bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrodes of Nontoxic Solid Amalgams for Electrochemical Measurements
Authors: Yosypchuk Bogdan , Novotný Ladislav 
Published: December 2002

AbstractThe preparation, activation and electrochemical pretreatment of electrodes based on nontoxic solid amalgams were described. Testing of metal solid amalgam electrodes (MeSAEs) proved their broad applicability in many respects, e.g., as to the range of working potentials and the level of background currents, well comparable with those of the hanging mercury drop electrode (HMDE). A regeneration of their surfaces before each measurements could be simply automatized using a PC‐controlled system providing a reasonable repeatability of voltammetric measurements down to 3% RSD. Combination with stripping techniques at accumulation times tac=300 s the detection limit amounted to the concentration level of 1 ppb Cu(II), Pb(II), Cd(II), Zn(II), etc. Best electrochemical properties were exhibited by the silver solid amalgam electrode (AgSAE). For example, polished AgSAE (p‐AgSAE), completely free of liquid mercury, proved satisfactory even at more negative potentials enabling the determination of Zn(II), Mn(II), IO$\rm{ {_{3}^{-}}}$, etc. Moreover, even better repeatability of mercury meniscus modified AgSAE (m‐AgSAE) was due to better quality and renewability of its surface. In many cases further testing confirmed that under appropriate conditions MeSAEs represent good, often cheaper and more users‐friendly alternatives to HMDE.
Msh2 deficiency increases the mutation frequency in all parts of the mouse colon
Authors: Zhang Shulin , Lloyd Ruth , Bowden Gregory , Glickman Barry W. , de Boer Johan G. 
Published: December 2002

AbstractThe Msh2 DNA mismatch repair gene is one of five genes implicated in the pathogenesis of hereditary nonpolyposis colorectal cancer (HNPCC). To address the possible mechanisms of the site‐specific occurrence of HNPCC, the effect of Msh2 deficiency on mutations in different parts of the colon was investigated using the BC‐1(lacI)/Msh2 double transgenic mouse. Compared to the Msh2+/+ mice, Msh2‐/‐ mice had an 8–9‐fold increase of mutation frequency (MF) in the lacI gene from the cecum and the proximal and distal colon. The mutational spectra were also significantly different between Msh2+/+ and Msh2‐/‐ mice, with a significant increase in the frequency of −1 frameshifts and G:C→A:T base substitutions in the repair‐deficient mice. However, in spite of the site‐specific predisposition of HNPCC in humans, we found no significant difference in the MF or mutation spectrum between the three parts of the colon in Msh2+/+, Msh2+/‐, or Msh2‐/‐ mice. In addition, 11 independent mutants harboring complex mutations within the lacI gene were recovered in the Msh2‐/‐ mice. Interestingly, while the Msh2+/‐ mice displayed an overall MF similar to that observed in the wild‐type mice, sequencing revealed a significantly different mutational spectrum between Msh2+/+ and Msh2+/‐ mice, mainly characterized by an increase in −1 frameshifts. Due to the prevalence of frameshift mutations in HNPCC patients, this haploinsufficiency effect of the Msh2 gene in safeguarding genomic integrity may have important implications for human carrier status. Environ. Mol. Mutagen. 40:243–250, 2002. © 2002 Wiley‐Liss, Inc.
Transmission of mutations in the lacI transgene to the offspring of ENU‐treated Big Blue® male mice
Authors: Barnett Lois B. , Tyl Rochelle W. , Shane Barbara S. , Shelby Michael D. , Lewis Susan E. 
Published: December 2002

