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Notes: Cited By (since 1996): 9 Export Date: 12 March 2010 Source: Scopus URL - Supplemental materials for


Notes:

Cited By (since 1996): 9

Export Date: 12 March 2010

Source: Scopus

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Author Address:

GSF-Institute fur Toxikologie, D-8042 Neuherberg/Munchen, Germany

Reference Type:

Journal Article

Record Number:

7596

Author:

W. Xu and I. D. Adler

Year:

1990

Title:

Clastogenic effects of known and suspect spindle poisons studied by chromosome analysis in mouse bone marrow cells

Journal:

Mutagenesis

Volume:

5

Issue:

4

Pages:

371-374

Short Title:

Clastogenic effects of known and suspect spindle poisons studied by chromosome analysis in mouse bone marrow cells

Abstract:

The present study was performed within the project 'Genomic Mutations' (sponsored by the Commission of the European Communities) in order to gather all possible experimental information on 10 chemicals selected on the basis of their possible capacity to induce aneuploidy. An analysis of chromosomal aberrations was carried out in bone marrow cells of mice with the first five chemicals: colchicine (COL), econazole (EZ), choralhydrate (CH), hydroquinone (HQ) and diazepam (DIAZ). The experiments were performed in parallel to micronucleus tests with the objective to distinguish a positive micronucleus response due to chromosomal breakage from that obtained by lagging chromosomes. The results of the micronucleus tests will be reported elsewhere. COL, CH, EZ and DIAZ showed no clastogenic effects in mouse bone marrow cells after single intraperitoneal injection. Polyploid cells were significantly more frequent after COL treatment. HQ showed a dose-dependent induction of chromosomal aberrations at 6 and 24 h after treatment. After 24 h, cells with multiple aberrations up to complete chromosome fragmentation were frequently observed. They indicate that a small fraction of the cell population, probably related to a specific stage of the cell cycle, was particulary sensitive to HQ. A sex difference in clastogenic response to HQ was not observed. It is concluded that of the five chemicals tested only HQ was clastogenic in mouse bone marrow cells under the present experimental conditions.

Notes:

Cited By (since 1996): 25

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Author Address:

Department of Biology, Yunnan Normal University, Kunming, Yunnan, China

Reference Type:

Journal Article

Record Number:

7597

Author:

D. Liu, X. Yin, H. Wang, Y. Zhou and Y. Zhang

Year:

1990

Title:

Antimutagenicity screening of water extracts from 102 kinds of Chinese medicinal herbs

Journal:

Zhongguo zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica

Volume:

15

Issue:

10

Pages:

617-622, 640

Short Title:

Antimutagenicity screening of water extracts from 102 kinds of Chinese medicinal herbs

Abstract:

Our observation shows that out of 102 kinds of Chinese medicinal herbs tested, 17 have remarkable antimutagenic effect on the mutation induced by aflatoxin B1, in Ames test. Among the 17 herbs Glycyrrhiza uralensis, Bupleurm chinense, Portulaca grandiflora and Cnidium monnieri have been found in other tests to be effective against mutagenesis induced by cyclophosphamide in mice.

Notes:

Cited By (since 1996): 4

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Author Address:

Laboratory of Medical Genetics, Western Region Hospital, Urumqi.

Reference Type:

Journal Article

Record Number:

7598

Author:

H. Glatt, I. Gemperlein, F. Setiabudi, K. L. Platt and F. Oesch

Year:

1990

Title:

Expression of xenobiotic-metabolizing enzymes in propagatable cell cultures and induction of micronuclei by 13 compounds

Journal:

Mutagenesis

Volume:

5

Issue:

3

Pages:

241-249

Short Title:

Expression of xenobiotic-metabolizing enzymes in propagatable cell cultures and induction of micronuclei by 13 compounds

Notes:

Cited By (since 1996): 53

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http://www.scopus.com/inward/record.url?eid=2-s2.0-0024993931&partnerID=40&md5=558ccd1dfc3aa66d25f2da404b7f2f6a

