bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low‐Valent Nickel and Palladium Complexes with 1,1′‐Bis(phosphanyl)ferrocenes: Syntheses and Structures of Acrylic Acid and Ethylene Complexes
Authors: Langer Jens , Fischer Reinald , Görls Helmar , Walther Dirk 
Published: February 2007

AbstractThermally stable acrylic acid complexes with low‐valent nickel or palladium of the type [(L)M(η2‐CH2=CH‐COOH)] [1a: M = Ni, L = 1,1′‐bis(diphenylphosphanyl)ferrocene (dppf), 1b: M = Ni, L = 1,1′‐bis(diisopropylphosphanyl)ferrocene (dippf), 1c: M = Pd, L = dippf] were obtained by reaction of [Ni(cod)2] or [(L)Pd(nb)] with acrylic acid in the presence of the phosphane ligands. X‐ray diffraction analysis of 1a and 1c, respectively display that only the olefin part is coordinated. Hydrogen bonds between two carboxyl groups result in dimers in the solid state. The isomeric nickela‐cyclic carboxylates of the type [(L)Ni(CH2CH2COO)] are stable complexes in case of 2a (L = dppf) and 2b (L = dippf) whereas the unstable compound 2c [L = 1,1′‐bis(di‐tert‐butylphosphanyl)ferrocene (dtbpf)] undergoes fast reductive decoupling to form CO2 and the ethylene complex [(dtbpf)Ni(ethylene)] (3c). The related complex [(dippf)Ni(ethylene)] (3b) was prepared from nickel(0) complexes by ligand exchange reaction. 3b and 3c were characterized by elemental analyses, NMR spectroscopy and X‐ray structure analysis of single crystals.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Analysis of human lymphoblast mutation assays by using historical negative control data bases
Authors: Penman Bruce W. , Crespi Charles L. 
Published: February 2007

AbstractWe describe here historical negative control data bases for gene locus mutation assays at the thymidine kinase locus and hypoxanthine‐guanine phosphoribosyl transferase locus in TK6 and AHH‐1 human lymphoblasts, respectively. Protocols have been designed which minimize the variability among independent experiments and thus facilitate the use of historical negative control data bases for assay analysis. The historical negative control data bases for both cell lines can be accurately modeled as gamma or Poisson distributions; confidence limits can be calculated from these distributions. We describe and justify a mutagenicity assay analysis procedure which uses a comparison to the concurrent negative control cultures via a t‐test in conjunction with a comparison to the historical negative control data base. The incorporation of a comparison to the historical negative control data base allows the use of a higher confidence level without substantially sacrificing the sensitivity of the mutation assays. The analysis of the mutagenicity of saccharin in TK6 cells is presented as an example; saccharin was found to be nonmutagenic under the conditions tested.
Plant activation of m‐phenylenediamine by tobacco, cotton, and carrot cell suspension cultures
Authors: Lhotka Monica A. , Plewa Michael J. , Gentile James M. 
Published: February 2007

AbstractTobacco, cotton, and carrot plant cell suspension cultures activated the promutagen m‐phenylenediamine into a mutagen as detected by Salmonella typhimurium strain TA98 with the use of the plant cell/microbe coincubation assay. For each cell line, mid‐log phase plant cells at a density of 100–150 mg/ml were coincubated for 1 hr with concentrations of m‐phenylenediamine that ranged from 0.1 to 10 μmol per reaction tube in the preincubation test of the plant cell/microbe coincubation assay. Further experiments were conducted to optimize the activation response for each plant cell line. The density of plant cells in the reaction mixture, the time of coincubation of the reaction mixture, and the stage of the growth curve at which the plant cells were harvested for use in the reaction mixture all affected the response. Experiments that used the conditions determined as optimum for each plant cell line were then conducted. With each cell line, the optimized conditions enhanced the activation response that had been observed with the preliminary conditions. A ranking order based on the concentration‐response curves indicated a relationship of tobacco cells >> carrot cells > cotton cells. Tobacco cells were able to activate m‐phenylenediamine into a mutagen at concentrations of less than 10 nmol per plate when using TA98 as the genetic indicator organism. Finally, experiments to determine the type of genetic lesion induced by plant‐activated m‐phenylenediamine were conducted. By using five of the Ames strains, m‐phenylenediamine was shown to be active in inducing revertants in strains TA1538 and TA98 following activation by tobacco cells under the optimized conditions. We conclude that m‐phenylenediamine is activated by plant cells into a mutagen that primarily induces frameshift mutations.
Predicting the carcinogenic potential of environmental nitropyrenes
Authors: Rosenkranz Herbert S. 
Published: February 2007

