bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of ultraviolet light‐, ethyl methanesulfonate‐, and 7, 12‐dimethylbenz[a]anthracene‐induced unscheduled dna synthesis by retinol and retinoic acid in the primary rat hepatocyte
Authors: Budroe John D. , Shaddock Joseph G. , Casciano Daniel A. 
Published: February 2007

AbstractThe effects of retinol and retinoic acid on unscheduled DNA synthesis (UDS) in primary Sprague‐Dawley rat hepatocytes were studied in the presence and absence of known chemical and physical mutagens. Neither retinol nor retinoic acid caused a significant increase in UDS over solvent control at concentrations ranging from 1 μM to 50 μM. Retinol and retinoic acid did not significantly affect 200 μg/mL ethyl methanesulfonate(EMS)‐ or 32 J/m2 ultraviolet light(UV)‐induced UDS at concentrations ranging from 1 μM to 50 μM. In contrast, retinol and retinoic acid significantly inhibited 2.5 μg/mL and 5.0 μg/mL 7,12‐dimethyl‐benz[a]anthracene(DMBA)‐induced UDS at concentrations of 1 μM or greater. Retinol‐and retinoic acid‐induced hepatocytotoxicity was studied in vitro using lactate dehydrogenase (LDH) release as an indicator of cytoxicity. Neither retinol nor retinoic acid caused significant increases in LDH release over solvent control 3 hours after treatment, whereas retinol caused a biologically significant increase in LDH release 24 hours posttreatment at concentrations of 50 μM and 100 μM. These data suggest that nontoxic concentrations of retinol and retinoic acid do not inhibit the DNA excision repair process but apparently affect the effective DNA adduct load due to the ultimate species of DMBA metabolite responsible for hepatocellular DNA damage.
Mutagenicity testing of some medicinal herbs
Authors: Riazuddin S. , Malik M. M. , Nasim A. 
Published: February 2007

AbstractExtracts of four brands of a Pakistani local medicine called naswar and six indigenous herbs commonly used as medicine in children were tested for their ability to induce mutations to prototrophy in Salmonella typhimurium tester strains TA98, TA100, TA1535, and TA1537. Petroleum ether extracts of one brand of naswar, namely green naswar of Peshawar, exhibited mutagenicity in all of the four tester strains. Organic extracts of three herbs, Saussurea lappa, Swertia chiraita, and Skimmia laureola, exhibited mutagenic activity in tester strain TA98. Green naswar of Bannu, grey naswar, red naswar, and the remaining three herbs, namely, Acorous calamus, Azadarachta indica, and Zanthozylum alatum, exhibited no mutagenic activity under the present experimental conditions. The abilities of green naswar of Peshawar and Saussurea lappa to induce mutations was shown to be related to the presence of cyclic aromatic compounds with molecular formulas C34 H44 O9 and C15 H18 O2, respectively. The experimental data are discussed as they relate to the potential hazards of such naturally occurring compounds and to synthetic compounds in excessive and uncontrolled use by the general public in villages in Pakistan.
Mitomycin C‐induced sister chromatid exchanges in vivo and in vivo/in vitro in mice and Chinese hamsters
Authors: Krishna G. , Nath J. , Ong T. 
Published: February 2007

AbstractMouse and Chinese hamster models have been extensively used for assessing the cytogenetic effects of environmental carcinogens and mutagens. However, there is little information on comparative analysis of chromosomal damage in these species under in vivo and in vivo/in vitro (culturing of cells from animals exposed to the test compound) systems. To obtain such information, mice and Chinese hamsters were injected with varying concentrations (0.5–6.0 mg/kg) of mitomycin C, an antineoplastic drug. The bone marrow and spleen cells were analyzed for the number of sister chromatid exchanges (SCEs) under in vivo and in vivo/in vitro conditions. The results indicated a dose‐related SCE response that varied with species, tissues, and assay conditions. The mouse cells appeared more sensitive to the effects of mitomycin C than did Chinese hamster cells. In general, the SCE frequencies were relatively higher under in vivo conditions than under in vivo/in vitro conditions in both species. The spleen cells had higher SCE values than bone marrow cells under in vivo/in vitro conditions in both species. These differences may be related to the pharmacokinetic properties of the drug in different species and tissues, to treatment conditions, or to the repair capabilities of the cells. This study also indicates the usefulness of recently established bone marow and spleen in vivo/in vitro cell cultures for comparative cytogenetic analysis.
Genotoxic effects of cisplatin in somatic tissue of Drosophila melanogaster
Authors: Katz Alan J. 
Published: February 2007