AbstractThe purpose of the study was to determine: 1) if male germ cells of Big Blue® mice carrying newly induced mutations in the lacI transgene were effective in fertilization; 2) if offspring arising from such mutant sperm had the mutation in germ cells and multiple somatic tissues; and 3) how the frequency of mutants induced in the lacI transgene compared to the frequency induced in endogenous genes traditionally employed to study germ cell mutagenesis in mice. Male B6C3F1 mice hemizygous for the lambda/lacI transgene were treated weekly with 100 mg/kg body weight of the mammalian germ cell mutagen N‐ethyl‐N‐nitrosourea (ENU). The cumulative dose for each treated animal was 300 mg ENU/kg body weight. Ten weeks later the treated mice were mated to T stock females and the resulting offspring were screened for specific‐locus mutations at six loci affecting external appearance, as well as for mutations in the lacI transgene in multiple somatic tissues and germ cells. Five offspring carrying recessive specific‐locus mutations were observed among 597 offspring screened (mutant frequency = 139.6 × 10‐5 per locus). Four offspring carrying lacI mutations were observed among 280 offspring screened (mutant frequency = 35.7 × 10‐5 per locus (assuming 40 target loci)). Each of the four lacI mutant offspring carried a different mutation. Three of the mutations were A:T→G:C transitions and one a G:C→A:T transition. Consistent with the expectation that a mutation induced in a parental germ cell and transmitted to a conceptus would exist in every cell of the offspring, each mutant mouse had identical mutations in all somatic tissues sampled, as well as in its germ cells. These data provide preliminary evidence for the biological validity of assessing induced, heritable mutations using transgenic mice, without the need for generating an F1 generation. Environ. Mol. Mutagen. 40:251–257, 2002. © 2002 Wiley‐Liss, Inc.
Genotoxicity biomonitoring in regions exposed to vehicle emissions using the comet assay and the micronucleus test in native rodent Ctenomys minutus
Authors: Heuser Vanina D. , da Silva Juliana , Moriske Heinz‐Jörn , Dias Johnny F. , Yoneama Maria Lúcia , de Freitas Thales R.O. 
Published: December 2002

AbstractExposure to motor vehicle emissions represents an important concern for possible long‐term health effects. The present report describes: 1) the application and verification of the alkaline comet assay in Ctenomys minutus to detect the possible genotoxicity of automobile emissions; 2) a comparison of the comet assay results with peripheral blood micronucleus (MN) assay results performed in the same animals; and 3) the identification of agents involved in the responses and in the seasonal variation of the effects. Ctenomys minutus (Octodontidae‐Rodentia) were captured in two different fields from both sides of RS/030, a highway on the coastal plain of the Brazilian state of Rio Grande do Sul. Reference animals were obtained from a nearby field that was about 3 km distant from any road. By the end of this study, 123 rodents (73 females and 50 males) were live‐trapped. Our results indicate that there was an increase in cells with DNA damage for C. minutus environmentally exposed to automobile emissions, as demonstrated by the alkaline comet assay, but there was no increase in micronucleated cells. The alkaline comet assay showed age and gender differences in the response. The comet assay results suggest that adult females are the principal population affected by air pollutants from vehicle emissions. Chemical data were also collected from areas exposed to automobile exhaust and these indicated that elevated levels of hydrocarbons, metals, and NO2 were associated with the elevated levels of damaged cells observed in the wild rodent C. minutus. Our results agree with previous data on engine and fuel components, where weak increases in damage for native rodents exposed to emissions have been observed. Other larger, controlled studies are needed to better understand how the metabolism of C. minutus affects its response to emission exposure. Environ. Mol. Mutagen. 40:227–235, 2002. © 2002 Wiley‐Liss, Inc.
Effects of heat shock protein 70 (Hsp70) on arsenite‐induced genotoxicity
Authors: Barnes J.A. , Collins B.W. , Dix D.J. , Allen J.W. 
Published: December 2002

AbstractArsenic, a human carcinogen, is genotoxic, although its mechanism(s) of action for tumorigenesis is not well understood. Among the toxicity‐related properties of this chemical are its clastogenic and aneugenic activities, as well as its capacity for inducing stress‐response in the form of elevated heat shock protein (HSP) expression. In the present study, we evaluated the effects of Hsp70 expression on arsenite (As)‐induced structural and numerical chromosome anomalies in human cells. Human MCF‐7 Tet‐off cells stably transfected with a pTRE/Hsp70‐1 transgene construct were used to regulate Hsp70 levels prior to in vitro As exposures. Separate cultures of relatively high vs. low Hsp70‐expressing cells were established. A cytokinesis block micronucleus assay with kinetochore immunostaining was used to detect micronuclei (MN) derived from chromosome breakage (K−MN) or loss (K+MN). These studies demonstrated significant increases in micronucleus frequencies in response to As following either a long exposure (5 or 10 μM for 46 hr), or short exposure (10 or 40 μM for 8 hr) protocol. Overall, the long protocol was more efficient in producing K+MN and cells with multiple MN. Overexpressing Hsp70 resulted in significant reductions in the percent of cells positive for MN for both the long and short As exposure protocols. Both K+ and K− types of As‐induced MN were lower in cells with elevated Hsp70 as compared to cells without overexpression of Hsp70. We conclude that the dose and duration of As exposure influence the type as well as amount of chromosomal alteration produced and that inducible Hsp70 protects against both the clastogenic and aneugenic effects of this chemical. Environ. Mol. Mutagen. 40:236–242, 2002. Published 2002 Wiley‐Liss, Inc.
Mutagenic activity of cisplatin in the lacZ plasmid‐based transgenic mouse model
Authors: Louro Henriqueta , Silva Maria J. , Boavida Maria G. 
Published: December 2002