AbstractNitrated polycyclic aromatic hydrocarbons (nitroarenes) constitute a large group of anthrapogenic environmental contaminants. Some members of the group are mutagenic and genotoxic in a wide spectrum of systems while others are either mutagenic only in Salmonella typhimurium or devoid of activity altogether. Additionally, some nitroarenes are uniformly carcinogenic in rodents while others are not. In view of the logistic and economic problems involved in preparing large quantities of individual nitroarenes in pure (>99.5%) form and assaying them for carcinogenicity in animals, we have analyzed the results that nitropyrenes and related chemicals yield in short‐term tests by CPBS, the Carcinogen Prediction, and Battery Selection method, and demonstrate that CPBS classifies them correctly with respect to carcinogenicity.
The simultest: A new approach to screening chemicals with the Salmonella reversion assay
Authors: Nestmann Earle R. , Brillinger Renata L. , McPherson Marcia F. , Maus K. Laurie 
Published: February 2007

AbstractA new Salmonella mutagenicity test method is under development to test a chemical with more than one strain simultaneously (the “SIMULTEST”), that is, different Salmonella typhimurium tester strains are used in combination on the same plate. Strains are combined in two sets: strains with plasmid pKM101 (TA97, TA98, TA100, and TA102) and strains without the plasmid (TA1535, TA1537, and TA1538). The SIMULTEST combinations successfully detect the mutagenic activity of five mutagens in different chemical classes. This approach may be useful in reducing the workload associated with mutagenicity testing with Salmonella.
Lack of uds activity in the livers of mice and rats exposed to dichloromethane
Authors: Trueman R. W. , Ashby J. 
Published: February 2007

AbstractDichloromethane (DCM) has been evaluated for its ability to initiate unscheduled DNA synthesis (UDS) in the livers of male mice and rats in vivo. Two types of experiment were conducted. In the first, Alpk:AP rats were exposed by oral gavage to 100, 500, or 1,000 mg/kg DCM and hepatocytes assessed for UDS via autoradiography 4 and 12 hours later. In the second, Fischer F344 rats or B6C3F1 mice were exposed by inhalation to either 2,000 or 4,000 ppm of DCM for either 2 or 6 hours, and hepatocytes assessed for UDS immediately after exposure. The dose levels and strains of rodent employed in the latter protocol correspond to those employed in a recent cancer bioassay of DCM conducted by the U.S. National Toxicology Program. DCM failed to induce UDS in any of the experiments. These data are discussed within the context of other evidence indicating DCM to be nongenotoxic in vivo, despite its reported carcinogenicity in the mouse.
A review of the mutagenicity of chloroform
Authors: Rosenthal Sheila L. 
Published: February 2007