Author Address:

Department of Toxicology, University of Mainz, Obere Zahlbacher Strasse 67, D-6500 Mainz, Germany

Reference Type:

Journal Article

Record Number:

7599

Author:

L. R. Ferguson, C. M. Hill and B. C. Baguley

Year:

1990

Title:

Genetic toxicology of tricyclic carboxamides, a new class of DNA binding antitumour agent

Journal:

European Journal of Cancer

Volume:

26

Issue:

6

Pages:

709-714

Short Title:

Genetic toxicology of tricyclic carboxamides, a new class of DNA binding antitumour agent

Abstract:

(N-[2-(Dimethylamino)ethyl]acridine-4-carboxamide (acridine carboxamide; NSC 601316) is an acridine-derived experimental antitumour agent with curative properties against Lewis lung carcinoma in mice. Although it intercalates into DNA and also appears to interact with topoisomerase II, its DNA binding properties appear distinct from other acridine derivatives such as the clinical antitumour drug, amsacrine. The mutagenic properties of acridine carboxamide, together with three related compounds containing either 9-aminoacridine or phenazine chromophores, were studied at the 6-thioguanine and ouabain loci in cultured V79 Chinese hamster fibroblasts. Each compound, when tested at concentrations causing up to 90% kill, had weak but significant activity at the 6-thioguanine but not at the ouabain locus. All drugs were potent inducers of micronuclei, indicating high clastogenic activity. There was a highly significant relationship between mutation frequency (as resistance to 6-thioguanine) and either cytotoxicity (measured as D37 in a clastogenicity assay) or clastogenicity. A broader range of compounds was also tested for microbial mutagenicity. In Salmonella typhimurium strains, none were mutagenic in TA98, TA100 or TA102 but several were mutagenic in TA1537, a frameshift tester strain. Some drugs also caused 'petite' mutagenisis in Saccharomyces cerevisiae. In general, compounds with the phenazine chromophore, which has no positive charge, were the most mutagenic in these systems. However, activity was not related to mammalian mutagenicity or antitumour effect. The results suggest that in mammalian cells, the cytotoxity, clastogenicity and mutagenic activity of these drugs are mediated by similar mechanisms to those for amsacrine analogues, probably involving the enzyme DNA topoisomerase II.

Notes:

Cited By (since 1996): 3

Export Date: 12 March 2010

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Author Address:

Cancer Research Laboratory, University of Auckland, Medical School, Auckland, New Zealand

Reference Type:

Journal Article

Record Number:

7600

Author:

G. T. Arce, D. R. Vincent, M. J. Cunningham, W. N. Choy and A. M. Sarrif

Year:

1990

Title:

In vitro and in vivo genotoxicity of 1,3-butadiene and metabolites

Journal:

Environmental Health Perspectives

Volume:

86

Pages:

75-78

Short Title:

In vitro and in vivo genotoxicity of 1,3-butadiene and metabolites

Abstract:

1,3-Butadiene and two major genotoxic metabolites 3,4-epoxybutene (EB) and 1,2:3,4-diepoxybutane (DEB) were used as model compounds to determine if genetic toxicity findings in animal and human cells can aid in extrapolating animal toxicity data to man. Sister chromatid exchange (SCE) and micronucleus induction results indicated 1,3-butadiene was genotoxic in the bone marrow of the mouse but not the rat. This paralleled the chronic bioassays which showed mice to be more susceptible than rats to 1,3-butadiene carcinogenicity. However, 1,3-butadiene did not induce unscheduled DNA synthesis (UDS) in the rat or mouse hepatocytes following in vivo exposure. Likewise, UDS in rat and mouse hepatocytes in vitro was not induced by EB or DEB. Salmonella typhimurium gene mutation (Ames) tests of 1,3-butadiene using strains TA1535, TA97, TA98, and TA100 and employing rat, mouse, and human liver S9 metabolic systems were barely 2-fold above background only in strain TA1535 at 30% 1,3-butadiene in air with induced and uninduced rat S9 and mouse S9 (uninduced). 1,3-Butadiene was negative in in vitro SCE studies in human whole blood lymphocytes cultures treated in the presence of rat, mouse, or human liver S9 metabolic activation. In general, 1,3-butadiene is genotoxic in vivo but is a weak in vitro genotoxin.