AbstractCis‐diamminedichloroplatinum (II) (cisplatin) is a well characterized antitumor drug used for the treatment of a variety of human cancers. The cytotoxicity of cisplatin is mainly mediated through the formation of DNA adducts, which are also believed to be responsible for the secondary malignancies produced by the drug. The aim of this study was to determine the in vivo mutagenic activity of cisplatin in the lacZ plasmid‐based transgenic mouse model. The mutant frequency (MF) and the spectrum of mutations induced by cisplatin in the mouse liver were analyzed and compared to controls. The mean MF in the lacZ gene was increased 2‐fold in mice treated with a single 6 mg/kg body weight dose of cisplatin and sacrificed after 17 and 28 days (P = 0.001 and P < 0.0001). Restriction analysis and sequencing of mutant DNA showed that cisplatin was able to induce both large deletions and point mutations. A specific profile of base substitution and frameshift mutations was identified in treated mice, consisting primarily of G:C→A:T transitions at GpG and ApG sites, the preferential DNA binding sites of cisplatin, and single basepair deletions/insertions. The present results provide the first evidence that cisplatin has mutagenic activity in vivo and induces a characteristic pattern of mutations in the mouse liver. This mutagenicity may be responsible for its tumorigenic activity. Environ. Mol. Mutagen. 40:283–291, 2002. © 2002 Wiley‐Liss, Inc.
Induction of epithelial tumors in Drosophila melanogaster heterozygous for the tumor suppressor gene wts
Authors: Eeken Jan C.J. , Klink Ilse , van Veen Bert L. , Pastink Albert , Ferro Wouter 
Published: December 2002

AbstractThe imaginal disk cells of Drosophila have a cell cycle that is very similar to that of mammalian cells. Data concerning factors inducing tumors in these cells may directly relate to the risk of these factors for inducing cancer in humans. One of the genes involved in the regulation of cell cycle control is wts (warts), the Drosophila homolog of the mammalian tumor suppressor gene LATS1. The Drosophila wts mutations are recessive lethal. However, homozygous clones that arise in heterozygous flies in the imaginal disk cells lead to epithelial tumors, spectacular outgrowths visible on the cuticle of the adult. We have treated Drosophila larvae, heterozygous for wts, with the chemical mutagen MMS (methyl methanesulfonate) or with X‐rays and measured the appearance of epithelial tumors in the eclosing adult flies. This test is a variation of the well‐known Drosophila somatic mutation and recombination test (SMART), where mostly recessive markers have been used leading to visible phenotypes in the eyes and wings of the fly. We show that the sensitivity of this test is far greater than the comparable test system using the recessive eye marker white. Environ. Mol. Mutagen. 40:277–282, 2002. © 2002 Wiley‐Liss, Inc.
Overexpression of heme oxygenase‐1 (HO‐1) in V79 cells results in increased resistance to hyperbaric oxygen (HBO)‐induced DNA damage
Authors: Rothfuss Andreas , Speit Günter 
Published: December 2002