AbstractThird instar larvae of Drosophila melanogaster transdihybrid for mwh and flr were exposed to varying concentrations of cisplatin by feeding on dry media wetted with aqueous solutions of the test compound. Larval feeding continued until pupation, and surviving transdihybrid adults were collected seven days following commencement of feeding. Wings of adults were removed and scored under 400X magnification for the presence of twin spots and single spots comprised of clones of cells possessing malformed wing hairs. Cisplatin was found to induce both twin spots and single spots, and significant (p < 0.05) linear concentration‐response relationships were obtained with respect to the induction of all endpoints. Induction of twin spots demonstrates that cisplatin induces mitotic recombination in the somatic tissue of Drosophila larvae. This capacity to induce mitotic exchange in the somatic tissue of Drosophila compares well with the compound's reported ability to induce chromosome breaks in Drosophila germ cells [Brodberg et al, 1983]. However, not all compounds possess similar genotoxic profiles in the somatic and germ tissue of Drosophila.
Structure‐mutagenicity relationships of benzidine analogues
Authors: Messerly E. A. , Fekete J. E. , Wade D. R. , Sinsheimer J. E. 
Published: February 2007

AbstractThe mutagenic activities of benzidine, its dihydrochloride salt, and 12 of their analogues were compared in the Ames test using strains TA100 and TA98 with and without rat liver S9 activation. With the exceptions of 4,4′‐methylenebis(3‐nitroaniline) in both strains and 3,3′‐dichlorobenzidine in TA98, little or no mutagenicity was observed in the series when tested without S9 activation. All compounds, except tetramethylbenzidine, exhibited some activity in TA100 with S9 activation; dichlorobenzidine and 4‐aminobiphenyl were significantly more mutagenic than the other compounds. This was in contrast to the TA98 results where the bridged diphenyl compounds, with the exception of the nitroaniline derivative, were only slightly mutagenic compared to the more planar biphenyl series. Only the nitroaniline compound was mutagenic in both strains in the presence or absence of S9 activation. For benzidine and the 3,3′‐disubstituted benzidines (the dimethoxy‐, diamino‐, and dichloro‐ compounds), an increase in mutagenicity correlated to a decrease in basicity of the parent anilines in both TA100 and TA98.
Mutagenic and lethal effects of near‐ultraviolet radiation (290–400 nm) on bacteria and phage
Authors: Eisenstark A. 
Published: February 2007

AbstractDespite decades of study of the effect of near‐ultraviolet radiation (NUV) on bacterial cells, insights into mechanisms of deleterious alterations and subsequent recovery are just now emerging. These insights are based on observations that 1) damage by NUV may be caused by a reactive oxygen molecule, since H2O2 may be a photoproduct of NUV; 2) some, but not all, of the effects of NUV and H2O2 are interchangeable; 3) there is an inducible regulon (oxyR) that responds to oxidative stress and is involved in protection against NUV; 4) a number of NUV‐sensitive mutants are defective either in the capacity to detoxify reactive oxygen molecules or to repair DNA damage caused by NUV; and 5) recovery from NUV damage may not directly involve induction of the SOS response. Since several distinctly different photoreceptors and targets are involved, it is unknown whether NUV lethality and mutagenesis result from an accumulation of damages or whether there is a particularly critical photoeffect. To fully understand the mechanisms involved, it is important to identify the chromophore(s) of NUV, the mechanism of toxic oxygen species generation, the role of the oxidative defense regulon (oxyR), the specific lesions in the DNA, and the enzymatic events of subsequent repair.
Genetic effects of methylmercury in human chromosomes: I. A cytogenetic study of people exposed through eating contaminated fish
Authors: Monsalve M. V. , Chiappe C. 
Published: February 2007

AbstractAn analysis of chromosomal aberrations (structural and numerical) and sister chromatid exchange (SCE) was carried out on 16 people exposed to methylmercury through eating fish caught in Cartagena Bay (Colombia), an area of known methylmercury contamination. Fourteen people whose diet consisted mainly of fish caught in another, noncontaminated area of the Atlantic acted as controls. The results showed a significant difference between the experimental and control groups in methylmercury (MM) concentrations measured in hair and peripheral blood. Subsequently, significant differences between levels of organic mercury in blood and hair were found when all the individuals studied were classified in two groups according to their blood mercury levels. When achromatic lesions were included, the frequency of structural chromosome aberrations differed significantly between the exposed and control groups. Furthermore, a significant correlation (p < 0.05) was found between structural chromosome aberrations and groups (exposed and control). When achromatic lesions were excluded from the analyses, these differences were not found. There was a significant correlation between SCE and age. This is the first report of a study on the frequency of SCE in a population exposed to methylmercury.
Increased chromosome damage in pediatric heart catheterization patients after diagnostic fluoroscopy and cineangiography
Authors: Shafer David A. , Raviele Anthony A. , Dunbar Virginia G. , Click Lorie A. 
Published: February 2007

