacco mosaic virus and its isolated nucleic acid.

When tobacco mosaic virus (TMV) and its isolated nucleic acid (TMV-RNA) were treated with nitrous acid, the nucleic acid was inactivated six times faster than the intact virus. Inactivation of both the infectious entities was exponential with treatment time to 0.1% level of survival. Eight different mutant phenotypes were scored after inactivation of TMV and TMV-RNA to 50, 10, 1.0, and 0.1% survival levels. Significantly more mutants in relation to unaltered isolates were induced at all levels of survival upon nitrous acid treatment of TMV than of TMV-RNA. Furthermore, the proportion of two specific mutant phenotypes was significantly greater in treated TMV than in treated TMV-RNA. No qualitative differences, however, were observed between the mutational spectra of nitrous acid-treated TMV and TMV-RNA. These results indicate that, in the intact virus, the viral capsid protects some of the sites involved in lethality; thus, proportionately more mutants are induced on nitrous acid treatment of TMV versus TMV-RNA.

Chemical Phenomena↗
PubMed2004

Exposure to NO2 and nitrous acid and respiratory symptoms in the first year of life.

BACKGROUND: Effects of nitrogen dioxide (NO2) on respiratory health have been the subject of extensive research. The outcomes of these studies were not consistent. Exposure to nitrous acid, which is a primary product of combustion, and is also formed when NO2 reacts with water, may play an important role in respiratory health. We estimate the independent effects of exposure to nitrogen dioxide and nitrous acid on respiratory symptoms during the first year of life. METHODS: Nitrogen dioxide and nitrous acid concentrations were measured once (1996-1998) in the homes of 768 infants who were at risk for developing asthma. Infants were living in southern New England. The frequency of respiratory symptoms in these children was recorded during the first year of life. RESULTS: Infants living in homes with an NO2 concentration exceeding 17.4 ppb (highest quartile) had a higher frequency of days with wheeze (rate ratio = 2.2; 95% confidence interval = 1.4-3.4), persistent cough (1.8; 1.2-2.7), and shortness of breath (3.1; 1.8-5.6) when compared with infants in homes that had NO2 concentrations lower than 5.1 ppb (lowest quartile), controlling for nitrous acid concentration. Nitrous acid exposure was not independently associated with respiratory symptoms. CONCLUSIONS: Among infants at risk for developing asthma, the frequency of reported respiratory symptoms in the first year of life was associated with levels of NO2 not currently considered to be harmful.

Air Pollution, Indoor↗
PubMed1999

Nitrous acid pretreatment of tendon xenografts cross-linked with glutaraldehyde and sterilized with gamma irradiation.

Collagenous xenografts made from kangaroo tail tendon cross-linked with glutaraldehyde have a potential application in the reconstruction of massive digital tendon deficits. However, a limitation to the clinical use of these xenografts has been the optimization of collagen cross-linking, and subsequent bio-incorporation and retention of mechanical properties following implantation. The purpose of this study was to evaluate the effect of nitrous acid on modulating the biologic and mechanical properties of tendon xenografts cross-linked with glutaraldehyde. Tendon xenografts were pretreated with 0.1 or 0.01 M nitrous acid solution, prior to cross-linking in 2% glutaraldehyde and sterilization by gamma irradiation. Xenografts were implanted intramuscularly in rabbits to examine biocompatability, and also used to repair ovine digital extensor tendon deficits to evaluate functional incorporation. Histologically, intramuscularly implanted nitrous acid pretreated xenografts in rabbits had a greater degree of diffuse cellular infiltration into interstitial splits in the graft than controls after 12 weeks. Xenografts implanted in an ovine extensor tendon deficit were evaluated after 26 and 52 weeks. Rate of failure of tenorrhaphies between host tendon and xenografts overall (15/21) was significantly greater (P < 0.05) than for autografts (1/21), suggesting that the holding power of sutures in xenografts was inferior to that obtained in autografts. Tensile failure stress of midsections of both nitrous acid pretreated and control xenografts was about 100 MPa prior to implantation (time zero). After 26 and 52 weeks, failure stress of both types of xenografts was significantly less than at time zero (P < 0.05). At 52 weeks, failure stress of nitrous acid pretreated xenografts (47.4 +/- 3.1 MPa) was significantly less than control xenografts (63.7 +/- 5.4 MPa); (P < 0.05). However, nitrous acid pretreated xenografts were similar to control xenografts in failure load (357 +/- 29 and 354 +/- 26 N, respectively), but they tended to have larger cross-sectional areas (7.6 +/- 0.5 versus 5.7 +/- 0.6 mm2, respectively) which were responsible for the lower calculated value for failure stress. Histologically, autografts maintained their normal tissue architecture and evoked a more limited cellular response in surrounding tissues than xenografts (P < 0.05). Both types of xenograft were surrounded by a thicker cuff of cellular response than autografts. However, compared to control xenografts, nitrous acid pretreated xenografts had more extensive fragmentation and splitting of collagen bundles, and more diffuse cellular and vascular infiltration into these interstitial splits, and these alterations were apparently contributing to the greater 'swelling' of these xenografts. It was concluded that pretreatment of tendon xenografts with nitrous acid modulated their biologic and material properties. Further studies are needed to elucidate the mechanism of these effects, and to determine if the protocol for tendon xenograft preparation could be optimized for improved clinical performance.