AbstractAlthough chloroform (CHCI3) is metabolized in vivo and in vitro to a substance that covalently interacts with protein and lipid, its potential for binding to DNA is low. In addition, most of the assays for genotoxicity are negative. However, many of the genotoxicity results are inconclusive because of inadequacies in the experimental protocols. The types of genotoxicity tests this report is based on include bacterial, yeast, host‐mediated, Drosophila sex‐linked recessive lethal, mammalian cell mutagenicity, sperm head abnormality, cytogenetic, and DNA damage. On the basis of presently available information, no definitive conclusion on the mutagenic potential of CHCI3 can be reached.
Radiation‐induced micronuclei in peripheral erythrocytes of Rana catesbeiana: An aquatic animal model for in vivo genotoxicity studies
Authors: Krauter P. W. , Anderson S. L. , Harrison F. L. 
Published: February 2007

AbstractAn in vivo micronucleus assay for peripheral erythrocytes of Rana catesbeiana tadpoles was developed and evaluated. The assay was used to determine the spontaneous frequency of micronuclei in circulating erythrocytes in tadpoles from two different populations, to define the time from administering the clastogen to the maximum micronucleus frequency in peripheral erythrocytes, and to determine the response to radiation.The spontaneous frequency of micronuclei in circulating erythrocytes of early‐stage tadpoles was low (3.6 ± 2.8 micronuclei per 1,000 erythrocytes, MN o/oo), but higher than that of late‐stage tadpoles (1.7 ± 0.7 MN o/oo). The time from the exposure of early‐stage tadpoles to radiation (2.1 Gy) to the maximum micronucleus frequency was about 2 wk.The increase in frequency of micronuclei in peripheral erythrocytes of late‐stage tadpoles receiving doses ranging from 0.5 to 3.0 Gy was linear with dose; a 3‐fold increase was obtained with a dose of 3.0 Gy. The spontaneous frequency of micronuclei in erythrocytes and the increase in frequency induced by radiation appeared to differ in tadpoles from different populations. Quantification of micronuclei in the peripheral erythrocytes of R catesbeiana tadpoles provides a promising whole‐animal system for studies of genotoxicity in aquatic environments.
Re‐evaluation of the need for multiple sampling times in the mouse bone marrow micronucleus assay: Results for DMBA
Authors: Ashby J. , Mirkova E. 
Published: February 2007

Abstract7,12‐dimethylbenzanthracene (DMBA) is confirmed as active in the mouse bone marrow micronucleus assay 24 hr after dosing as a corn‐oil homogenate via either oral gavage or intraperitoneal (ip) injection. These data are consistent with recent observations made by several investigators. However, when dosed via ip injection as a solution in DMSO, peak activity was evident 48 hr after dosing and a dramatic reduction in erythropoiesis was observed. The latter results are consistent with early observations made by Salamone and Heddle. The early observations of Salamone and Heddle were highlighted in the Gene‐Tox review of this assay and led the OECD to recommend the use of 3 sampling times for this assay (between 12 and 72 hr). The present data indicate that this advice should be reviewed. In particular, it suggested that a maximum of two sampling times is adequate and that, as a consequence, the number of animals employed in the conduct of the test could be reduced with no loss of sensitivity. The present data also suggest that the use of a corn‐oil homogenate of insoluble test agents may provide an efficient replacement for the use of ground suspensions or solutions in DMSO.
Mutagenic and clastogenic properties of 3‐chloro‐4‐(dichloromethyl)‐5‐hydroxy‐2 (5H)‐furanone: A potent bacterial mutagen in drinking water
Authors: Meier John R. , Blazak William F. , Knohl Richard B. 
Published: February 2007