AbstractHeme oxygenase (HO) catalyzes the rate‐limiting step in the oxidative degradation of heme to biliverdin. The isoform HO‐1 is inducible by a variety of agents causing oxidative stress and has been suggested to play an important role in cellular protection against oxidant‐mediated cell damage. Using treatment of cell cultures with hyperbaric oxygen (HBO) as a model for oxidative stress, we have shown an induction of HO‐1 in isolated human lymphocytes after a single HBO exposure and protection of these cells against DNA damage by subsequent oxidative stress. In contrast, V79 Chinese hamster cells showed neither a comparable adaptive protection nor an induction of HO‐1 after HBO exposure, which makes this cell line an attractive model system for a further characterization of HO‐1‐mediated protection. In the present study, we investigated whether overexpression of HO‐1 renders V79 cells more resistant to DNA damage induced by HBO. Transient transfection of V79 cells with a full‐length human HO‐1 cDNA resulted in a 2–3‐fold increase in HO‐1 protein levels. Comet assay experiments with and without FPG posttreatment for the determination of oxidative DNA base damage showed that HO‐1 overexpressing V79 cells were significantly protected against oxidative DNA damage induced by a single HBO exposure. Furthermore, HO‐1‐transfected cells exhibited a clearly reduced induction of micronulei after HBO treatment. Since the observed protective effects were abolished by cotreatment with the HO‐1 inhibitor tin‐mesoporphyrin, our study suggests that a low‐level overexpression of HO‐1 provides protection against oxidative DNA damage induced by HBO. Environ. Mol. Mutagen. 40:258–265, 2002. © 2002 Wiley‐Liss, Inc.
Evaluation of the clastogenic, DNA intercalative, and topoisomerase II‐interactive properties of bioflavonoids in Chinese hamster V79 cells
Authors: Snyder Ronald D. , Gillies Peter J. 
Published: December 2002

AbstractBioflavonoids are naturally occurring polyphenols with intriguing and varied therapeutic and chemoprotective activities generally ascribed to their antioxidant properties. However, many flavonoids have also been shown to be genotoxic in a variety of prokaryotic, eukaryotic, and in vivo systems. The mechanistic basis for this genotoxicity has not been fully elucidated, although structure–activity relationship studies have identified requisite flavonoid structural features. We utilized Chinese hamster V79 cells to evaluate the relationships between DNA intercalation ability, topoisomerase II interactions, reactive oxygen species (ROS) generation, and clastogenicity in a series of 14 bioflavonoids. Five of the flavonoids examined, luteolin, quercetin, genistein, apigenin, and acacetin, were strongly clastogenic. This clastogenicity was shown to require DNA intercalation (with the exception of genistein) and was substantially reduced by catalytic inhibitors of DNA topoisomerase II. The transition metals Cu(II) and Mn(II) formed chelates with and/or modified the structure and biological activity of some flavonoids but no consistent relationship could be demonstrated between metal reactivity and clastogenicity. There was no clear association between generation of ROS and clastogenicity. The data presented herein are consistent with a model in which the genotoxicity of most flavonoids arises via DNA intercalation and topo II poisoning, likely mediated through metabolism to flavonoid quinones. Interestingly, other flavonoids such as myricetin, daidzein, baicalein, fisetin, and galangin were catalytic topo II inhibitors, rather than poisons. These studies further validate the use of cell‐based approaches for detecting drug/topo II interactions and raise interesting questions relating to biological and chemical mechanisms of flavonoids. Environ. Mol. Mutagen. 40:266–276, 2002. © 2002 Wiley‐Liss, Inc.
Mouse lymphoma thymidine kinase gene mutation assay: Follow‐up International Workshop on Genotoxicity Test Procedures, New Orleans, Louisiana, April 2000
Authors: Moore Martha M. , Honma Masamitsu , Clements Julie , Harrington‐Brock Karen , Awogi Takumi , Bolcsfoldi George , Cifone Maria , Collard Deborah , Fellows Michael , Flanders Kathryn , Gollapudi Bhaskar , Jenkinson Peter , Kirby Paul , Kirchner Stephan , Kraycer Joann , McEnaney Stephen , Muster Wolfgang , Myhr Brian , O'Donovan Michael , Oliver Jo , Ouldelhkim Marie‐Claude , Pant Kamala , Preston Robert , Riach Colin , San Richard , Shimada Hiroyasu , Stankowski Leon F. 
Published: December 2002