Animals↗
PubMed1999

Indoor, outdoor, and regional summer and winter concentrations of PM10, PM2.5, SO4(2)-, H+, NH4+, NO3-, NH3, and nitrous acid in homes with and without kerosene space heaters.

Twenty-four-hour samples of PM10 (mass of particles with aerodynamic diameter < or = 10 microm), PM2.5, (mass of particles with aerodynamic diameter < or = 2.5 microm), particle strong acidity (H+), sulfate (SO42-), nitrate (NO3-), ammonia (NH3), nitrous acid (HONO), and sulfur dioxide were collected inside and outside of 281 homes during winter and summer periods. Measurements were also conducted during summer periods at a regional site. A total of 58 homes of nonsmokers were sampled during the summer periods and 223 homes were sampled during the winter periods. Seventy-four of the homes sampled during the winter reported the use of a kerosene heater. All homes sampled in the summer were located in southwest Virginia. All but 20 homes sampled in the winter were also located in southwest Virginia; the remainder of the homes were located in Connecticut. For homes without tobacco combustion, the regional air monitoring site (Vinton, VA) appeared to provide a reasonable estimate of concentrations of PM2.5 and SO42- during summer months outside and inside homes within the region, even when a substantial number of the homes used air conditioning. Average indoor/outdoor ratios for PM2.5 and SO42- during the summer period were 1.03 +/- 0.71 and 0.74 +/- 0.53, respectively. The indoor/outdoor mean ratio for sulfate suggests that on average approximately 75% of the fine aerosol indoors during the summer is associated with outdoor sources. Kerosene heater use during the winter months, in the absence of tobacco combustion, results in substantial increases in indoor concentrations of PM2.5, SO42-, and possibly H+, as compared to homes without kerosene heaters. During their use, we estimated that kerosene heaters added, on average, approximately 40 microg/m3 of PM2.5 and 15 microg/m3 of SO42- to background residential levels of 18 and 2 microg/m3, respectively. Results from using sulfuric acid-doped Teflon (E.I. Du Pont de Nemours & Co., Wilmington, DE) filters in homes with kerosene heaters suggest that acid particle concentrations may be substantially higher than those measured because of acid neutralization by ammonia. During the summer and winter periods indoor concentrations of ammonia are an order of magnitude higher indoors than outdoors and appear to result in lower indoor acid particle concentrations. Nitrous acid levels are higher indoors than outdoors during both winter and summer and are substantially higher in homes with unvented combustion sources.

Air Pollutants↗
PubMed1977

Repair of nitrous acid damage to DNA in Escherichia coli.

A number of mutant strains of Escherichia coli have been examined for their sensitivity to nitrous acid and in some instances to methylmethanesulfonate. All ung- mutants tested are abnormally sensitive to nitrous acid. Since the ung mutation is phenotypically expressed as a defect in uracil DNA glycosidase, this observation supports the contention that treatment of cells with nitrous acid causes deamination of cytosine to uracil. In addition the observed sentitivity indicates that the ung gene is involved in the repair of uracil in DNA. Studies with other mutants suggest that both exonuclease III and DNA polymerase I of E. coli are involved in the repair of nitrous acid damage in vivo.

