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PubMed1995

The antitumor drug, 1,3-bis(2-chloroethyl)-1-nitroso-urea, inactivates human nicotinamide mononucleotide adenylyltransferase.

Nicotinamide mononucleotide (NMN) adenylyltransferase (EC 2.7.7.1) from human placenta is rapidly inactivated by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). A similar inactivation is observed with other C- and N-nitroso compounds. The inactivation by BCNU is dependent on incubation time, temperature and BCNU concentration. Protective reagents for -SH groups, dithiothreitol and beta-mercaptoethanol, and the substrate NMN are very effective in protecting NMN adenylyltransferase from BCNU inactivation and in preserving its catalytic properties, while ATP is less efficient. Incubation of BCNU-inactivated and dialysed NMN adenylyltransferase with dithiothreitol results in a partial recovery of the enzymatic activity.

Adenosine Triphosphate↗
PubMed1983

Alkylation of isolated chromatin with N-methyl-N-nitrosourea and N-ethyl-N-nitrosourea.

When isolated chromatin is incubated with the carcinogens N-methyl-N-nitrosourea (MeNU) and N-ethyl-N-nitrosourea (EtNU), DNA and chromosomal proteins become alkylated to increasingly greater extents as the carcinogen concentrations increase. With either MeNU or EtNU, the core and linker DNA of chromatin are alkylated to essentially identical extents. Alkylation of chromatin DNA as well as free DNA is drastically reduced at physiological ionic strengths (e.g. 0.15 M NaCl). The presence of 0.15 M NaCl, on the other hand, enhances alkylation of chromosomal proteins. While EtNU is much less reactive to DNA than MeNU, alkylation of chromosomal proteins relative to that of chromatin DNA has been found to be markedly greater with EtNU than with MeNU. Such a difference in their relative reactivities toward DNA and proteins may be related to the known difference of carcinogenic potency between these N-nitroso compounds.

Alkylation↗
PubMed1990

Nitrosamines as potential environmental carcinogens in man.

Nitrosamines are ubiquitous in our environment and diet. Many nitroso compounds are carcinogenic in animals and most probably in man. Nitrosamines are formed from the reaction of nitrite with primary, secondary, or tertiary amines in an acid medium. Nitrate should be considered as a nitrosating agent because it can be converted to nitrite by microbial action. Many aliphatic and nitrogen-containing heterocyclic compounds can be nitrosated to form carcinogenic substances. The occurrence in food and in some drugs of several nitrosamines or their nitrosatable precursors is described. Several tobacco-specific nitrosamines have been considered as possible causative agents for human cancer. Nitrosamines may be implicated in the induction of certain human gastric cancers.

Animals↗
PubMed1982

Chemical probes for tRNA tertiary structure. Comparative alkylation of tRNA with methylnitrosourea, ethylnitrosourea and dimethylsulfate.

The tertiary structure of tRNA in solution can be proved by chemical modification experiments. Three reagents, N-ethyl-N-nitrosourea, N-methyl-N-nitrosourea and dimethylsulfate which are known to alkylate nucleic acids at nucleophilic centers were compared. It is found that N-ethyl-N-nitrosourea and N-methyl-N-nitrosourea mainly react with phosphate residues and dimethylsulfate only with the bases. With dimethylsulfate the extent of alkylation of guanosines is about one order of magnitude higher than that of the phosphates by the nitroso compounds.

Alkylating Agents↗
PubMed1992

Involvement of the L-arginine-nitric oxide pathway in internal anal sphincter relaxation.

The purpose of this study was to examine the role of the L-arginine-nitric oxide pathway in neurogenic relaxation of the internal anal sphincter. Muscle strips representing the internal anal sphincter were prepared from 17 adult opossums. The preparations were mounted in organ baths for recording of isometric tension. N omega-nitro-L-arginine, an agent known to inhibit the L-arginine-nitric oxide pathway, concentration-dependently reduced relaxations induced by transmural field stimulation. At the highest concentration of N omega-nitro-L-arginine (10(-4) mol/L), no relaxation was evoked at any frequency tested (0.5-40 Hz). The inhibitory response to exogenous vasoactive intestinal polypeptide was unaffected by N omega-nitro-L-arginine pretreatment, indicating that vasoactive intestinal polypeptide relaxation does not use the L-arginine-nitric oxide pathway. In addition, responses to forskolin and sodium nitroprusside were not influenced by N omega-nitro-L-arginine preincubation, suggesting that the effect observed was not caused by a direct influence on the adenylate or the guanylate cyclases. It is concluded that the nonadrenergic, noncholinergic innervation of the internal anal sphincter involves an inhibitory substance generated from the L-arginine-nitric oxide pathway. Whether this substance is nitric oxide or a related nitroso compound remains to be settled.

