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PubMed1987

Urinary and faecal mutagenicity in Sprague-Dawley rats dosed with the food mutagens quercetin and rutin.

The natural flavonoid quercetin was administered to Sprague-Dawley rats by ip injection or gastric intubation of a single dose of 500, 1000 or 2000 mg/kg body weight. Mutagenicity assays with Salmonella typhimurium strain TA98 showed moderate mutagenic activity in the urines and faecal extracts but not in plasma samples from the treated animals. The mutagenic activity detected in the urines accounted for about 0.5% of the administered dose, irrespective of the route of administration and the dose level. Higher mutagenicity was demonstrated in faecal extracts. Rutin (quercetin-3-O-rutinoside) was administered by gavage and ip injection at 2000 mg/kg. Although the chemical was inactive as a mutagen in vitro, significant mutagenicity was detected in the urines and faecal extracts of the treated rats. Such activity was similar to that detected after administration of free quercetin in a dose some four times lower (by weight).

Animals↗
PubMed1998

Lack of mammalian mutagenicity of the potent bacterial mutagen tris(2,3-dibromopropyl) phosphate and its metabolite 2-bromoacrolein.

The flame retardant tris(2,3-dibromopropyl)phosphate (Tris-BP) and its metabolite 2-bromoacrolein (2BA) are very potent bacterial mutagens in Salmonella typhimurium (S. typhimurium) TA 100. In this study, we showed that 2BA and Tris-BP are also mutagenic in S. typhimurium TA 104, which detects mutations at AT base pairs, while TA 100 detects mutations at CG basepairs. We also studied the mutagenicity of 2BA in mammalian cells in vitro and in the rat in vivo. Firstly, 2BA was tested in the human lymphoblastoid cell line TK6. The results showed that there was no increase in mutation frequency at the hprt locus, whereas there was a large decrease in cell survival. Secondly, a shuttle vector system was used to study the induction of mutations by 2BA:DNA adducts. The vector was modified by insertion of a single-stranded oligonucleotide containing on average one 2BA:DNA adduct. No increase in mutation frequency above background was detected after replication of this vector in SV40 transformed normal human fibroblasts. Because the liver is a major site for bioactivation of Tris-BP to 2BA in vivo, we tested the initiating capacity of Tris-BP in the rat liver in a modified Solt & Farber initiation and promotion system. Administration of Tris-BP resulted in a small increase in the number of preneoplastic gamma-glutamyl-transpeptidase positive (GGT+) foci in the liver compared to control animals (only significant in the lowest size class). Modification of the experimental protocol by performing partial hepatectomy 24 h after the administration of Tris-BP, did not increase the number of GGT+ or glutathione S-transferase-P (GST-P+) positive foci above the control level. Taken together, these results indicate that, in spite of a high mutagenicity in S. typhimurium, 2BA and Tris-BP have low or negligible mutagenic effects in mammalian systems. The lack of mutagenic activity may explain why Tris-BP is not a carcinogen in the rat liver.

Acrolein↗
PubMedDate not supplied

Effect on mutagenicity of the stepwise removal of hydroxyl group and chlorine atoms from 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone: 13C NMR chemical shifts as determinants of mutagenicity.

The response of mutagenicity to the stepwise replacement of chlorine atoms and the hydroxyl group by hydrogen in 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX, 1) was determined in several assays by using Salmonella typhimurium tester strain (TA100). In all, eight MX derivatives were assayed. Several were studied together in at least one assay. In addition to MX, the seven included 3-chloro-4-(dichloromethyl)-2(5H)-furanone (RMX, 2), 3-chloro-4-(chloromethyl)-5-hydroxy-2(5H)-furanone (3), 3-chloro-4-(chloromethyl)-2(5H)-furanone (4), 4-(chloromethyl)-5-hydroxy-2(5H)-furanone (5), 4-chloromethyl-2(5H)-furanone (6), and 4-(dichloromethyl)-2(5H)-furanone (8). Compounds 1-6 were mutagenic. Compound 8 gave erratic results. 4-(Acetoxymethyl)-2(5H)-furanone (11) was nonmutagenic. The largest drop in mutagenicity amounted to a factor of about 10(2) for the replacement of the hydroxyl group or a C-3 chlorine atom from 3. Other replacements of the hydroxyl group or a C-3 or C-6 chlorine atom amounted to mutagenicity diminished by a factor of only 10. On the basis of the rates of UV spectral changes under assay conditions, chemical half-life values (ct 1/2) for 1-6 and 8 were estimated as indicators of compound stability. However, mutagenicity differences were shown to result principally from the intrinsic mutagenicities of the six compounds 1-6 rather than from differences in stability.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon Isotopes↗
PubMed1995

A new mutagenicity assay method for frameshift mutagens based on deleting or inserting a guanosine nucleotide in the beta-lactamase gene.