Cell Survival↗
PubMed1980

Nitrous acid damage to duplex deoxyribonucleic acid: distinction between deamination of cytosine residues and a novel mutational lesion.

The rate of nitrous acid deamination of labeled cytosine residues in native Escherichia coli deoxyribonucleic acid was monitored in vitro by release of acid-soluble counts after treatment with uracil deoxyribonucleic acid glycosylase. The reaction exhibited a lag and was not stimulate by several agents previously shown to enhance base substitution mutagenesis during nitrous acid treatment of duplex deoxyribonucleic acid. We conclude that a significant proportion of nitrous acid induced mutagenic lesions are novel lesions and not cytosine deaminations.

Cytosine↗
PubMed2006

Reactions of indoles with nitrogen dioxide and nitrous acid in an aprotic solvent.

The reaction of 2-phenyl- and 1-methyl-2-phenylindole with nitrogen dioxide or with nitrous acid (NaNO2-CH3COOH) in benzene leads mainly to the formation of the isonitroso and 3-nitroso indole derivatives, respectively. When reacted with nitrous acid, 1-methyl-2-phenylindole gives also the corresponding azo-bis-indole in good yields. The reaction of indole with nitrogen dioxide leads to 2-(indol-3-yl)-3H-indol-3-one as the main product together with small amounts of 2-(indol-3-yl)-3H-indol-3-oxime; whereas the major product obtained when the same indole is reacted with nitrous acid is represented by 2-(indol-3-yl)-3H-indol-3-oxime. The reaction of 3-alkyl substituted indoles with nitrogen dioxide is rather complex and results in the formation of different nitro indoles, whereas nitrosation is observed when nitrous acid is used. Crystal structures of 2-(indol-3-yl)-3H-indol-3-one and of 4-nitro-N-acetyltryptamine have been determined by X-ray analysis.

Magnetic Resonance Spectroscopy↗
PubMed1965

NITROUS ACID MUTATION OF TRANSFORMING DNA: CONSIDERATION OF MODE OF ACTION.

Apparently nitrous acid produces genetic alterations, expressed as antibiotic-resistant markers, directly on heat-denatured transforming DNA of Haemophilus influenzae, rather than producing DNA which acts as a non-specific mutagen. The markers which arise as a result of treatment with nitrous acid behave similarly to naturally occurring antibiotic markers. In addition, data comparing the expression and replication of induced markers to natural markers suggest that the nitrous acid-induced markers express and multiply in the same fashion as do "normal" markers. Therefore, mutations which require additional time to produce a functional DNA by a base-pair substitution, or by replication of the introduced DNA, are not responsible for the mutants observed.

Anti-Bacterial Agents↗
PubMed1975

A search for Saccharomyces cerevisiae mutants with an increased sensitivity to nitrous acid.

Six strains with an increased nitrous acid sensitivity were isolated (Fig. 1). The putative HNO2-sensitive mutants, as well as the parental strain 55R5 behaved abnormally in crosses, so that studies on the segregation of the sensitivity were difficult and unreliable. During 1.5 years the oversensitivity of the mutants gradually decreased to disappear completely (Tab. V). The differences in HNO2 sensitivity between respiratory-sufficient and cytoplasmic respiratory-deficient strains (Tab. I), as well as between different respiratory-sufficient strains (Tab. II-IV) are analysed.

Cell Nucleus↗
PubMed1995

Effects of nitrous acid exposure on human mucous membranes.