Anal Canal↗
PubMed1996

Analysis of N-nitrosamines by high-performance liquid chromatography with post-column photohydrolysis and colorimetric detection.

N-Nitrosamines eluted from reversed-phase HPLC were quantitatively photohydrolysed in a UV photoreactor in aqueous solution to give the nitrite ion which could be determined colorimetrically with the Griess reagent. The chromatographic behavior of N-nitroso compounds (including 19 volatile dialkyl and 7 non-volatile N-nitrosamines) was studied on three octadecylsilane columns. The capacity factor varies linearly with the number of carbons atom of the n-dialkyl chains. N-nitrosamines bearing di-n-alkyl chains with the same number of carbon atoms could be separated with a highly polar mobile phase. The yield of photohydrolysis depends upon pH and time of exposure under UV light. The response was shown to be linear in the 0-200 ng range with a limit of detection of 8 pmoles injected for N-dialkyl nitrosamines. This limit was 20 pmoles for N-nitrosamines bearing two phenyl groups. Although N-nitrosamines could be detected at 230 nm without post-column reaction, such a reaction enhances the specificity of detection in biological matrices such as gastric juice or alcoholic beverages.

Beer↗
PubMed1994

Diazotization reaction of nitric oxide trapped by hemoglobin.

The present study addresses to determine whether hemoglobin within red blood cells can be utilized as a spin-trap agent for nitric oxide. We demonstrate the diazotization method coupled with a gel filtration chromatography, which is simply due to the separation of nitrosylhemoglobin from nitrite, nitrate or other low molecular nitroso-compounds in biological systems and to the liberation of nitric oxide from nitrosyl heme-complexes in the acidic condition. The amount of nitric oxide can be estimated by the difference of absorbances at 542 nm between diazo-compounds formed by Griess reagent and hemichrome by phosphoric acid. Our results indicate that hemoglobin in red cells as a spin-trap agent would be useful for monitoring nitric oxide in the circulation under the several disease states.

Chromatography, Gel↗
PubMed1976

Fixation and loss of hydrazine-induced premutational damage in Haemophilus influenzae.

Premutational damage induced in Haemophilus influenzae by hydrazine appears to be fixed as final mutation only at replication as judged by the transformation assay. Fixation at replication is independent of the rec1 gene, unlike the case with nitrosocarbaryl. Prior to replication premutational damage induced by hydrazine disappears by an unknown process that is not dependent on the presence of a pyrimidine dimer excision system nor on the rec1 gene. Hydrazine does not produce detectable single-strand breaks or alkali-labile sites in the treated DNA nor gaps in DNA newly synthesized after treatment. In these respects it also differs from nitroso compounds. It is concluded that hydrazine acts to produce and altered base, possibly N(4)-aminocytosine, that produces mutations by mispairing at replication rather than by error-prone repair.

Chromosomes, Bacterial↗
PubMed1976

A correlative study on the genetic damage induced by chemical mutagens in bone marrow and spermatogonia of mice. I. CNU-ethanol.

Cytogenetic damage induced by a wide range of concentrations of CNU-ethanol in mice was evaluated by determining the frequencies of (a) micro-nuclei in polychromatic erythrocytes of the bone marrow, (b) chromatid aberrations in bone marrow, (c) chromatid aberrations in spermatogonia, and (d) reciprocal translocations induced in spermatogonia and scored in spermatocytes. For CNU-ethanol the following order of sensitivity was found between the tests performed: micronuclei greater than aberrations in bone marrow greaer than aberrations in spermatogonia greater than translocations in spermatocytes. Correlation coefficients were calculated for the first three parameters. Positive correlations existed (a) between micronuclei in polychromatic erythrocytes and chromatid aberrations in bone marrow on the first day after treatment, and (b) between chromatid aberrations in bone marrow and spermatogonia at the first day after treatment. Three reciprocal translocations were induced in spermatogonia and recorded in primary spermatocytes; all were of a rare type, namely between an X chromosome and an autosome.

