bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phototoxic effects of fluoranthene, a polycyclic aromatic hydrocarbon, on bacterial species
Authors: Tuveson R. W. , Kagan J. , Shaw M. A. , Moresco G. M. , v. Behne E. M. , Pu H. , Bazin M. , Santus R. 
Published: February 2007

AbstractFluoranthene, a non‐carcinogenic polycyclic aromatic hydrocarbon, inactivatesEscherichia colicells in the presence of near‐ultraviolet light (NUV; 300–400 nm).E colicells carrying defects in theuvrA6orkatFgenes are sensitized to inactivation by the simultaneous treatment with fluoranthene and NUV, suggesting that DNA is a target and that hydrogen peroxide is generated.Haemophilus influenzaetransforming DNA can be inactivated by the simultaneous treatment with fluoranthene and NUV confirming DNA as a target. Using the photooxidation of imidazole and histidine as probes, fluoranthene was found to generate singlet oxygen in organic and aqueous media. In water, it participated in electron transfer reactions, reducing nitro blue tetrazolium as well as ferricytochrome C. This reduction took place both in the presence of air, where superoxide anion was formed, and under argon. Simultaneous treatment with fluoranthene and NUV was incapable of inducing histidine‐independent mutations. Simultaneous treatment with fluoranthene and NUV was incapable of inducing theuvrAgene product as evidenced by the absence of the induction of beta‐galactosidase in anE colioperon fusion strain [uvrA215::Mud(Ap,lac)].
Specific reduction of N,N‐dimethylnitrosamine mutagenicity in Drosophila melanogaster by dimethyl sulfoxide
Authors: Brodberg R. K. , Mitchell M. J. , Smith S. L. , Woodruff R. C. 
Published: February 2007

AbstractDimethyl sulfoxide (DMSO) used as a solvent has been observed to complicate mutagenicity screens by interacting with tested chemicals to yield false positives or negatives. We have used DMSO as a solvent in the Drosophila melanogaster recessive sex‐linked lethal mutation assay and find that it reduces, but does not abolish, the detectable mutagenicity of N,N‐dimethylnitrosamine (DMN). Its use as a solvent with procarbazine, another promutagen, shows no effect on mutagenicity in Drosophila. DMSO does not exhibit a general inhibitory action on microsome activity when ecdysone 20‐monooxygenase activity is used as a measure of cytochrome P‐450 activity. We were unable to detect the low DMN demethylase activity in the strain used. Hence, the inhibitory effect of DMSO in Drosophila at both the physiological and biological level appears to be limited and not general in action. Because DMN and DMSO are similar in structure, it is possible that DMSO is interacting with a DMN demethylase in Drosophila. This might lead to a reduction in the conversion of DMN to a mutagen. Consequently, from the results of this study and others DMSO should be used cautiously as a solvent in Drosophila mutagen screening.
Genotoxicity of acrylic acid, methyl acrylate, ethyl acrylate, methyl methacrylate, and ethyl methacrylate in l5178y mouse lymphoma cells
Authors: Moore Martha M. , Amtower Amanda , Doerr Carolyn L. , Brock Karen H. , Dearfield Kerry L. 
Published: February 2007

AbstractA series of monomeric acrylate/methacrylate esters (methyl acrylate, ethyl acrylate, methyl methacrylate, and ethyl methacrylate) as well as acrylic acid were examined for genotoxic activity in L5178Y mouse lymphoma cells without exogenous activation. All five compounds induced concentration‐dependent increases in mutant frequency. Small‐colony, trifluorothymidine‐resistant mutants were primarily induced, which suggests that these compounds may act via a clastogenic mechanism. This prediction was confirmed by the finding that all five compounds produced gross chromosome aberrations in mouse lymphoma cells. The two acrylates were much more potent in their response than acrylic acid. Methyl acrylate (22 μg/ml, survival = 18%) induced 385 mutants/106 survivors (total mutant frequency less the spontaneous mutant frequency) and 45 chromosome aberrations/100 cells analyzed (total aberrations less the spontaneous background). Ethyl acrylate (37.5 μg/ml, survival = 15%) induced 683 mutants/106 survivors.
Flavone mutagenicity in salmonella typhimurium: Dependence on the PKM101 plasmid and excision‐repair deficiency
Authors: Macgregor J. T. , Wilson R. E. 
Published: February 2007