Nitrous acid (HONO) is formed both indirectly from the reaction of nitrogen dioxide (NO2) with water on indoor surfaces, and directly during combustion. This gaseous pollutant may be a previously unrecognized causal factor in assessments of nitrogen oxide exposure effects. The present study is the first attempt to evaluate exposure effects of HONO on the human airways and the mucous membranes of the eyes and nose. Fifteen healthy adult nonsmokers were exposed for 3.5 h in a double-blind, balanced protocol to clean air, 77, and 395 ppb HONO. Each exposure was preceded by a 1-h baseline measurement period, and exposures were separated by 1 wk. There was a 10-min exercise period during exposure. Effects measurements included assessment of bronchial reactivity, measurement of specific airway conductance, spirometry, acoustic rhinometry, nasal lavage, tear-fluid cytology, a CO2 eye-provocation test, evaluation of eye redness, and subjective sensations. Effects of HONO exposure on the eyes were found as exposure-related changes in tear-fluid cytology. In particular, the number of squamous cells increased by 20, 67, and 80% following exposure to clean air, 77, and 395 ppb HONO, respectively (p = 0.004). Possible indications of exposure effects on sensitivity to CO2 eye provocation and on specific airway conductance were also measured. For specific airway conductance there was an approximate 10% decrease in conductance following exercise in association with HONO exposure, compared with a 2% decrease with clean air (p = 0.038).

Adult↗
PubMed2000

Chemical synthesis of cross-link lesions found in nitrous acid treated DNA: a general method for the preparation of N2-substituted 2'-deoxyguanosines.

Treatment of DNA with nitrous acid results in the formation of DNA-DNA cross-links. Two cross-link lesions have previously been isolated and their structures assigned based on spectroscopic data. The major lesion has been proposed to consist of two deoxyguanosine (dG) nucleosides sharing a common N2 atom (1), while the structure of the minor lesion has been proposed to consist of a common nitrogen atom linking C2 of a dG nucleoside to C6 of deoxyadenosine (2). The chemical synthesis of 1 and 2, utilizing a palladium-catalyzed coupling, is described herein. It is demonstrated that the spectroscopic properties of synthetic 1 are identical to that of lesion 1 obtained from nitrous acid cross-linked DNA, thus providing a proof of its structure. Comparison of the limited spectroscopic data available for lesion 2 originating from nitrous acid cross-linked DNA to synthetic 2 supports its structural assignment. The synthetic approach used for synthesis of 1 and 2 is shown to be a general method for the preparation of a variety of N2-substituted dG nucleosides in good yields.

Catalysis↗
PubMed1977

Lethla effect of nitrous acid on Escherichia coli.

The effect of nitrous acid (NA) on viability, integrity of cellular DNA and on membrane transport were studied in 5 strains of Escherichia coli. Stationary phase cells, grown on mineral salts medium, were exposed to NA. The viability of strains decreased in thefollowing order: W3110 wild-type greater than WP2 wild-type, WP2 uvrA greater than NG30 recA greater than P3478 polA. Alterations were found in the DNA sedimentation profile in alkaline sucrose gradient. Disturbance of DNA synthesis was measured by 3H-labelled thymidine ([3H]Thd) incorporation. No degradation of DNA was found after NA treatment. Low doses of NA caused significant inhibition of leucine and glucose transport into whole cells. The results are interpreted in terms of the multi-target action of NA causing the death of cells.

Biological Transport, Active↗
PubMed2000

Mechanisms of killing of spores of Bacillus subtilis by iodine, glutaraldehyde and nitrous acid.

Treatment of wild-type spores of Bacillus subtilis with glutaraldehyde or an iodine-based disinfectant (Betadine) did not cause detectable mutagenesis, and spores (termed alpha-beta-) lacking the major DNA-protective alpha/beta-type, small, acid-soluble proteins (SASP) exhibited similar sensitivity to these agents. A recA mutation did not sensitize wild-type or alpha-beta- spores to Betadine or glutaraldehyde, nor did spore treatment with these agents result in significant expression of a recA-lacZ fusion when the treated spores germinated. Spore glutaraldehyde sensitivity was increased dramatically by removal of much spore coat protein, but this treatment had no effect on Betadine sensitivity. In contrast, nitrous acid treatment of wild-type and alpha-beta- spores caused significant mutagenesis, with alpha-beta- spores being much more sensitive to this agent. A recA mutation further sensitized both wild-type and alpha-beta- spores to nitrous acid, and there was significant expression of a recA-lacZ fusion when nitrous acid-treated spores germinated. These results indicate that: (a) nitrous acid kills B. subtilis spores at least in part by DNA damage, and alpha/beta-type SASP protect against this DNA damage; (b) killing of spores by glutaraldehyde or Betadine is not due to DNA damage; and (c) the spore coat protects spores against killing by glutaraldehyde but not Betadine. Further analysis also demonstrated that spores treated with nitrous acid still germinated normally, while those treated with glutaraldehyde or Betadine did not.