The conventional method of site-directed mutagenesis was used to develop two Salmonella strains, JK-1 and JK-2, for detecting frameshift mutagens. The JK-1 strain was derived from Salmonella typhimurium TA1537 strain transformed by a mutant construct. A guanosine nucleotide was inserted between nucleotide residues 312 and 313 of the beta-lactamase gene. The JK-2 strain was obtained by the same procedure, but a guanosine nucleotide in position 315 of the beta-lactamase gene was deleted. The strains were tested with ten frameshift mutagens and the revertants were selected by ampicillin resistance. Representative mutagens including 2-nitrofluorene (2-NF), 2-acetylaminofluorene (AAF), 9-aminoacridine (9-AA), 2,7-diaminofluorene (2,7-DAF) and 2-methoxy-6-chloro-9-(3-(ethyl-2-chloro-ethyl)-aminopropylamino)acridine (ICR-170) were more potent in the JK-1 strain than the JK-2 strain, and the number of revertant colonies were dose related. Under the same conditions, the ampicillin test was more sensitive than the Ames test. Other types of compounds such as 2-methoxy-6-chloro-9-(2-chloroethylaminopropylamino)acridine (ICR-191), benzo[a]pyrene (BP), 4-nitroquinoline N-oxide (4-NQNO), hycanthone and aflatoxin B1 (AFB1) were not as mutagenic to these new strains. The method is quite promising for studying certain specific frameshift mutagens, but more chemical mutagens should be tested to validate its applicability and reproducibility in general use.

Amino Acid Sequence↗
PubMed1996

Distinction of mutagenic carcinogens from a mutagenic noncarcinogen in the big blue transgenic mouse.

The aromatic amines 2,4-diaminotoluene (2,4-DAT) and 2,6-diaminotoluene (2,6-DAT) are structural isomers that have been extensively studied for their mutagenic and carcinogenic characteristics. Both compounds are rapidly absorbed after oral administration and are equally mutagenic in the Ames test; however, 2,4-DAT is a potent hepatocarcinogen, whereas 2,6-DAT does not produce an increased incidence of tumors in rats or mice at similar doses. The Big Blue transgenic B6C3F1 mouse carries multiple copies of the lacl mutational target gene. Our studies were designed to determine whether the Big Blue system could be used to detect differences in the vivo mutagenic activity between the carcinogen-noncarcinogen pair 2,4-DAT and 2,6-DAT and to determine whether the in vivo mutagenesis assay results correspond to the rodent carcinogen bioassay results. Male B6C3F1 transgenic mice were exposed to 2,4-DAT or 2,6-DAT at 0 or 1,000 ppm in the diet for 30 and 90 days or to dimethylnitrosamine as a positive control. Mutant frequencies were nearly identical for all three groups at 30 days, while at 90 days the mutant frequency for the hepatocarcinogen 2,4-DAT (12.1 +/- 1.4 x 10(-5)) was significantly higher (p < 0.01) as compared to both age-matched (spontaneous) controls (5.7 +/- 2.9 x 10(-5)) and the 2,6-DAT-exposed group (5.7 +/- 2.4 x 10(-5)). Results from this study demonstrate that the Big Blue transgenic mutation assay can distinguish differences in vivo between the mutagenic responses of hepatic carcinogens ad a noncarcinogen; is sensitive to mutagens through subchronic dietary exposure; and yields a differential response depending upon the length of time mice are exposed to a mutagen.

Animals↗
PubMed2001

Relationships between chemical structures and mutagenicity: a preliminary survey for a database of mutagenicity test results of new work place chemicals.