AbstractFlavones mutagenic in Salmonella typhimurium fall into two distinct classes, characterized by different structural and metabolic activation requirements and by different strain responses. The mutagenic potencies of a prototype agent of each class, quercetin (3,3′,4′,5,7‐hydroxyflavone) and norwogonin (5,7,8‐hydroxyflavone), were determined in tester strains differing in excision‐repair capability and in the presence or absence of plasmid pKM101. Two series of strains were used, one with the hisD3052 frameshift mutation and one with the hisG46 missense mutation. With both agents and for both series of strains, the mutagenic response was markedly dependent on the absence of excision repair and the presence of the pKM101 plasmid.
Mutagenicity of nitro compounds in Salmonella typhimurium in the presence of flavin mononucleotide in a preincubation assay
Authors: Dellarco Vicki L. , Prival Michael J. 
Published: February 2007

AbstractA series of nitro compounds (18 aromatic and one aliphatic) was evaluated using a modification of the standard Salmonella typhimurium mutagenicity assay. A preincubation protocol was used with flavin mononucleotide (FMN) incorporated into the assay mixture to facilitate nitro reduction. Several aromatic nitro compounds (m‐nitroaniline, p‐nitroaniline, 2, 6‐dinitrotoluene, 2,4‐dinitrotoluene,2,3‐dinitrotoluene, 1,8‐dinitro‐naphthalene), which were negative or only weakly mutagenic when tested in the standard plate incorporation assay, showed FMN‐dependent mutagenic responses with this procedure. For some nitro compounds, the addition of FMN was not needed for the detection of mutagenicity in the modified protocol. Not all nitro compounds were positive using the preincubation procedure with FMN. The lack of mutagenicity, however, does not appear to be the result of the inability of the modified method to reduce nitro compounds, since it was found that reduction does occur under the assay conditions for the two nonmutagens evaluated for nitro reduction (nitrobenzene and p‐nitrophenol). It is suggested that the modified protocol may be useful for evaluating the mutagenicity of many nitro compounds.
Micronuclei in binucleated lymphocytes of mice following exposure to gamma radiation
Authors: Erexson Gregory L. , Kligerman Andrew D. , Halperin Edward C. , Honore Gerard M. , Allen James W. 
Published: February 2007

AbstractExperiments were designed to investigate the induction of micronuclei (MN) in mouse peripheral blood lymphocytes (PBLs) after in vitro or in vivo exposure to 60Co gamma radiation. For the invitro experiments, 4 ml of blood from male C57BL/6J mice were either irradiated in 6 ml Falcon culture tubes as whole blood or isolated to obtain mononuclear leukocytes (MNLs) that were pelleted by centrifugation and then irradiated in RPMI 1640. For the in vivo analysis, mice received whole body irradiation, blood was obtained by cardiac puncture, and the MNLs were isolated for each mouse. Exposures were at a rate of 0.82 to 0.90 Gy/min to yield doses of 0.5, 1, 2, 3, or 4 Gy. MNLs were cultured using cytochalasin B for MN analysis in binucleated PBLs. There was a significant dose‐dependent increase in MN observed at all doses. Dose‐response curves for the in vivo and in vitro whole blood experiment were not significantly different. However, for isolated pelleted MNLs irradiated in vitro, the MN frequency at 4 Gy was less than one‐half that seen in the in vivo experiment. The large difference in MN response is thought to be due to the radioprotective effect of hypoxia.
Conditions affecting the mutagenicity of trichloroethylene in Salmonella
Authors: McGregor D. B. , Reynolds D. M. , Zeiger E. 
Published: February 2007

AbstractTrichloroethylene (TCE) is a high production volume chemical frequently stabilized with oxiranes. These oxiranes may be responsible for the mutagenic activity of TCE in Salmonella, which has been occasionally, but not consistently, reported. High purity and oxirane‐stabilized TCE samples were tested for their mutagenic potential in Salmonella typhimurium strains TA 1535, TA 98, and TA 100. Stabilized TCE was tested using a preincubation protocol up to a dose level of 10,000 μ per plate, but no mutagenic response was observed in either the presence or absence of a supplementary metabolic activation system (S9 mix) derived from Aroclor 1254‐induced male rat liver. TCE without oxirane stabilizers also was nonmutagenic when tested in a vapor delivery system at nominal concentrations of up to 20% and using S9 mix derived from either rat or hamster. TCE containing 0.5–0.6% 1, 2‐epoxybutane did induce mutagenic responses from strains TA 1535 and TA 100 in the presence and absence of S9 mix. The lowest effective dose was about 0.63% in TA 1535 in the absence of S9 mix. Vapor‐phase tests with 1, 2‐epoxybutane showed that an atmospheric concentration of 0.009% could induce 12‐fold and 3‐fold increases, respectively, in strains TA 1535 and TA 100. These increases would account for the mutagenic activity of the stabilized TCE sample. Epichlorohydrin (another commonly used stabilizer) induced similar increases in mutant numbers at an atmospheric concentration of 0.0009%. The absence of a significant response caused by unstabilized TCE in the presence of S9 mix is probably due to a lack of assay sensitivity, since chloral, a metabolite of TCE, is a mutagen in TA 100 [Haworth et al.: Environ Mutagen [Supplement 1] 5:3–142, 1983].
The effects of acrylamide on mouse germ‐line and somatic cell chromosomes
Authors: Backer Lorraine C. , Dearfield Kerry L. , Erexson Gregory L. , Campbell James A. , Westbrook‐Collins Barbara , Allen James W. 
Published: February 2007