AbstractThe Mouse Lymphoma Assay (MLA) Workgroup of the International Workshop on Genotoxicity Test Procedures held a second harmonization meeting just prior to the U.S. Environmental Mutagen Society Meeting in New Orleans, LA, in April 2000. The discussion focused on several important aspects of the MLA, including: 1) cytotoxicity measures and their determination, 2) use of a 24‐hr treatment, 3) the ability of the assay to detect aneugens, and 4) concentration selection. Prior to the meeting the group developed Microsoft Excel Workbooks for data entry. Ten laboratories entered their data into the workbooks (primarily as coded chemicals). The Excel Workbooks were used to facilitate data analysis by generating an extensive set of graphs that were evaluated by the meeting participants. Based on the Workgroup's previous agreement that a single cytotoxicity measure should be established for both the microwell and soft agar versions of the assay, the Workgroup analyzed the submitted data and unanimously agreed that the relative total growth (RTG) should be used as the cytotoxicity measure for concentration selection and data evaluation. The Workgroup also agreed that the various cytotoxicity measures should be calculated using the same methods regardless of whether the soft agar or microwell version of the assay was used. In the absence of sufficient data to make a definitive determination, the Workgroup continued to endorse the International Committee on Harmonization recommendation for the use of 24‐hr treatment and made some specific 24‐hr treatment protocol recommendations. The Workgroup recognized the ability of the MLA to detect at least some aneugens and also developed general guidance and requirements for appropriate concentration selection. Environ. Mol. Mutagen. 40:292–299, 2002. © 2002 Wiley‐Liss, Inc.
Extreme events controlling erosion and sediment transport in a semi‐arid sub‐andean valley
Authors: Coppus R. , Imeson A. C. 
Published: December 2002

AbstractThe importance of extreme events in controlling erosion and sediment transport in semi‐arid areas has long been appreciated but in practice being by definition rare and episodic they are difficult to study. When they are observed this is frequently in catchments for which little data are available. Another difficulty is that even when catchments are being monitored the instruments that record discharge, sediment load and hillslope sediment fluxes perform inaccurately or unpredictably during extreme weather conditions. This paper describes slope and channel processes that were actually observed by the authors during a (at least) 1 : 30 year 30 minute event with a rainfall intensity of 240 mm h−1 in a second‐order tributary of the Rio Camacho near Tarija in southern Bolivia. During the event, it could be observed how different tributary streams and slope sections contributed sediments and flow to the main channel. Evidence for these contributions did not survive the event, which has implications for both modelling and monitoring. Before the onset of the event open erosion plots were functioning on the slopes where rainfall and runoff were being measured. Rainfall experiments were used to obtain infiltration rates.The storm began with a moderate intensity of about 5 cm per hour but increased after 5 minutes to 30 cm per hour and continued for 30 minutes. At this time, the rainfall intensity greatly exceeded the infiltration capacity and water started draining the steep slopes. The ephemeral channel rapidly filled up with runoff. Erosion by hailstones was considerable.Provisionally, the discharge during peak runoff was estimated at 43·7 m3 s−1 (Manning equation). On the basis of sediment loads carried by previous storms, (average concentration of 21 g l−1) the total suspended load discharge during the storm would have been 15 ton ha−1. Within the ephemeral channel, 10 to 50 cm thick layers of coarse sediments were deposited. The collectors of the open erosion plots could not handle the large amounts of runoff and sediment and were completely filled to overflowing.Comparing these data with soil losses during less intense storms it can be concluded that extreme events largely contribute to erosion and sediment transport and that the majority of the rainstorms play only a minor role. The results also show how limited the values of rainfall experiments are in understanding geomorphic events. This makes modelling of erosion and soil losses a difficult and hazardous task. Copyright © 2002 John Wiley & Sons, Ltd.
Slope–channel linkage and sediment delivery on North Carolina coastal plain cropland
Authors: Slattery Michael C. , Gares Paul A. , Phillips Jonathan D. 
Published: December 2002

AbstractThis paper presents the results of field measurements conducted in a small (19·4 ha) agricultural basin on the North Carolina coastal plain. The overall objective of the study is to determine the magnitude of soil erosion and sediment delivery as a result of storm runoff. The results suggest that erosion in the region is more rapid and extensive than previously thought. Fields at the site are experiencing accelerated soil loss, with rates often comparable to those of the southeastern Piedmont, a region long recognized as having rapid and problematic soil loss. This casts doubt on some assessments of the coastal plain as being a stable, non‐eroding landscape. However, much of the soil mobilized is redistributed and stored within the watershed with only a small portion of the soil eroded from slopes leaving the basin on an event time frame. Copyright © 2002 John Wiley & Sons, Ltd.