A database of mutagenicity test results of new chemicals has been developed. Based on the amendment of the Industrial Safety and Health Law (ISHL) in 1979, manufacturers and importers in Japan are required to register any new work place chemicals with bacterial mutagenicity test results. At present more than ten thousand substances have been examined. We have surveyed correlations between 44 substructures and mutagenicity in 2,857 ISHL data as well as in 1,207 National Toxicology Program data as a preliminary analysis. The percentages of the mutagenic compounds were calculated. High percentages were found for electrophilic reagents such as epoxides (63%), aromatic nitro compounds (49%) and primary alkyl monohalides (46%). 71% of peroxides was found to be mutagenic. The results suggest that several types of reactions such as nucleophilic substitution reaction, nitrenium cation reaction and radical reaction are included in the process of the mutagenic alterations of DNA.

Databases, Factual↗
PubMed2001

Mutagenicity and identification of mutagenic compounds of fumes obtained from heating peanut oil.

Since the fume of cooking oil has been reported to increase the risk of lung cancer, the objectives of this study were to evaluate the mutagenicity and to find the mutagens in the fumes of peanut oil heated to the smoke point. Peanut oil prepared from roasted peanut kernel showed a lower smoke point, less unsaturated fatty acids, more fume formation, and stronger mutagenicity than that from unroasted kernel. Further investigation of mutagenic compounds was performed by the Ames test and gas chromatography/mass spectrometry analysis. Among the 12 compounds identified from the neutral fraction of methanol extract, four compounds at a dose of 10 microg per plate were mutagenic to Salmonella Typhimurium TA98 and TA100 in the order of trans-trans-2,4-decadienal > trans-trans-2,4-nonadienal > trans-2-decenal > trans-2-undecenal. Results report the enal compounds formed as the mutagens in the fumes of peanut oil and indicate that inhaling cooking fumes might cause carcinogenic risk.

Gas Chromatography-Mass Spectrometry↗
PubMed2006

The mutagenic and anti-mutagenic effects of Ecballium elaterium fruit juice in human peripheral lymphocytes.

The aim of this study was to investigate the mutagenic and anti-mutagenic effects of Ecballium elaterium (EE) fruit juice which has an anti inflammatory effect using in vitro human peripheral lymphocytes. For the investigating the mutagenic effects of EE fruit juice, human peripheral lymphocytes was treated with three doses (18, 36 and 72 microl/1) of fruit juice alone for 24 and 48 h. For the investigating the anti-mutagenic effects of the EE fruit juice, the human lymphocytes also treated with the mixture of the fruit juice and 0.25 microg/ml MMC. EE fruit juice induced the percentage of total CA when used alone (especially the percentage of structural CA than the percentage of the numerical CA) and synergically induced the percentage of total CA when used as a mixture with MMC. EE fruit juice did not affect the SCE frequency for 24 and 48 h treatment time. In contrast, EE and MMC as a mixture, sinergically induced the SCE frequency at the highest concentration for 48 h treatment time only. EE alone did not decrease the RI while it decreased the MI as a dose dependent manner. EE and MMC as a mixture have the higher cytotoxic effect than the cytotoxic effects of EE alone. As a result, it can be concluded that, EE had no anti-mutagenic effect while EE had a mutagenic and a cytotoxic effect in human peripheral lymphocytes.

Antimutagenic Agents↗
PubMed1984

Mutagenicity of various Japanese foodstuffs treated with nitrite. II. Directly-acting mutagens produced from N-containing compounds in foodstuffs.

Various Japanese foodstuffs show mutagenicity after nitrite treatment at pH 4.2. Among 13 groups of foodstuffs, classified by the 'market basket' method, the group containing fish showed the highest mutagenicity in the absence of metabolic activation. Taking the daily intake of these foodstuffs into consideration, the combination of groups V (soya bean paste), VI (juice), VIII (pickles and seaweed), IX (alcoholic beverages, coffee), X (fish) and XI (meat) represents 90% of the total mutagenic activity that may be supplied by food each day. The mutagenic activities of foodstuffs in groups VII (vegetables), VII and IX were increased remarkably by nitrite treatment; the mutagenicity of alcoholic beverages was particularly affected by nitrite. The separation of wine, sake and beer into acidic, basic and neutral fractions scattered the premutagenic activities, with a large decrease in total activity. The chemical properties of the basic fraction of beer, which gave the highest mutagenicity after nitrite treatment, were examined, and two tetrahydro-beta-carboline derivatives were identified.

