bluuebunny/crossref_metadata_2025_split huggingface dataset:
Structural and Theoretical Insights into Metal–Scorpionate Ligand Complexes
Authors: Schwalbe Matthias , Andrikopoulos Prokopis C. , Armstrong David R. , Reglinski John , Spicer Mark D. 
Published: February 2007

AbstractThe syntheses of the complexes [M(TmMe)(CO)2(NO)] (M = Mo, W) by reaction of NOBF4 with [M(TmMe)(CO)3]– are reported and their spectroscopic characterisation and crystal structures are described. The analogous Cr complex could not be prepared by this methodology. The complexes adopt the expected pseudo‐octahedral geometry. Complexes [M(L)(CO)2(NO)] (M = Cr, Mo, W; L = Cp, Tp and TmMe) together with the hypothetical [Mo(CO)2(NO)]+ cation were subjected to DFT calculations. Geometry‐optimised structures closely parallel the crystallographic determinations and indicate that the complex [Cr(TmMe)(CO)2(NO)] is not inherently unstable. The DFT calculations allow the assignment of the C–O and N–O stretches in the IR spectrum and give insight into both the M–NO bonding and the metal to tripodal ligand bonding. The electron‐donor strengths are confirmed to lie in the order TmMe > Tp > Cp. A side reaction of the B–H moiety of the TmMe anion with NO+ results in the isolation of the dimethylformamide adduct of (trismethimazolyl)borane, providing further evidence that the reaction pathways of the TmR ligands are more varied and less passive than in the chemistry of the nitrogen‐based scorpionates.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Preparation and Characterization of Dinuclear NiII Amine‐Thiophenolate Complexes Coligated by EO4– (E = Cl, Re) and EO42– Oxoanions (E = S, Cr, Mo, W)
Authors: Lozan Vasile , Kersting Berthold 
Published: February 2007

AbstractThe ability of dinuclear nickel(II) complexes of the type [(LMe)NiII2(L′)] to coordinate tetrahedral main group and transition metal oxoanions (L′ = EO4–, EO42–) has been examined ((LMe)2– is the deprotonated form of the 24‐membered macrocyclic hexaaza‐dithiophenolate ligand H2LMe). The following complexes have been synthesized: [(LMe)Ni2(ClO4)][ClO4] (2[ClO4]), [(LMe)Ni2(ReO4)][ReO4] (3[ReO4]), [(LMe)Ni2(SO4)] (4), [(LMe)Ni2(CrO4)] (5), [(LMe)Ni2(MoO4)] (6), and [(LMe)Ni2(WO4)] (7). Complexes 2[ClO4], 3[ReO4], 4, 5, and 7 have been characterized by X‐ray crystallography. The complexes are isostructural, with the EO4– and EO42– groups bonded in a μ1,3‐bridging mode to generate dioctahedral N3Ni(μ‐S)2(μ1,3‐EO4)NiN3 core structures. The doubly charged EO42– groups interact more strongly with the [(LMe)Ni2]2+ fragment than the EO4– groups as reflected by the Ni–O distances which are significantly longer in 2 and 3 than in 4–7. The nickel(II) ions in 4 and 6 are weakly ferromagnetically coupled (J = 24.8 and 3.75 cm–1, respectively) and the magnitude of the coupling appears to correlate with the Ni–S–Ni angle. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Electrocatalytic Oxidation and Voltammetric Determination of Hydrazine on the Tetrabromo‐p‐Benzoquinone Modified Carbon Paste Electrode
Authors: Raoof Jahan‐Bakhsh , Ojani Reza , Ramine Maryam 
Published: February 2007

AbstractThe electrochemical properties of hydrazine studied at the surface of a carbon paste electrode spiked with p‐bromanil (tetrabromo‐p‐benzoquinone) using cyclic voltammetry (CV), double potential‐step chronoamperometry and differential pulse voltammetry (DPV) in aqueous media. The results show this quinone derivative modified carbon paste electrode, can catalyze the hydrazine oxidation in an aqueous buffered solution. It has been found that under the optimum conditions (pH 10.00), the oxidation of hydrazine at the surface of this carbon paste modified electrode occurs at a potential of about 550 mV less positive than that of a bar carbon paste electrode. The electrocatalytic oxidation peak current of hydrazine showed a linear dependent on the hydrazine concentrations and linear analytical curves were obtained in the ranges of 6.00×10−5 M–8.00×10−3 M and 7.00×10−6 M–8.00×10−4 M of hydrazine concentration with CV and differential pulse voltammetry (DPV) methods, respectively. The detection limits (3σ) were determined as 3.6×10−5 M and 5.2×10−6 M by CV and DPV methods. This method was also used for the determination of hydrazine in the real sample (waste water of the Mazandaran wood and paper factory) by standard addition method.
Histochemical staining and quantification of dihydrolipoamide dehydrogenase diaphorase activity using blue native PAGE
Authors: Yan Liang‐Jun , Yang Shao‐Hua , Shu Hongjun , Prokai Laszlo , Forster Michael J. 
Published: February 2007