Animals↗
PubMed1977

Evidence that UV-inducible error-prone repair is absent in Haemophilus influenzae Rd, with a discussion of the relation to error-prone repair of alkylating-agent damage.

Haemophilus influenzae Rd and its derivatives are mutated either not at all or to only a very small extent by ultraviolet (UV) radiation, X-rays, methyl methanesulfonate, and nitrogen mustard, though they are readily mutated by such agents as N-methyl-N'-nitro-N-nitrosoguanidine, ethyl methanesulfonate, and nitrosocarbaryl. In these respects H. influenzae Rd resembles the lexA mutants of Escherichia coli that lack the SOS or reclex UV-inducible error-prone repair system. This similarity is further brought out by the observation that chloramphenicol has little or no effect on post-replication repair after UV irradiation. In E. coli, chloramphenicol has been reported to considerably inhibit post-replication repair in the wild type but not in the lexA mutant. Earlier work has suggested that most or all the mutations induced in H. influenzae by NC result from error-prone repair. Combined treatment with NC and either X-rays or UV shows that the NC error-prone repair system does not produce mutations from the lesions induced by these radiations even while it is producing them from its own lesions. It is concluded that the NC error-prone repair system or systems and the reclex error-prone system are different.

Alkylating Agents↗
PubMed1979

Nitrous acid mutagenesis of duplex DNA as a three-component system.

Purified native Hemophilus influenzae DNA is relatively insusceptible to nitrous acid (NA) mutagenesis in vitro, but is readily mutated following denaturation. NA mutagenicity for duplex DNA is significantly increased in the presence of various alcohols, glycols, phenols or primary amines. Phenol-extracted DNA contains dissociable contaminants of low molecular weight that enhance NA mutagenesis. Enhancement of NA mutagenesis by phenol and by spermine is due to the formation of unstable molecular species. We propose that reactive organic nitroso compounds are formed which then serve as delivery vehicles to promote mutagenicity of native DNA, perhaps via transnitrosation reactions. Similar reactions probably occur in vivo to promote NA-induced base substitution (but not frameshift) mutations in Salmonella typhimurium and in Escherichia coli. The possible significance of these observations to carcinogenesis is discussed.

DNA, Bacterial↗
PubMed1981

The influence of methyl substitution of the mutagenicity of nitronaphthalenes and nitrobiphenyls.

A series of nitrobiphenyls, nitronaphthalenes, and their methyl-substituted derivatives were assayed for mutagenicity toward S. typhimurium TA98 and TA100. In assays conducted in the absence of rat liver S9 fraction, substitution of a methyl group ortho to the nitro group decreased mutagenicity (3-methyl-4-nitrobiphenyl, 2-methyl-1-nitronaphthalene, and 3-methyl-2-nitronaphthalene). The mutagenicity of 4-nitrobiphenyl was also inhibited by methyl substitution at the 2'-position (2'-methyl-4-nitrobiphenyl), and at both the 3- and 2'-positions (3,2'-dimethyl-4-nitrobiphenyl). In assays conducted in the presence of rat liver S9 fraction, inhibition of mutagenicity by methyl substitution was demonstrated for 2-methyl-1-nitronaphthalene, 3-methyl-2-nitronaphthalene and 3,2'-dimethyl-4-nitrobiphenyl. Thus, methyl substitution of nitrobiphenyls and nitronaphthalenes generally decreased mutagenicity, when assays were conducted in the absence of rat liver S9 fraction. However, in the presence of rat liver S9 fraction, the inhibitory effect of methyl substitution on mutagenicity was less pronounced. These results contrast to the usual enhancing effect of ortho-methyl substitution of the corresponding aromatic amines and their N-oxidized derivatives (hydroxylamines and C-nitroso compounds).

Animals↗