Chemical Phenomena↗
PubMed2001

Lack of mutagenic and co-mutagenic effects of magnetic fields during magnetic resonance imaging.

Mutagenic and co-mutagenic effects of static, pulsed bipolar gradient, and high-frequency magnetic fields, as well as combinations of them, were examined using the Ames test. The Ames test using Salmonella typhimurium bacteria, wild-type strain RTA, preincubation assay, without metabolic activation, was performed. All combinations of magnetic fields were tested with and without co-exposure to N-methyl-N'-nitro-N-nitrosoguanidine and benzo[a]pyrene-4,5-oxide, ethylene oxide, carboplatin, or cisplatin. As expected, chemical mutagens caused a clear-cut increase of the revertants in the Ames test. However, neither the static fields nor a combination of a static magnetic field with the time-varying bipolar gradient field or a pulsed high-frequency magnetic field caused an alteration in the number of revertants in the Ames test. No co-mutagenic effect of any magnetic field combination was observed. In conclusion, magnetic fields used during clinical magnetic resonance imaging (MRI) were neither mutagenic nor co-mutagenic.

Animals↗
PubMed1985

Mutagenic activity of various chemicals in Salmonella strain TA100 and glutathione-deficient derivatives. On the role of glutathione in the detoxification or activation of mutagens inside bacterial cells.

Several mutants with decreased levels of reduced glutathione (GSH) were isolated from the sensitive mutagen tester strain Salmonella typhimurium TA100 after treatment with u.v. and selection for resistance to N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) and its methyl analogue MNNG. Estimation of the GSH concentration and GSH S-transferase activity in extracts of these strains and of TA100 indicates that the GSH- derivatives contain 10-30% of the GSH level found in TA100, and that they exhibit normal GSH S-transferase activity. The mutagenic activities of 7 chemicals, namely, MNNG, ENNG, 1,2-dibromoethane (DBE), 1-chloro-2,4-dinitrobenzene (CDNB), styrene-7,8-oxide (STOX), N-ethyl-N-nitrosourea (ENU) and methyl methane sulphonate (MMS) were compared in TA100 and in one representative GSH- strain, denominated NG-57. MNNG, ENNG, DBE and CDNB are potent to extremely potent mutagens in TA100, but induce very low levels of His+ mutants in NG-57. Pretreatment of NG-57 with 1 mM GSH (partially) restores the mutant yields to the levels usually found in TA100. The mutagenic activities of STOX, ENU and MMS are similar in both strains. These results support some previous findings, namely that ENNG, MNNG and DBE, but not ENU are activated to mutagens inside the test bacteria, and also suggest that CDNB is activated by bacterial GSH. The latter finding is in contrast with the current view that CDNB is detoxified by GSH, as is also presently evidenced by a strong reduction of the compound's mutagenicity in the presence of extracts of rat liver, which contains GSH and GSH S-transferase activity. The results with STOX indicate that GSH plays in bacteria a much less important role in the detoxification of xenobiotics than in mammalian tissue, presumably due to a much lower GSH S-transferase activity in the first organism.

Biotransformation↗
PubMed1983

Mutagenicities of glycidyl ethers for Salmonella typhimurium: relationship between mutagenic potencies and chemical reactivity.

The lethal and mutagenic effects of ethyl, benzyl, 1-naphthylmethyl, 2-naphthylmethyl, 1-naphthylethyl, 2-naphthylethyl and 9-anthrylmethyl glycidyl ethers on Salmonella typhimurium (TA100, TA1535, TA98 and TA1538) were investigated. LD30-value became smaller with an increase in compound hydrophobicity. The mutagenicities of these compounds in TA100 increased in the order: 1-naphthylethyl glycidyl ether less than 2-naphthylethyl glycidyl ether less than benzyl glycidyl ether less than 2-naphthylmethyl glycidyl ether less than 1-naphthylmethyl glycidyl ether less than 9-anthrylmethyl glycidyl ether. 1-Naphthylmethyl and 2-naphthylmethyl glycidyl ethers were mutagenic toward TA1535. In TA98, 1-naphthylmethyl and 9-anthrylmethyl glycidyl ethers showed mutagenic activity and 9-anthrylmethyl glycidyl ether was more mutagenic than 1-naphthylmethyl glycidyl ether. 9-Anthrylmethyl glycidyl ether was also active in TA1538. In the reaction of glycidyl ethers with deoxyguanosine and related compounds, glycidyl ethers attacked at only N-7 of guanine. The alkylation rates of glycidyl ethers toward guanine residues in DNA were determined and the exciplex-formation ability of 7-substituted guanines was studied. The reactivity of glycidyl ethers with guanine residues in DNA has not provided a sufficient explanation for the variation in mutagenic potencies of glycidyl ethers.