AbstractThe industrial chemical acrylamide is suspected to induce potentially heritable genetic damage. While several studies in rodents have indicated that this substance can damage spermiogenic cells, resulting in dominant lethals and heritable translocations, cytogenetic assessments of premeiotic and meiotic cells after exposure have produced equivocal results. In the present study, various cytogenetic endpoints in both somatic and germ‐line cells from acrylamide‐treated mice were evaluated. Sister chromatid exchanges and micronuclei, but not chromosome aberrations, were induced in spleen cells; synaptonemal complex irregularities (asynapsis), but not chromosome aberrations, were induced in germ cells.
Mutagenicity of airborne particles from a nonindustrial town in Italy
Authors: Barale Roberto , Zucconi Donatella , Giorgelli Francesco , Carducci Anna Laura , Tonelli Margherita , Loprieno Nicola 
Published: February 2007

AbstractThe mutagenic activity of airborne particulate matter collected in Pisa, a small nonindustrial town located in Italy, has been monitored over 1 year using the Ames Salmonella Test. Airborne particulate was collected on fibreglass filters using a Hi‐Vol sampler and extracted by sonication and Soxhlet acetone extraction in sequence. TA 98 and TA 100 salmonella strains gave positive results with the great majority of samples. The mutagenicity trend fits with a harmonic regression with a peak during December/January and inversely correlates with the temperature. No correlations were observed with other meteorological conditions such as wind, cloud, rainfall, atmospheric pressure, and humidity. The ratio between mutagenicity/μg of particulate matter with S9 and that without S9 remains more or less constant regardless of seasonal fluctuations, suggesting that during cold months quantitative increases of mutagens onto particulate matter have probably occurred. The comparison of air mutagenicity in different sites suggests that motor vehicle exhaust fumes are the major source of air pollution. Finally, because of high‐traffic volume, air mutagenicity at street level is comparable to that observed in several metropolitan areas all over the world.
Absence of mutagenic interaction between microwaves and mitomycin C in mammalian cells
Authors: Meltz Martin L. , Eagan Phyllis , Erwin David N. 
Published: February 2007

AbstractEvidence in the literature from in vitro and in vivo studies as to whether or not radiofrequency radiation (RFR) in the microwave range is mutagenic is predominantly negative, with some positive reports. No evidence is available as to whether RFR will alter the mutagenic activity of genotoxic chemicals during a simultaneous exposure, a likely real‐life situation. Two hypotheses have been proposed: a) that RFR by itself can cause mutations in a mammalian cell in vitro assay system; and b) that a simultaneous exposure to RFR during a chemical treatment of the cells with a known genotoxic agent, mitomycin C (MMC), will alter the extent of mutagenesis induced by the treatment of the cells by the chemical alone. These studies were performed using the forward mutation assay at the thymidine kinase locus in L5178Y mouse leukemic cells. The pulsed wave RFR was broadcast from an antenna horn at a frequency of 2.45 GHz. The power density was 48.8 mW/cm2 and the measured specific absorption rate (SAR) in this system was 30 W/kg (600 W forward power), which is well above current safety guidelines. The conclusions from five different experiments, employing three different concentrations of MMC, were that a) RFR exposure alone, at moderate power levels which resulted in a temperature increase in the cell culture medium of less than 3°C, is not mutagenic; and b) when cells are simultaneously treated with MMC and RFR at these same moderate power levels, the RFR does not affect either the inhibition of cell growth or the extent of mutagenesis resulting from the treatment with the chemical MMC alone.
In vitro genotoxicity of dyes present in colored smoke munitions
Authors: Brooks A. L. , Seiler F. A. , Hanson R. L. , Henderson R. F. 
Published: February 2007