AbstractMammalian mitochondrial dihydrolipoamide dehydrogenase (DLDH, EC 1.8.1.4) catalyzes NAD+‐dependent oxidation of dihydrolipoamide in vivo and can also act as a diaphorase catalyzing in vitro nicotinamide adenine dinucleotide (reduced form) (NADH)‐dependent reduction of electron‐accepting molecules such as ubiquinone and nitroblue tetrazolium (NBT). In this paper, we report a gel‐based method for histochemical staining and quantification of DLDH diaphorase activity using blue native PAGE (BN‐PAGE). Rat brain mitochondrial extracts, used as the source of DLDH, were resolved by nongradient BN‐PAGE (9%), which was followed by diaphorase activity staining using NADH as the electron donor and NBT as the electron acceptor. It was shown that activity staining of DLDH diaphorase was both protein amount‐ and time‐dependent. Moreover, this in‐gel activity‐staining method was demonstrated to be in good agreement with the conventional spectrophotometric method that measures DLDH dehydrogenase activity using dihydrolipoamide as the substrate. The method was applied to determine levels of DLDH diaphorase activity in several rat tissues other than the brain, and the results indicated a similar level of DLDH diaphorase activity for all the tissues examined. Finally, the effects of thiol‐reactive reagents such as N‐ethylmaleimide (NEM) and nitric oxide donors on DLDH diaphorase activity were evaluated, demonstrating that, with this method, DLDH diaphorase activity can be determined without having to remove these thiol‐reactive reagents that may otherwise interfere with spectrophotometric measurement of DLDH dehydrogenase activity. The gel‐based method can also be used as a means to isolate mitochondrial DLDH that is to be analyzed by mass spectral techniques in studying DLDH post‐translational modifications.
EDTA alkaline elution characteristics and measurement of DNA damage in unlabeled DNA using hoechst 33258 fluorescence
Authors: Ducore Jonathan M. 
Published: February 2007

AbstractHoechst 33258 fluorescence of single stranded DNA has been used to perform alkaline elution with unlabeled DNA. The high background fluorescence of “standard” elution solutions has prompted others to use EDTA but the elution characteristics of DNA in EDTA‐containing solutions and the comparability of results with those using “standard” tetrapropyl ammonium hydroxide solutions have not previously been examined. We report here the elution characteristics of DNA in EDTA and the relevant parameters for the successful use of EDTA as an elution solution. An increase in elution pH to 12.4 is required but elution solutions of higher pH cause alkaline hydrolysis of undamaged DNA. Drug‐treated DNA from which DNA‐protein crosslinks have been removed can be completely removed from the filters at the end of the elution by a Pronase filter digestion. The simplest and most efficient removal of DNA‐protein crosslinks is through the inclusion of proteinase‐K in an SDS containing lysis solution. EDTA elution can measure interstrand crosslinks and single strand breaks as easily as is performed using radiolabeled DNA under “standard” elution conditions and requires only 1.5–2 × 106 cells per elution filter. DNA‐protein crosslinking measurements were unsatisfactory, however, since even the Pronase digestion failed to completely remove protein‐crosslinked DNA from the elution filters.Portions of this work were presented at the 77th Meeting of the American Association for Cancer Research, May 1986.
Measurement of unscheduled DNA synthesis and S‐phase synthesis in rodent hepatocytes following in vivo treatment: Testing of 24 compounds
Authors: Mirsalis Jon C. , Tyson C. Kim , Steinmetz Karen L. , Loh Erica K. , Hamilton Carol M. , Bakke James P. , Spalding Judson W. 
Published: February 2007