Deoxyguanosine↗
PubMed1993

Mutagenic effects of restriction enzymes in Chinese hamster cells: evidence for high mutagenicity of Sau3AI at the hprt locus.

CHO cells were exposed to seven different restriction endonucleases by electroporation and their cytotoxicity and mutagenicity measured. Cell killing as determined by a colony formation assay occurred in a concentration-dependent manner for each enzyme. The D0 of the survival curves were: MspI = 24U; AluI = 31U; Sau3AI = 106U; HaeIII = 46U; HinfI = 30U; PvuII = 35U; BamHI = 163U. BamHI and Sau3AI were particularly ineffective in cell killing. For the 6-base recognition sequence enzymes, PvuII (a blunt-ended cutter) was much more cytotoxic per unit electroporated than BamHI (a sticky-ended cutter). Among the 4-base cutters, Sau3AI and HaeIII were generally less cytotoxic than HinfI or PvuII. Cell killing appeared to depend on the nature of the recognition sequence and cutting sites rather than on the cutting frequency. The mutagenic effects of these restriction endonucleases were investigated by measuring the induced frequencies of hprt gene mutations. The mutagenicity of Sau3AI was dramatically higher than the other enzymes, increasing linearly with dose up to 35U. When normalized for survival, the mutagenicity of Sau3AI relative to the other enzymes was even greater. The mutagenic effect of BamHI, which has the same 5' protruding site as Sau3AI, was much lower at similar dose and survival levels. MspI, BamHI, and PvuII which have no recognition sites within the hprt coding sequence were marginally- or non-mutagenic. Based on these results and the distribution of cutting sites within the hprt cDNA for the enzymes studied, the hypothesis is discussed that a region in exon 4 is highly sensitive to the induction of mutants by DNA double-strand breaks.

Animals↗
PubMed1995

[Mutagenicity and anti-mutagenicity assay of airborne suspended particles in Shijiazhuang city].

Samples of airborne suspended particles collected from five air monitoring sites in Shijiazhuang City in 1993 were analyzed with rapid synchronous mutagenicity and anti-mutagenicity tests. It revealed airborne suspended particles collected had direct and indirect mutagenicity, but no anti-mutagenicity, and there was seasonal difference in their mutagenicity, which showed a decreasing trend with an order of winter, spring, summer and autumn. Mutagenicity related positively to air concentrations of total suspended particles and sulfur dioxide, inversely to those of ozone, and did not related to those of nitrogen oxide and carbon monoxide.

Air Pollutants↗
PubMed1975

[The mutagenic effect of new chemical substances. III. The mutagenic effect of several hydroxylamine derivatives].

The mutagenic effect of 21 new hydroxylamine derivatives was studied on biochemical mutants of Escherichia coli P-678 and Actinomyces rimosus 222. The Iver--Szybalsky method was used for the preliminary selection of mutagens. Dose-effect curves were plotted for the most efficient mutagens. Among the compounds studied 4 hydroxylamine derivatives were observed to have a mutagenic effect. The most efficient among them proved to be 0-(4-metoxybenzyl)-hydroxylamine and 0-(gamma-chlorocrotyl) hydroxylamine that induced reversions in the threonine locus of E. coli P-678 and in the lysine locus of Act. rimosus 222, being more efficient than hydroxylamine, the generally known mutagen. The dependence of the mutagenic activity of the compounds studied on their chemical structure is investigated.