AbstractGenetic toxicology studies were conducted on organic dyes and mixtures used in colored smoke munitions. The dyes studied included Solvent Red 1; two different batches (Lot 1 and Lot 2) of Disperse Red 11; terephthalic acid; and a mixture of 25 parts Solvent Red 1, 5 parts Disperse Red 11, and 16 parts terephthalic acid. The dyes were evaluated for their ability to produce mutations in Salmonella bacterial strains and in Chinese hamster ovary (CHO) cells. The dyes were also tested in CHO cells to determine cytotoxicity and the induction of sister chromatid exchanges and chromosome aberration. None of the dyes were genotoxic in the standard Ames assay using bacterial strain TA1535 or TA100 with or without the addition of S‐9 or in TA98 and TA1538 without S‐9. With S‐9, Disperse Red 11 (Lot 2) showed significant mutagenic activity in TA98 and TA1538 which increased as a function of S‐9 concentration. However, the maximum level of mutagenic activity detected was low (3.8 revertants/μg). The azo dye Solvent Red 1 was also negative in a pre‐incubation assay designed to reduce azo compounds to free amines. Solvent Red 1 was cytotoxic to mammalian cells, caused a significant increase in SCE, but was not mutagenic or clastogenic. Disperse Red 11 (Lot 1 and Lot 2) were not cytotoxic or clastogenic but produced an increase in cell cycle time and SCE frequency. Only Disperse Red 11 (Lot 2) increased mutations in the CHO/hypoxanthine‐guanine phosphoribosyltransferase (HGPRT) assay. The mutagenic activity of the dye mixture was not significant, suggesting no synergistic interaction between the dyes. These studies demonstrated that none of the dyes was clastogenic and that a contaminant in Disperse Red 11 (Lot 2) may be responsible for the weak mutagenic activity in both mammalian and bacterial cell systems.
Increased chromosome fragility as a consequence of blood folate levels, smoking status, and coffee consumption
Authors: Chen Andrew T. L. , Reidy John A. , Annest Joseph L. , Welty Thomas K. , Zhou Huan‐Geng 
Published: February 2007

AbstractChromosome fragility in 96 h, low‐folate cultures was found to be associated with smoking status, coffee consumption, and blood folate level. The higher proportion of cells with chromosome aberrations in cigarette smokers was attributable to lower red cell folate levels in smokers compared with nonsmokers. There was a positive linear relationship between the average cups of coffee consumed per day and the proportion of cells with aberrations. This association was independent of the effects of smoking and red cell folate level. These data suggest that smoking history, coffee consumption, and red cell folate level are important considerations for the design and interpretation of fragile site studies in cancer cytogenetics.
Mutagenicity of the human carcinogen treosulphan in Salmonella
Authors: Zeiger Errol , Pagano Dennis A. 
Published: February 2007

AbstractThe human carcinogen treosulphan was mutagenic in Salmonella typhimurium TA100 and TA1535, as was dl‐1,2:3,4‐diepoxybutane (DEB), a proposed hydrolysis product of treosulphan. Another proposed hydrolysis product, methane‐ sulfonic acid, was not mutagenic in these strains. The pattern of the mutagenic responses at pH 6, 7, and 8 to treosulphan and DEB suggests that DEB formation may be responsible for the mutagenicity of treosulphan.
A procedure for data analysis of the rodent micronucleus test involving a historical control
Authors: Hayashi M. , Yoshimura I. , Sofuni T. , Ishidate M. 
Published: February 2007

AbstractNo standard procedure of data analysis for rodent micronucleus tests involving historical controls has been established. In the present paper, under the presumption that the distribution of the historical control is stable and reliable, a procedure with three statistical steps is proposed to analyze the frequency of micronucleated polychromatic erythrocytes (MNPCEs). In the first step, the frequencies of MNPCEs in negative and positive control groups of a current experiment of the micronucleus test are compared with the distribution of historical negative and positive controls to examine the technical validity of the current experiment. In the second step, the frequency of MNPCEs in each treatment group is compared with the distribution of the historical negative control. In the third step, the dose‐response relation is tested with the Cochran‐Armitage trend test. A Monte Carlo simulation study shows that the power of this procedure is acceptable and also this procedure is robust. An application of this procedure on real data reveals that it is effective in detecting clastogenic chemicals when the probability of a type I error is nearly .01.
Initiating carcinogen, triethylenemelamine, induces micronuclei in skin target cells
Authors: He Shuilin , Baker Robert S. U. 
Published: February 2007