AbstractChromosome damage (CD) and sister chromatid exchange (SCE) levels were studied in lymphocytes from 30 pediatric heart catheterization patients receiving radiation during diagnostic fluoroscopy and cineangiography procedures. Forty‐eight‐hour CD and 72‐hr SCE cultures were prepared from sequential samples taken from each patient: samples 1–3 via the catheter the same day (1) before exposure, (2) after fluoroscopy, and (3) after cineangiography; and sample 4 by venipuncture the next morning. Significant increases in CD (dicentrics, rings, and fragments), but not SCE, were observed. From a mean base level of 0.4% cells with CD, the CD levels increased 2‐3‐fold in samples 3 and 4 (p = .001). Rings only occurred in samples 3 and 4. While increased CD levels also correlated with increasing age, body surface area, and weight, partial correlations controlling for these factors clearly indicate that the CD effects are principally attributable to the radiological procedures (p = .001). Increased CD levels correlated with both the roentgen dose of cineangiography exposure (p = .002) and the volume of contrast medium (p = .000); however, partial correlations, controlling for either factor, indicate that the contrast medium was the principal factor (p = .006).
Presence and measurement of sample histidine in the ames test: Quantification and possible elimination of a source of false‐positive mutagenicity test results
Authors: Busch David B. , Bryan George T. 
Published: February 2007

AbstractBoth histidine and dipeptides that can be converted to histidine can potentially interfere with the Ames test by increasing the number of spontaneous revertants. Such interference might be especially evident when urine and other biological samples are studied in this assay. We have developed a turbidimetric bioassay that utilizes a nonrevertible Salmonella typhimurium histidine auxotroph, NS1135. The assay is linear with histidine over at least a 300‐fold range (0.015‐5 μg/ml of L‐histidine·HCl·H2O). Data indicate that several histidine‐containing dipeptides can be utilized as efficiently as free histidine. Our data suggest that this assay may be used to measure biological samples accurately for their histidine content and thereby permit an adjustment for sample histidine during the setup of Ames assays, thus eliminating increased reversion caused by sample histidine.
Cytogenetic and chemical detection of human exposure to polyhalogenated aromatic hydrocarbons
Authors: Lundgren K. , Collman G. W. , Wang‐Wuu S. , Tiernan T. , Taylor M. , Thompson C. L. , Lucier G. W. 
Published: February 2007

AbstractPeripheral lymphocytes from Taiwanese women (n = 35) exposed to polychlorinated aromatic hydrocarbons and from matched controls (n = 24) were assessed for the levels of sister chromatid exchanges (SCEs) after a 72‐hour incubation of whole blood in the presence or absence of alpha‐naphthoflavone (ANF) and for chromosome aberrations after 48 hours of incubation. Serum levels of polychlorinated biphenyl (PCB) congeners were measured for all individuals, and serum levels of several polychlorinated dibenzofurans (PCDFs) were measured for 12 exposed individuals by gas chromatography‐mass spectometry. Blood concentrations of total PCBs in the exposed population averaged approximately 15 ppb, whereas mean PCDF values were 14 ppt. Major PCB congeners detected were 2,2′ 4,4′, 5,5′‐hexa CB and 2,2′3,4,4′,5‐hexa CB. PCDFs detected were primarily 1,2,3,4,7,8,‐hexachlorodibenzofuran (10.8 ppt) and 2,3,4,7,8‐pentachlorodibenzofuran (2.7 ppt). Average SCE frequencies were 7.61 for controls and 7.30 for exposed individuals when assays were conducted in the absence of ANF, whereas respective values were 8.85 and 10.75 in the presence of ANF. Differences in the level of ANF‐induced SCEs between the two populations were highly significant (P < .001). Moreover, the ANF‐induced SCEs were highly correlated with the serum concentrations of total PCBs and of several PCB congeners (P < .001). Increases in ANF‐induced SCEs appeared to be linear up to a PCB concentration of approximately 30 ppb. Chromosome aberration frequencies were similar in control and exposed populations. These studies demonstrate that in vivo exposure to PCBs and PCDFs result in an enhanced sensitivity of lymphocytes to the SCE‐causing actions of ANF.
Use of the microscreen phage‐induction assay to assess the genotoxicity of 14 hazardous industrial wastes
Authors: Houk Virginia Stewart , Demarini David M. 
Published: February 2007