Bacillus subtilis↗
PubMed1995

Molecular weight manipulation of chitosan. I: Kinetics of depolymerization by nitrous acid.

The kinetics of the depolymerization of chitosan in dilute aqueous HCl solutions by nitrous acid were studied. The rate of depolymerization is independent of the molecular weight of chitosan, first order with respect to the concentrations of both nitrous acid and glucosamine moieties, not catalysed by either hydrogen or chloride ions, and Arrhenius temperature dependent. Chitosan exhibits significantly decreased reactivity as the degree of deacetylation of the polymer increases. These results are consistent with a depolymerization reaction mechanism in which the rate-limiting step is nitrosation of the unprotonated amine by nitrous acidium ion.

Carbohydrate Sequence↗
PubMed1976

Effects of growth temperature and caffeine on genetic responses of Candida albicans to ethyl methanesulfonate, nitrous acid and ultraviolet radiation.

Ultraviolet radiation is more effective than either ethyl methanesulfonate or nitrous acid in inducing reverse mutation from auxotrophy to prototrophy in C. albicans. The killing effect of each of the mutagens is greater for cells grown at 37 C than at 25 C after treatment; mutation frequencies are unaffected by post-treatment growth temperatures. Though caffeine depresses survival of mutagen treated cells at both 25 C or 37 C, its effect is more pronounced at 37 C. Caffeine has no effect on mutagenesis by nitrous acid or ethyl methanesulfonate; it depresses UV mutagenesis, but only at 37 C and at high UV dosages. These findings indicate that UV mutagenesis in C. albicans is mediated by a caffeine-sensitive, recombinational system for DNA repair analogous to those known to occur in other species of yeasts. The repair system of C. albicans is unique in being susceptible to caffeine only at high temperature and when the number of DNA lesions to be repaired is large. The caffeine-sensitive steps in repair critical to UV mutagenesis are not involved in fixing mutations induced by the chemical mutagens tested.

Amino Acids↗
PubMed1978

Cell-cycle variation in the induction of lethality and mitotic recombination after treatment with UV and nitrous acid in the yeast, Saccharomyces cerevisiae.

Exponentially growing yeast cultures separated into discrete periods of the cell cycle by zonal rotor centrifugation show cyclic variation in both UV and nitrous acid induced cell lethality, mitotic gene conversion and mitotic crossing-over. Maximum cell survival after UV treatment was observed in the S and G2 phases of the cell cycle at a time when UV induction of both types of mitotic recombination was at a minimum. In contrast, cell inactivation by the chemical mutagen nitrous acid showed a single discrete period of sensitivity which occurred in S phase cells which are undergoing DNA synthesis. Mitotic gene conversion and mitotic crossing-over were induced by nitrous acid in cells at all stages of the cell cycle with a peak of induction of both events occurring at the time of maximum cell lethality. The lack of correlation observed between maximum cell and the maximum induction of mitotic intragenic recombination suggest that other DNA-repair mechanisms besides DNA-recombination repair are involved in the recovery of inactivated yeast cells during the cell cycle.

Cell Cycle↗
PubMed1963

NITROUS ACID REACTIVATION OF ULTRAVIOLET-IRRADIATED TRANSFORMING DNA FROM HEMOPHILUS INFLUENZAE.

Partial recovery of ultraviolet-damaged denatured or native transforming DNA from Hemophilus influenzae, has been obtained by exposing the irradiated DNA in the denatured form to nitrous acid. Some factors that affect this recovery are described. An erythromycin marker (E(20)) was not reactivated. The UV damage reactivable by nitrous acid is different from that repaired by the photoreactivating enzyme from bakers' yeast. The pretreatment with nitrous acid affords a slight protection for denatured C(25) DNA and Sm(250) DNA against ultraviolet irradiation, but this pretreatment sensitized the E(20) DNA to this irradiation.

DNA↗