AbstractKeratinocytes from mouse skin were cultured for a short period in vitro following single or multiple treatments at low dose levels in vivo with the known chromosome‐damaging agent triethylenemelamine (TEM). The chemical was applied to the skin of HRA/Skh hairless mice at concentrations corresponding to those reported to initiate cancer in initiation‐promotion assays. A significant dose‐related depression in keratinocyte cell recovery occurred over the dose range 0.3–1 mg TEM/mouse (single or multiple treatments). Under the same conditions, a dose‐related induction of micronuclei was observed using the cytokinesis‐block method with cytochalasin B. A similar frequency of micronuclei was detected in binucleate cells from mice treated with single or multiple applications of TEM. Mice held for 12–48 h post‐treatment, before removal of skin for in vitro culture, yielded highest micronuclei frequencies. These results indicate that the same target cell population, skin keratinocytes, can be used to investigate both genotoxicity and carcinogenesis, and that micronucleus induction in these cells may be a sensitive signal of skin cancer initiation.
Synergistic induction of cytogenetic damage by alkylating antineoplastics and 5‐azacytidine in human lymphocytes
Authors: Loannidou E. , Lialiaris T. , Mourelatos D. , Dozi‐Vassiliades J. 
Published: February 2007

AbstractWe studied the effects of the inhibitor of DNA methylation, 5‐azacytidine (Aza‐C), alone and in combination with three antitumor alkylating agents, on sister chromatid exchanges (SCEs) and lymphocyte proliferation kinetics. Aza‐C was found to act synergistically on induction of SCEs when administered in combination with either melphalan (MEL) or chlorambucil (CBC) or cis‐platinum‐(ll)diamine dichloride (cis‐Pt). Cell‐division delays were consistently observed in cultures treated with each of the antineoplastics when introduced concomitantly with Aza‐C, compared with cultures treated with antineoplastics alone. Mitotic indices (Ml) in cultures treated with each of the three alkylating agents were found to be suppressed by Aza‐C. These results support the premise that hypomethylation of DNA causes cytotoxic effects by interfering with DNA repair mechanisms and by inhibiting DNA synthesis, or other cell growth mechanisms, which human lymphocytes undertake after being damaged by alkylation.
Cytogenetic effects of cigarette smoke on pulmonary alveolar macrophages of the rat
Authors: Rithidech Kanokporn , Chen Bean T. , Mauderly Joe L. , Whorton Elbert B. , Brooks Antone L. 
Published: February 2007

AbstractTo determine accurately the potential genetic damage induced by toxic inhaled agents, the cells that receive a high concentration of such agents should be analyzed. Pulmonary alveolar macrophages (PAMs) represent such cells. We compared the cytogenetic effects of cigarette smoke on PAMs of rats exposed repeatedly by different methods. This study was part of a larger investigation of the health effects resulting from different methods of exposing rats to cigarette smoke. Fischer 344/N male rats (4/group) were randomly selected from five different exposure groups: (1) nose‐only sham‐exposed (air) control, (2) whole‐body sham‐exposed control, (3) nose‐only intermittent, (4) nose‐only continuous, and (5) whole‐body continuous. The rats were exposed 6 hr/day, 5 days/week for 22–24 days. All smoke‐exposed rats received the same daily concentrations x time product (600 mg.hr.m−3 for the first week, 1200 mg.hr.m−3 thereafter) of cigarette smoke. Rats were injected intraperitoneally with colchicine at the end of exposure. PAMs were obtained by lung lavage and chromosomal damage was measured. Highly significant smoke‐induced differences in both structural and numerical aberrations were observed in continuously exposed rats vs. sham controls, regardless route of exposure. The structural aberrations observed were chromatid‐type deletions. Both hypoploid and hyperploid cells were detected. Our data suggest that cigarette smoke is clastogenic and may disrupt spindle‐fiber formation. These activities may play a role in the induction of human carcinogenesis caused by cigarette smoke exposure.
Exposure level monitor of 3‐amino‐1,4‐dimethyl‐5H‐pyrido[4, 3‐b]indole, a dietary carcinogen, in rabbits
Authors: Manabe Shigeo , Kanai Yoshikatsu , Wada Osamu 
Published: February 2007

AbstractThe present investigation describes a method for the detection of minute amounts of 3‐amino‐1, 4‐dimethyl‐5H‐pyrido[4, 3‐b]indole (Trp‐P‐1), a carcinogenic tryptophan pyrolysate, bound to the hemoglobin of erythrocytes and plasma from rabbits dosed orally with the dietary carcinogen. The method consists of the acid‐induced release of the dietary carcinogen adducts as the free carcinogen and their extraction with methylene chloride and subsequent quantitation by high‐performance liquid chromatography (HPLC). With this method, Trp‐P‐1 levels in plasma, platelets, and red blood cells were monitored for 12 weeks to determine a suitable indicator for estimating the exposure levels of the dietary carcinogen. The results suggest that Trp‐P‐1 in red blood cells that bound covalently to the hemoglobin is the most suitable for monitoring the long‐term exposure levels.