Escherichia coli↗
PubMed1987

Chromosomal instability in mutagen-sensitive mutants isolated from mouse lymphoma L5178Y cells. II. Abnormal induction of sister-chromatid exchanges and chromosomal aberrations by mutagens in an ionizing radiation-sensitive mutant (M10) and an alkylating agent-sensitive mutant (MS1).

To determine the mutual relationships between cell survival and induction of sister-chromatid exchanges (SCEs) as well as chromosomal aberrations (CAs), mutagen-induced SCEs and CAs were analyzed in an ionizing radiation-sensitive mutant (M10) and an alkylating agent-sensitive mutant (MS 1) isolated from mouse lymphoma L5178Y cells. The levels of CA induction in both mutants strictly corresponded to the sensitivity to lethal effects of mutagens, except that caffeine-induced CAs in M10 are considerably lower than those in L5178Y. The results clearly indicate that except for caffeine-induced CAs in M10, mutagen-induced lethal lesions are responsible for CA induction. In contrast, SCE induction in mutants was complicated. In M10, hypersensitive to killing by gamma-rays, methyl methanesulfonate (MMS), and 4-nitroquinoline 1-oxide (4NQO), but not sensitive to UV or caffeine, the frequency of SCEs induced by gamma-rays was barely higher than that in L5178Y, and the frequencies of MMS- and UV-induced SCEs were similar to those in L5178Y, but 4NQO- and caffeine-induced SCEs were markedly lower than those in L5178Y. MS 1, which is hypersensitive to MMS and caffeine, but not sensitive to UV or 4NQO, responded to caffeine with an enhanced frequency of SCEs and had a normal frequency of MMS-induced SCEs, but a reduced frequency of UV- and 4NQO-induced SCEs. Thus, susceptibility to SCE induction by mutagens is not necessarily correlated with sensitivity of mutants to cell killing and/or CA induction by mutagens. Furthermore, the spontaneous levels of SCEs are lower in M10 and higher in MS 1 than that in L5178Y (Tsuji et al., 1987). Based on these results, we speculate that M10 may be partially defective in the processes for the formation of SCEs caused by mutagens. On the other hand, MS 1 may modify SCE formation-related lesions induced by UV and 4NQO to some repair intermediates that do not cause SCE formation. In addition, MMS-induced lethal lesions in MS 1 may not be responsible for SCE induction whereas caffeine-induced lethal lesions are closely correlated with SCE induction. Thus, the lesions or mechanisms involved in SCE production are in part different from those responsible for cell lethality or CA production.

4-Nitroquinoline-1-oxide↗
PubMedDate not supplied

Mutagenicity of chloro-olefins in the Salmonella/mammalian microsome test. I. Allyl chloride mutagenicity re-examined.

Contrary to findings published up to now, allyl chloride, a well known directly acting mutagen for Salmonella typhimurium, is efficiently activated by rat-liver homogenate (S9 mix) under non-standard mutagenicity testing conditions. Its indirect, S9-mediated mutagenic activity is greatly enhanced when longer than standard preincubation times are applied. The indirect mutagenicity of allyl chloride, thus revealed, greatly exceeds its direct mutagenic activity. Obviously, standard mutagenicity testing conditions cannot be regarded as reliable tools for the evaluation of the full genotoxic potential of allyl chloride and, possibly, of other related compounds.

Allyl Compounds↗
PubMed1992

A QSAR investigation of the role of hydrophobicity in regulating mutagenicity in the Ames test: 1. Mutagenicity of aromatic and heteroaromatic amines in Salmonella typhimurium TA98 and TA100.

Quantitative structure-activity relationships (QSAR) have been derived for the mutagenic activity of 88 aromatic and heteroaromatic amines acting on Salmonella typhimurium TA98 + S9 and 67 amines acting on TA100 + S9. Mutagenic activity is linearly dependent on hydrophobicity, the energy of the highest occupied molecular orbital, and the energy of the lowest unoccupied molecular orbital of the amine. The dependence of mutagenic activity on hydrophobicity and electronic effects is nearly identical for TA98 and TA100. Mutagenic activity in TA98 is also found to depend on the size of the aromatic ring system. Different QSARs are derived for the mutagenic activity of hydrophilic amines (log P less than 1) acting on either TA98 or TA100. The mechanism of amine activation and reaction with DNA is considered in light of these findings.

Amines↗