AbstractThe in vivo‐in vitro hepatocyte DNA repair assay has been shown to be useful for studying genotoxic hepatocarcinogens. In addition, measurement of S‐phase synthesis (SPS) provides an indirect indicator of hepatocellular proliferation, which may be an important mechanism in rodent carcinogenesis. This assay was used to examine 24 chemicals for their ability to induce unscheduled DNA synthesis (UDS) or SPS in Fischer‐344 rats or B6C3F1 mice following in vivo treatment. Hepatocytes were isolated by liver perfusion and incubated with 3H‐thymidine following in vivo treatment by gavage. UDS was measured by quantitative autoradiography as net grains/ nucleus (NG). Controls from both sexes of both species yielded <0.0 NG. Chemicals chosen for testing were from the National Toxicology Program (NTP) genetic toxicology testing program and most were also evaluated in long‐term animal studies conducted by the NTP. 11‐Aminoun‐decanoic acid, benzyl acetate, bis(2‐chloro‐1‐methylethyl)ether (BCMEE), C.I. Solvent Yellow 14, cinnamaldehyde, cinnamyl anthranilate, dichloromethane, dichlorvos, glutaraldehyde, 4,4′‐methylenedianiline (MDA), 4‐nitrotoluene, 4,4′‐oxydianiline, a polybrominated biphenyl mixture (PBB), reserpine, 1,1,2,2‐tetrachloroethane, 1,1,2‐trichloroethane, trichloroethylene, and 2,6‐xylidine all failed to induce UDS in rats and/or mice. Dinitrotoluene and Michler's Ketone induced positive UDS response in rat, while N‐nitrosodiethanolamine and selenium sulfide induced equivocal UDS results in mouse and rat, respectively. BCMEE, bromoform, chloroform, PBB, 1,1,2‐trichloroethane, and trichloroethylene were all potent inducers of SPS in mouse liver, while C.I. Solvent Yellow 14, and 1,1,2,2‐tetrachloroethane yielded equivocal SPS results in rat and mouse, respectively. These results indicate that most of the test compounds do not induce UDS in the liver; however, the significant S‐phase response induced by many of these compounds, especially the halogenated solvents, may be an important mechanism in their hepatocarcinogenicity.
Comparative study of the mutagenic and genotoxic activity associated with inhalable particulate matter in Rio de Janeiro air
Authors: Miguel Ann G. , Daisey Joan M. , Sousa Judy A. 
Published: February 2007

AbstractWe have determined the genotoxic and mutagenic activities associated with inhalable particulate matter (IPM) collected in Rio de Janeiro, Brazil, Camden, NJ, and Caldecott Tunnel, CA, and used these results to compare three different bioassays. Samples collected every 12 hr (Rio) or every 24 hr (Camden) were extracted sequentially with cyclohexane (CX), dichloromethane (DCM), and acetone (ACE), for a rough fractionation by polarity, and composites of the extracts were tested for mutagenicity using the Salmonella frame shift (TA98) and base substitution (TA100) tester strains, as well as for genotoxicity using the Rossman Microscreen bioassay based on the induction of γ‐prophage in a lysogenic Escherichia coli strain. All samples were tested without and with S9 metabolic activation. Maximum mutagenic and genotoxic activities were in the nonpolar (CX) and polar (ACE) fractions, respectively, indicating that these two assays detect different classes of compounds with different efficiencies. Oxidative aging of the Rio aerosol is indicated by a shift in activities in both tests from the less polar fractions in the day to the polar (ACE) fraction at night. The Rio TA98 mutagenic (18 rev/m3) and genotoxic (1.4 × 105 PFU/m3) activities were higher than those fcr Camden, an Eastern U.S. city, by factors of 1.4 and 2.8, respectively.
Sister chromatid exchange and chromosome aberrations in mice after in vivo exposure of green S‐A food colorant
Authors: Giri A. K. , Sivam S. Sai , Khan K. A. , Sethi N. 
Published: February 2007

AbstractSister chromatic exchanges (SCE) and chromosome aberrations (CA) in mice after in vivo exposure of Green S were carried out following single acute treatment. Except for the lowest dose (25 mg/kg body weight) a significant increase in the SCEs were observed in all the other doses (50, 100, and 200 mg/kg) tested. In CA study two higher doses (200 and 400 mg/kg) showed a significant increase in CA when compared with control. The minimum effective dose which induced SCE and CA was 50 and 200 mg/kg of body weight, respectively. The trend tests for the evidence of dose response effects were also significant for both SCE and CA. No significant differences were observed in cell replication kinetic (Rl) analysis. A significant increase in the mitotic index (Ml) was also observed in the highest dose (400 mg/kg) tested when compared with control. Thus the present study indicates that Green S can induce both SCE and CA in vivo in bone marrow cells of mice.
Genetic method for pre‐classification of genotoxins into monofunctional or cross‐linking agents
Authors: Vogel Ekkehart W. , Zijlstra Jaap A. , Nivard Madeleine J. M. 
Published: February 2007