Abstract3‐Chloro‐4‐(dichloromethyl)‐5‐hydroxy‐2(5H)‐furanone (MX) was found to be a direct‐acting mutagen in the Ames test for strains TA1535, TA1538, TA92, TA97, TA98, TA100 and TA102. The highest mutagenic response (∼13,000 revertants/nmol) was seen in strain TA100. The TA100 response was six‐ to tenfold higher than in TA98, TA97, and TA102, and 100‐ to 500‐fold higher than in TA1535, TA92, and TA1538. The addition of a 9,000 × g supernatant fraction (S‐9) from livers of polychlorinated biphenyl‐treated rats, along with cofactors for NADPH generation, resulted in a 90% reduction in the TA100 mutagenicity. MX induced chromosomal aberrations in Chinese hamster ovary cells after 6–8 hr exposure without S‐9 at a dose as low as 4 μg/ml, and after 2 hr exposure with S‐9 at a dose of 75 μg/ml. The oral dose of MX lethal to 50% (LD50) in Swiss‐Webster mice was determined to be 128 mg/kg. MX did not induce micronuclei in mouse bone marrow when administered by oral gavage at doses up to 70% of the LD50.
Detection of TEM‐induced reciprocal translocations in F1 sons of CD‐1 male mice: Comparison of sequential fertility evaluation and cytogenetic analysis
Authors: Morris S. M. , Kodell R. L. , Domon O. E. , Bishop J. B. 
Published: February 2007

AbstractTo determine the positive and negative classification error rates associated with the HTA in our laboratory, F1 sons of TEM‐exposed CD‐1 male mice were evaluated by the sequential fertility method with subsequent cytogenetic analysis. Males who sired three litters of size 10 or less when mated to primiparous females from either the B6C3F1 or the BCF1 strain were classified as partial steriles. When meiotic chromosome analyses revealed the presence of at least two cells containing multivalent figures, males were classified as translocation heterozygotes. When the fertility evaluation and the cytogenetic analysis were compared, normal fertility was observed on 5 of 83 (6.02 %) translocation‐bearing F1 males mated to B6C3F1 tester females and on 3 of 83 (3.61 %) F1 males mated to BCF1 tester females. Thus, the false‐negative error rates were 6.02% and 3.61% with these two tester strains. Multivalent figures were not observed in the meiotic chromosomes of 410 F1 males. Of these, 12 (2.93%) had reduced fertility when mated to the B6C3F1 tester strain as did 7 (1.71%) mated to the BCF1 strain. Thus, the false‐positive error rates with these two tester strains were 2.93% for the B6C3F1 strain and 1.71 % for the BCF1 strain. Our results indicate that nonzero error rates, both false‐positive and false‐negative, are associated with the sequential mating method HTA. In addition, the magnitude of these error rates was influenced not only by the tester female strain but also by the genotype of the F1 male.
Clastogenicity of tritiated thymidine to the mouse bone marrow
Authors: Ratpan Flora , Ashby J. 
Published: February 2007

AbstractTritiated thymidine (3HTdR; 120 μCi/mouse) increases the incidence of micronucleated polychromatic erythrocytes (MPE) in bone marrow PE of both B6CF1 and CBA male mice. This effect observed in vivo reflects the clastogenicity reported by other investigators for 3HTdR in vitro. Thymidine itself was concluded to be inactive in the assay at a dose‐level 100 times greater than that required to show activity for 3HTdR. These observations are of relevance to those employing 3HTdR to monitor the mitogenic activity and the genotoxicity of chemicals.
Mutagenesis of bleomycin‐damaged lambda phage in SOS‐deficient and repair endonuclease‐deficient escherichia coli
Authors: Povirk Lawrence F. , Houlgrave C. Webster 
Published: February 2007