AbstractThe Microscreen phage‐induction assay, which quantitatively measures the induction of prophage λ in Escherichia coli WP2s(λ), was used to test 14 crude (unfractionated) hazardous industrial waste samples for genotoxic activity in the presence and absence of metabolic activation. Eleven of the 14 wastes induced prophage, and induction was observed at concentrations as low as 0.4 pg per ml. Comparisons between the ability of these waste samples to induce prophage and their mutagenicity in the Salmonella reverse mutation assay indicate that the phage‐induction assay detected genotoxic activity in all but one of the wastes that were mutagenic in Salmonella. Moreover, the Microscreen assay detected as genotoxic five additional wastes that were not detected in the Salmonella assay. The applicability of the Microscreen phage‐induction assay for screening hazardous wastes for genotoxic activity is discussed, as are some of the problems associated with screening highly toxic wastes containing toxic volatile compounds.
A method for studying the mutagenicity of some gaseous compounds in salmonella typhimurium
Authors: Victorin Katarina , Ståhlberg Margareta 
Published: February 2007

AbstractA dynamic flow‐through exposure system was designed for mutagenicity studies of gaseous compounds in Salmonella. Salmonella typhimurium strain TA100 was the primary tester strain. The dose ranges were 0.5–20% of vinyl chloride, ethene, propene, and 1,3‐butadiene, 1–200 ppm of ethylene oxide, 0.5–20 ppm of nitrogen dioxide, and 0.1–3.5 ppm of ozone. The gas flow rate was 250, 500, or 1,000 ml/min, and the exposure time was 6 or 7 hours. Of the tested gases, vinyl chloride, ethylene oxide, and nitrogen dioxide were mutagenic. Ethene, propene, and 1,3‐butadiene were not mutagenic in this system. Ozone is bacteriotoxic, and no mutagenic effect could be demonstrated in the nontoxic dose range. The exposure system was considered suitable for studies on gaseous chemicals.
Responses of the L5178Y tk+/tk− mouse lymphoma cell forward mutation assay ii: 18 coded chemicals
Authors: McGregor Douglas B. , Brown Alison , Cattanach Pamela , Edwards Ian , McBride Douglas , Caspary William J. 
Published: February 2007

AbstractEighteen chemicals were tested for their mutagenic potential in the L5178Y tk+/− mouse lymphoma cell forward mutation assay by the use of procedures based upon those described by Clive and Spector [Mutat Res 44:269–278, 1975] and Clive et al [Mutat Res 59:61–108, 1979]. Cultures were exposed to the chemicals for 4 hr, then cultured for 2 days before plating in soft agar with or without trifluorothymidine (TFT), 3 μg/ml. The chemicals were tested at least twice. Significant responses were obtained with benzofuran, benzyl chloride, bromodi‐chloromethane, butylated hydroxytoluene, chlorendic acid, o‐chlorobenzalmalo‐nitrile, 1,2,3,4‐diepoxybutane, dimethyl formamide, dimethyl hydrogen phosphite, furfural, glutaraldehyde, hydroquinone, 8‐hydroxyquinoline, and resorcinol. Apart from bromodichloromethane, butylated hydroxytoluene and dimethyl hydrogen phosphite, rat liver S9 mix was not a requirement for the activity of any of these compounds. Chemicals not identified as mutagens were water, tert‐butyl alcohol, pyridine, and witch hazel.
Occurrence in vivo of sister chromatid exchanges at the same locus in successive ceil divisions caused by nonrepairable lesions induced by gamma rays
Authors: Morales‐Ramírez Pedro , Vallarino‐Kelly Teresita , Rodríguez‐Reyes Regina 
Published: February 2007

AbstractThe capacity of lesions induced by gamma radiation to produce sister chromatid exchanges (SCE) in successive divisions in mouse bone marrow cells in vivo was evaluated using a protocol for the three‐way differentiation of sister chromatids.Evidence was obtained that exposure to gamma radiation induces DNA lesions that result in the formation of SCE at the same locus in two successive cell divisions. The relevance of this observation with respect to DNA repair and mutagenesis is discussed.
No evidence found for induction of dominant lethal mutations and heritable translocations in male mice by calcium cyclamate
Authors: Cain Katherine T. , Cornett Carolyn V. , Cacheiro Nestor L. A. , Hughes Lori A. , Owens James G. , Generoso Walderico M. 
Published: February 2007