AbstractTo characterize environmental carcinogens, there is a need to distinguish monofunctional genotoxic agents from those having cross‐linking potential, because chemicals which can cross‐link DNA are among the most potent carcinogens in rodents [Barbin and Bartsch, 1989] and humans [Allen et al., 1988; Kaldor et al., 1988]. Here we provide a genetic method for a pre‐classification of genotoxins with respect to their functionality—monofunctional versus cross‐linking. The procedure is based on the determination of relative clastogenic efficiency by a two‐endpoint comparison in Drosophila: (i) induction of chromosome loss (CL), (ii) incidence of recessive lethal mutations (RL). Analysis of CL/RL ratios of 53 genotoxins, all mutagens in Drosophila, permitted distinction of 45 into two major categories: (i) 21 monofunctional agents with CL/RL indices generally ≤1; (ii) 24 agents with ratios >2 exhibiting DNA cross‐linking properties. Within the group of monofunctional agents, CL/RL ratios tend to be low for SSN1 agents, i.e., for N‐ethyl‐N‐nitrosourea, N‐ethyl‐N′‐nitro‐N‐nitrosoguanidine, and for N‐nitroso‐diethylamine. With cross‐linking agents, the number of reactive groups appeared of minor importance as bi‐, tri‐, and tetrafunctional agents showed no significant differences in their CL/RL indices. Among 8 chemicals which could not be grouped into one of the two categories are two (adriamycin, daunomycin) regarded as intercalating agents. It is concluded that this two‐endpoint analysis in Drosophila has prognostic value and can assist in the characterization of genotoxic agents with unknown mode of action. © 1993 Wiley‐Liss, Inc.
Interchange and intra‐nuclear architecture
Authors: Savage John R. K. 
Published: February 2007

AbstractFor chromatin lesions to interact to form exchanges of any sort, it is obvious that contact between them must be made. However, the probability of such interaction is conditioned by other factors like time, initial separation, metabolic activity, and, in the case of chemically induced lesions, scheduled DNA synthesis.The irradiated nucleus was, for a long time, regarded as a “bag of broken chromosomes” with the severed ends free to move around and find partners with which to form illegitimate reunions. Many of these would be seen at following metaphase as intra‐ and interchanges.Evidence is rapidly accumulating which indicates that this picture of the nucleus is false. We know now that chromosomes occupy highly localised domains with limited movement, and that there is no massive intermingling; that much of the chromatin is compacted and splinted with proteins and so precluded from exchange‐type contact; that most of the chromatin is looped and “fixed” into an intra‐nuclear protein scaffold or skeleton; that some chromatin is spun‐out and associated with the nuclear envelope in the vicinity of the pore‐complexes.Thus it would appear that movement, in the sense envisaged by early workers, is curtailed, and that only a proportion (probably a small proportion) of the chromatin is actually “at‐risk” with respect to interchange formation.Where then does interchange take place? Are the “sites” pre‐existent, or can proximity requirements be realised after radiation exposure? In what ways will the intra‐nuclear architecture influence exchange? These are some of the questions which are considered in this paper. © 1993 Wiley‐Liss, Inc.
Genotoxic effects of the carbamate insecticide, methomyl. II. In vivo studies with pure compound and the technical formulation, “lannate 25”
Authors: Bolognesi Claudia , Peluso Marco , Degan Paolo , Rabboni Roberta , Munnia Armelle , Abbondandolo Angelo 
Published: February 2007

AbstractThe carbamate insecticide, methomyl, and the methomyl‐containing technical formulation, “Lannate 25”, were tested for the induction of DNA damage in vivo. Swiss CD1 mice were treated intraperitoneally with test substances and the following tests were performed: alkaline elution of liver and kidney DNA, 8‐hydroxy‐guanosine detection in liver DNA, and 32P‐postlabelling analysis of DNA adducts in liver DNA. The clastogenic activity of the two pesticide preparations was also evaluated as micronucleus frequency in bone marrow. No DNA adducts were detected in liver DNA of mice treated with pure methomyl, while a dose‐related increase in DNA adducts was found in Lannate 25‐treated animals. All other tests were positive with both methomyl and Lannate 25. A summary of genotoxic activity of methomyl is also presented. The hypothesis that the observed genotoxic effects of methomyl are induced indirectly, through formation of active oxygen species, is discussed. © 1994 Wiley‐Liss, Inc.
Preferential effects of the chemotherapeutic DNA crosslinking agent mitomycin C on inducible gene expression in vivo
Authors: Caron Rosemary M. , Hamilton Joshua W. 
Published: February 2007