AbstractPrevious DNA sequence analysis of bleomycin‐induced forward mutations in repackaged lambda phage has suggested SOS‐dependent replicative bypass of oxidized apyrimidinic sites as a possible mechanism of mutagenesis. In order to evaluate this hypothesis further, frequencies of mutation to a clear‐plaque phenotype were compared for bleomycin‐damaged phage grown in various repair‐deficient strains of Escherichia coli. Survival of bleomycin‐damaged phage was virtually identical in all host strains. Studies in SOS‐deficient strains indicated specific requirements for functional recA+ and umuC+ alleles in the generation of the majority of bleomycininduced mutations, as well as a less stringent requirement for induction of the SOS response by ultraviolet irradiation of the host cells. These results are expected for mutagenesis resulting from apyrimidinic sites. However, the mutation frequency for bleomycin‐damaged phage was the same whether the phage were grown in a wild‐type strain or in strains deficient in apurinic/apyrimidinic repair endonucleases; this was true even for an nth∼nfo∼xth∼ strain lacking all three major apurinic/apyrimidinic endonucleases (endonuclease III, endonuclease IV, and exonuclease III). Likewise, phage grown in an endonuclease IV‐overproducing strain showed the same mutation frequency as those grown in wild‐type cells. These data suggest that either i) bleomycin‐induced mutagenesis results from SOS‐dependent bypass of lesions other than apyrimidinic sites or ii) the number of apyrimidinic sites available for SOS processing is virtually independent of the level of apurinic/apyrimidinic endonuclease activity in the cell. It is possible that a fraction of the apyrimidinic sites induced by bleomycin either are intrinsically resistant to repair or undergo secondary reactions that render them resistant.
Induction of mitotic chromosome loss in the diploid yeast saccharomyces cerevisiae D61 M by genotoxic carcinogens and tumor promoters
Authors: Albertini S. , Friederich U. , Würgler F. E. 
Published: February 2007

AbstractThree genotoxic carcinogens and eight tumor promoters were tested for induction of aneuploidy, specifically chromosome loss, in Saccharomyces cerevisiae D61.M. This is a heterozygous diploid yeast strain that permits the scoring of segregants expressing three linked recessive markers (cyhR2, ade6, and leul), two of which (ade6 and leul) are located close to the centromere on opposite arms of chromosome VII. The centromere marker leu was routinely checked, and a positive control (bavistan) was run with every experiment. The three genotoxic carcinogens aflatoxin B1, benzo(a)pyrene, and 7,12‐dimethylbenz(a)anthracene did not induce aneuploidy, independent of the presence or absence of an exogenous metabolic activation system (rat liver homogenate; S9). Four of the eight tumor promoters tested induced chromosome loss but no mitotic recombination or mutation: cholic acid, lithocholic acid, phenobarbital, and saccharin. Diethylstilbestrol (DES) led to positive as well as to negative results in several independent experiments. In the case of the positive experiment, DES also induced putative recombinants. Three tumor promoters induced neither chromosome loss nor mitotic recombination: anthralin, 4,4′‐dichloro‐diphenyl‐ethane (DDT) and γ‐hexachlorcyclohexane (lindane). From our experiments it can be concluded that the hypothesis put forward by Parry et al. [Nature; 294:263–265], according to which tumor promoters induce chromosome loss in yeast, is not correct in a general sense. In our set of eight tumor promoters, only one half distinctly induced chromosome loss.
Molecular analyses of in vivo hprt mutant T cells from atomic bomb survivors
Authors: Hakoda Masayuki , Hirai Yuko , Kyoizumi Seishi , Akiyama Mitoshi 
Published: February 2007

AbstractIn vivo‐derived hprt‐deficient mutant T cells isolated from three nonirradiated controls and two atomic bomb survivors were studied by Southern blot analysis to investigate the molecular spectra of the mutations. Mutant frequencies for the three controls were 1.8, 2.3, and 7.3 × 10−6, and those for the two survivors (who had received radiation doses of 2.46 and 2.15 Gy, based upon the revised atomic bomb shielded kerma estimates) were 9.3 and 14.4 × 10−6, respectively. Fourteen (13%) of 105 mutant T‐cell colonies from the controls showed various structural changes in the hprt gene. The frequency of mutants with hprt gene structural changes in one atomic bomb survivor, who exhibited a mutant frequency of 9.3 × 10−6, was 26% (16/61), which was significantly higher than that of the controls. However, the frequency of structural changes in the other survivor (14%, 8/59) was not higher than that of the controls. Two sets of mutants (in total, eight mutants) from the survivor, who showed a significantly higher frequency of mutants with hprt gross alterations than did the controls, had the same hprt changes and the same rearrangements of T‐cell receptor (TcR) β‐ and γ‐chain genes, indicating a clonal expansion from one progenitor mutant. This phenomenon may reflect an in vivo recovery process of T cells in the periphery after exposure to atomic bomb radiation. However, when comparing the frequency of mutations, these two sets of mutants should be reduced. After reducing the total number of mutants from the number of gross hprt changes, the frequency was not significantly higher than that of the controls.
Induction of chromosomal aberrations by hypotonic culture conditions is independent of the S‐phase in V79 hamster cells
Authors: Nowak C. 
Published: February 2007