AbstractCalcium cyclamate, an artificial sweetener, was studied for its effectiveness in inducing transmissible chromosomal aberrations in germ cells of male mice. Both the dominant‐lethal and the heritable translocation tests were carried out following daily treatment (on weekdays) of males by oral intubation with the maximum tolerated dose for 6 weeks. Calcium cyclamate is negative in both tests; therefore, there is no evidence of induced chromosome breakage and exchange.
Adaptive response of escherichia coli to alkylation damage
Authors: Volkert Michael R. 
Published: February 2007

AbstractTreatment of cells with low levels of alkylating agents for extended periods of time causes them to become resistant to the lethal and mutagenic effects of subsequent high‐level challenge treatments with alkylating agents. This increased resistance has been called the adaptive response to alkylation damage and results from the induction of an alkylation‐specific DNA repair response. The adaptive response is most efficiently induced by methylating agents and is most effective against the lethal and mutagenic effects of methylation damage to DNA. Four genes have been identified as components of this response, ada, alkA, alkB and aidB. The functions of two of these genes are known. AlkA protein functions as a glycosylase that repairs N3‐meA, N3‐meG, O2‐meT, and O2‐meC residues in DNA, and Ada protein functions as an alkyltransferase that removes alkyl groups from O6‐meG, O4‐meT residues as well as methylphosphotriesters. After it interacts with methylated DNA, Ada protein functions as a positive regulatory element that controls the expression of the adaptive response by stimulating the expression of the ada‐alkB operon, and the alkA and aidB genes.
Effect of treatment medium on induction of aneuploidy by nocodazole in saccharomyces cerevisiae
Authors: Taylor‐Mayer Rhoda E. , Mayer Vernon W. , Goin Carol J. 
Published: February 2007

AbstractWhile studying ways to improve responsiveness of Saccharomyces cerevisiae strain D61.M to agents that induce aneuploidy, we noted that nocodazole, which strongly induces aneuploidy when yeast cells are treated in yeast extract‐peptone‐dextrose (YEPD) medium, had no effect when a synthetic complete (SC) medium was used. Further study revealed that the presence of peptone was necessary for induction. Other aneuploidy‐inducing agents, including ethyl acetate, acetone, and methyl benzimi‐dazoie‐2‐yl‐carbamate (MBC), were equally active in either medium. Benomyl, which degrades to MBC, was less active in SC than in YEPD medium.
Recontacting subjects in mutagen‐exposure‐monitoring studies: II. Results of a questionnaire study of mutagenesis researchers, with review of the pertinent literature
Authors: Busch David B. , Easterling Douglas , Leventhal Howard , Bryan George T. 
Published: February 2007

AbstractA questionnaire on the attitudes of mutagenesis researchers regarding the health significance of and the use of data from tests of human mutagen exposure or genetic damage was completed by 71 of 312 (23%) individuals who had been participants in meetings or organizations concerned with mutagenesis research. On a point scale of 0 to 10, with 0 indicating strong disagreement, 5 indicating uncertainty, and 10 indicating strong agreement, the average respondent felt (8.31 ± 2.27) that data indicating a probable health hazard should be shared automatically with the subjects, but was also moderately concerned about psychological distress of subjects learning of study results indicating abnormally high mutagen exposure (6.14 ± 2.57) or genetic damage (6.94 ± 2.48). The average respondent felt that follow‐up of subjects could improve the quality of mutagen‐exposure‐monitoring studies (8.33 ± 1.49), disagreed that subjects whose laboratory data suggested unusually severe exposure or damage should not be asked about possible sources of exposure (1.15 ± 1.32), and disagreed that it was ethical to follow up but not discuss results with subjects having laboratory evidence of abnormal mutagen exposure (3.78 ± 3.43) or genetic damage (3.06 ± 3.17) to see how many developed cancer relative to a control group.Fifteen specific tests for measuring mutagen exposure or genetic damage were rated on a scale of 0 to 10, with 0 being “totally experimental” and 10 being “absolutely diagnostic of degree of exposure or genetic damage.” Values ranged from 6.13 ± 2.67 for karyotyping leukocytes to 3.43 ± 2.43 for quantifying frequency of rare red cells with mutant protein.