AbstractThe immediate effects of a single dose of the chemotherapeutic DNA crosslinking agent, mitomycin C (MMC), on the expression of several constitutive and drug‐inducible genes were examined in a simple in vivo system, the 14 day chick embryo. We observed no effect of MMC on the steady‐state mRNA expression of the constitutively expressed β‐action, transferrin, or albumin genes. In contrast, MMC treatment significantly altered both the basal and drug‐inducible mRNA expression of two glutethimide‐inducible genes, 5‐aminolevulinic acid (ALA) synthase and cytochrome P450 CYP2H1. The basal expression of these genes was transiently but significantly increased over a 24 hr period following a single dose of MMC. Conversely, MMC significantly suppressed the glutethimide‐inducible expression of these genes when administered 1 to 24 hr prior to the inducing drug. The effects of MMC on both basal and drug‐inducible ALA synthase and CYP2H1 mRNA expression were principally a result of changes in the transcription rates of these genes. In contrast, MMC treatment had little or no effect on glutethimide‐induced expression of ALA synthase or CYP2H1. when administered 1 hr after the inducing drug, suggesting that a very early event in the induction process represents the target for these MMC effects. Covalent binding studies demonstrated that the effects of MMC on gene expression were closely correlated temporally with formation of [3H]‐porfiromycin‐DNA adducts. These results support the hypothesis that genotoxic chemicals specifically target their effects to inducible genes in vivo. © 1995 Wiley‐Liss, Inc.
Software package for the management of sequencing projects using lacl transgenic animals
Authors: De Boer Johan G. 
Published: February 2007

AbstractThe bacterial lacl gene has been used for many years as a mutational target for the study of the mechanisms of mutation. A wealth of information has been collected for many mutagenic treatments and in strains with diverse DNA repair backgrounds. Recently this gene has been used in the construction of a transgenic mouse, named Big Blue®, and a transgenic rat, as well as a rat cell line. The lacl gene in these animals and cells can conveniently be recovered and analyzed in bacteria. This makes it possible to study mutagenic potential of chemical compounds in vivo using a mammal. Tissue, strain, and gender specificity can be addressed. In addition, mutations recovered from tumour tissues or from animals with specific genetic backgrounds can be analyzed conveniently. The mammalian systems can produce large numbers of mutants that require computer assistance to manage the samples and the resulting DNA sequence data. Accordingly, a computer software system was develped. The system maintains an inventory of bacteriophage lambda lacl mutants and allows entry of mutant sequences while performing accuracy checks on the data. The software features several options for displaying lists of mutants. The system can perform several analyses, including mutant class compilations, mutational spectra comparisons, and clonal expansions analysis. An extensive database obtained from the bacterial lacl system is included with the software and can be analyzed along with mutants derived from transgenic animals. © 1995 Wiley‐Liss, Inc.
Proto‐oncogene amplification and homogeneously staining regions in human breast carcinomas
Authors: Saint‐Ruf Claude , Gerbault‐Seureau Michéle , Viegas‐Péquignot Evani , Zafrani Brigitte , Cassingena Roland , Dutrillaux Bernard 
Published: February 2007

AbstractCytogenetic studies on fresh human breast cancers revealed that homogeneously staining regions (HSRs), which are assumed to represent DNA amplification, are observed in almost half of the cases. To search for a possible relationship between HSRs and proto‐oncogene amplification, 16 proto‐oncogenes, including ERBB2, were studied by Southern blot analysis in four tumors with two or three HSRs, and in three tumors without HSRs. Only four proto‐oncogenes were found to be amplified in at least one tumor each: HST and INT2 (x3), MYC (x2–3), and FES (x > 10). The large sizes of the HSRs, which each corresponded to several percent of the haploid genome, were hardly compatible with the low rate of amplification, except for FES and then only if a large adjacent segment was co‐amplified. This incomplete correlation was demonstrated by in situ hybridization, using biotinylated probes, which showed fluorescent spots on only one HSR for FES in one tumor and for INT2 in another one. Our results indicate that most of the large amplifications corresponding to HSRs do not involve the proto‐oncogenes usually studied in breast cancer. The large amplification of FES, detected in one tumor, may be coincidental.
Cytogenetic findings in six posterior uveal melanomas: Involvement of chromosomes 3, 6, and 8
Authors: Sisley Karen , Rennie Ian G. , Cottam David W. , Potter Anthony M. , Potter Christopher W. , Rees Robert C. 
Published: February 2007

AbstractSix posterior uveal melanomas were karyotyped after short‐term culture. One had a normal chromosome complement; the remaining five had limited chromosome changes. Involvement of chromosomes 1 and 6 was noted in two and four cases, respectively, and three ciliary body tumours demonstrated both monosomy 3 and i(8q).