AbstractA deviation from physiological osmolality (300 mOsm/kg H2O) can lead to genotoxic effects. A 30‐min treatment of V79 hamster cells with hy‐potonic sodium chloride of 60 mOsm/kg H2O or with diluted culture medium of the same osmolality induces extraordinarily high frequencies of chromosomal aberrations. In this study, multiple fixation times over a 24‐hr period were used to identify cells in various stages of the cell cycle at the time of treatment and to find out whether or not hypotonic conditions are able to induce aberrations in all cell cycle stages. Because of the aberration pattern observed, it is suggested that hypotonic treatment acts as an S‐independent agent, like X‐rays or restriction endonucleases. Whether the aberrations originate from directly induced DNA damage or from a release of DNase after lysosomal breakdown is discussed.
DNA strand breakage in normal and solar ultraviolet‐sensitive ICR 2A frog cell lines exposed to solar ultraviolet wavelengths
Authors: Rosenstein Barry S. 
Published: February 2007

AbstractICR 2A frog cells and two solar ultraviolet (UV)‐sensitive cell lines, DRP 36 and DRP 153, were irradiated with 150 kj/m2 of the UV radiation produced by a fluorescent sun lamp, the radiation from which was passed through a sheet of 48A Mylar (DuPont, Wilmington, DE) to eliminate wavelengths shorter than approximately 315 nm. The irradiated cultures were also exposed to photoreactivating light (PRL), resulting in the removal of most of the pyrimidine dimers induced by the sun lamp UV irradiation, and then incubated 0–4 hr. At the end of the incubations, the cells were subjected to the alkaline elution assay. In these elutions, the cell lysates were either treated with proteinase K (proK) to eliminate any DNA‐protein crosslinks (DPC) that may be present in the cells, or left untreated with proK. For the ICR 2A cells, the level of apparent DNA single‐strand breaks (ssb) detected in elutions using proK increased with the incubation time after irradiation and remained high. However, when the DNA was eluted without proK pretreat‐ment, the number of ssb fell rapidly. In contrast, the levels of ssb decreased in the DRP 36 and DRP 153 cells regardless of the use of proK in the elutions. Hence, this differential response in ssb induction may be indicative of a system involved with recovery following irradiation with solar UV wavelengths.
Sodium thiosulfate inhibits cisplatin induced mutagenesis in somatic tissue of Drosophila
Authors: Katz Alan J. 
Published: February 2007

AbstractThe antitumor agent cisplatin was evaluated for genotoxicity in the somatic tissue of Drosophila melanogaster in combination with the nucleo‐philic compound sodium thiosulfate (STS). Third instar larvae transheterozygous for mwh and flr3 were grown on media containing (1) water, (2) 200 mM STS, (3) 0.05 mM cisplatin in 200 mM STS, or (4) 0.05 mM cisplatin. Wings of surviving adults were scored for the presence of twin spots and both small and large single spots; 200 mM STS was nongenotoxic in the assay. Whereas 0.05 mM cisplatin significantly induced all three endpoints, 0.05 mM cisplatin in combination with 200 mM STS was found to have no genotoxic activity. Hence, STS possessed antimutagenic activity in the wing‐spot assay and completely inhibited cisplatin‐induced mutagenesis and mitotic recombination.