Notes:

Cited By (since 1996): 14

Export Date: 12 March 2010

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Author Address:

Haskell Laboratory for Toxicology and Industrial Medicine, E.I. du Pont de Nemours and Company, Inc., United States

Reference Type:

Journal Article

Record Number:

7601

Author:

B. C. Behera and S. P. Bhunya

Year:

1990

Title:

Genotoxic effect of isoproturon (herbicide) as revealed by three mammalian in vivo mutagenic bioassays

Journal:

Indian Journal of Experimental Biology

Volume:

28

Issue:

9

Pages:

862-867

Short Title:

Genotoxic effect of isoproturon (herbicide) as revealed by three mammalian in vivo mutagenic bioassays

Abstract:

Genotoxic effect of isoproturon was assessed by employing in vivo chromosomal aberration, micronucleus and sperm-shape abnormality assays. A significant dose-responsive mutagenic effect was observed in chromosome aberration and sperm-shape abnormality tests whereas in micronucleus assay the effect was significant only at the highest dose (200 mg/kg). Only the result for the chronic dose and the two different fixation times (6 and 48 hr) were not statistically significant. The results indicate the genotoxic property of isoproturon in mammalian in vivo test system.

Notes:

Cited By (since 1996): 15

Export Date: 12 March 2010

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http://www.scopus.com/inward/record.url?eid=2-s2.0-0025487524&partnerID=40&md5=541545d7b7646e72aebf696e35fc3c57

Author Address:

P.G. Department of Zoology, Utkal University, Bhubaneswar, India.

Reference Type:

Journal Article

Record Number:

7602

Author:

J. A. Heddle, A. Bouch, M. A. Khan and J. D. Gingerich

Year:

1990

Title:

Concurrent detection of gene mutations and chromosomal aberrations induced in vivo in somatic cells

Journal:

Mutagenesis

Volume:

5

Issue:

2

Pages:

179-184

Short Title:

Concurrent detection of gene mutations and chromosomal aberrations induced in vivo in somatic cells

Abstract:

A simple direct assay for gene mutations in vivo is the missing assay in genetic toxicology. Here we report that both gene mutations and chromosomal aberrations induced in vivo can be reliably detected and quantified in a single cell type. Lung cells were isolated and cultured from Chinese hamsters that had been exposed to model mutagenic carcinogens, and then analysed in culture for genetic alterations. Chromosomal aberrations were assayed by the frequency of micronuclei found in binucleate cells after growth in the presence of cytochalasin B. Mutations were assayed by the frequency of thioguanine-resistant colonies on the 10th day of culture. X-rays and ethyl nitrosourea produced detectable increases in both mutations and chromosomal aberrations. Ethyl methanesulphonate produced large numbers of mutations but no chromosomal aberrations and methyl methanesulphonate produced the inverse: large numbers of chromosomal aberrations but no mutations. Our experience with these agents and the procedure suggests a standard protocol for the assay, and confirms the value of measuring both gene mutations and chromosomal aberrations.

Notes:

Cited By (since 1996): 12

Export Date: 12 March 2010

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http://www.scopus.com/inward/record.url?eid=2-s2.0-0025168006&partnerID=40&md5=6b747b969dfd2427e0009460d26bdf8d

Author Address:

Department of Biology, York University, Toronto, Ont. M3J 1P3, Canada

Reference Type:

Journal Article

Record Number:

7603

Author:

V. Georgieva, R. Vachkova, M. Tzoneva and A. Kappas

Year:

1990

Title:

Genotoxic activity of benomyl in different test systems

Journal:

Environmental and Molecular Mutagenesis

Volume:

16

Issue:

1

Pages:

32-36

Short Title:

Genotoxic activity of benomyl in different test systems

Keywords:

Ames test

bone marrow cells

dominant lethals

human lymphocytes



Abstract:

Benomyl (methyl-1-[butylcarbamoyl]-2-benzimidazole carbamate), a benzimidazole derivative fungicide, was tested in the Ames test for point mutations; in human lymphocytes cultures for cell division disturbances, chromosomal aberrations, and SCE; in rat bone marrow cells in vivo for micronuclei; and in rats in vivo for dominant lethals. Benomyl was negative in the Ames test. In human lymphocytes, benomyl at concentrations of 0.5, 1.0, and 2.0 μg/ml decreased the number of cells undergoing third division whereas at the concentrations of 0.25 to 4.0 μg/ml it strongly increased the number of aneuploid cells. Benomyl was also shown to induce sister chromatid exchanges and micronuclei but not chromosome aberrations. Benomyl decreased the number of female rats with implants but did not cause any dominant lethals.

Notes:

Cited By (since 1996): 17

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http://www.scopus.com/inward/record.url?eid=2-s2.0-0025302676&partnerID=40&md5=b4d050e1c5c25729a4faabb25cf723bc

Author Address:

National Research Center, 'Democritus', P.O. Box 60228, Athens 15310, Greece

Reference Type:

Journal Article

Record Number:

7604

Author:

L. M. Bakhitova, V. Pashin Yu, S. N. Drobchenko and G. N. Bondarev

Year:

1990

Title:

Antimutagenic activity of modified polygluquin compounds

Journal:

Izevestiya Akademii Nauk SSSR - Seriya Biologicheskaya

Issue:

4

Pages:

625-628

Short Title:

Antimutagenic activity of modified polygluquin compounds

Notes:

Export Date: 12 March 2010

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URL:

http://www.scopus.com/inward/record.url?eid=2-s2.0-0025298262&partnerID=40&md5=c674ba197c94d3fb3cb63a3d530eced2

Author Address:

Institute of General Genetics, USSR Academy of Sciences, Moscow, Russia

Reference Type:

Journal Article

Record Number:

7605

Author:

L. S. Mullin, A. W. Ader, W. C. Daughtrey, D. Z. Frost and M. R. Greenwood

Year:

1990

Title:

Toxicology update Isoparaffinic hydrocarbons: A summary of physical properties, toxicity studies and human exposure data

Journal:

Journal of Applied Toxicology

Volume:

10

Issue:

2

Pages:

135-142

Short Title:

Toxicology update Isoparaffinic hydrocarbons: A summary of physical properties, toxicity studies and human exposure data

Abstract:

The Isoparaffins covered in this manuscript are branched aliphatic hydrocarbons with a carbon skeleton length ranging from approximately C10 to C15. They are used in the manufacturer of liquid imaging toners, paint formulations, charcoal lighter fluid, furniture polishes and floor cleaners. Potential exposure exists in the petroleum, printing and paint industries. Isoparaffins have a very low order of acute toxicity, being practically non-toxic by oral, dermal and inhalation routes. However, aspiration of liquid isoparaffins into the lungs during oral ingestion could result in severe pulmonary injury. Dermally, isoparaffins have produced slight to moderate irriation in animals and humans under occluded patch conditions where evaporation cannot freely occur. However, they are not irritating in non-occluded tests, which are a more realistic simulation of human exposure. They have not been found to be sensitizers in guinea pig or human patch testing. However, occasional rare idiosyncratic sensitization reactions in humans have been reported. Installation of isoparaffins into rabbit eyes produces only slight irritation. Several studies have evaluated sensory irritation in laboratory animals or odor or sensory response in humans. When evaluated by a standard procedure to assess upper airway irritation, isoparaffins did not produce sensory irritation in mice exposed to up to 400 ppm isoparaffin in air. Human volunteers were exposed for six hours to 100 ppm isoparaffin. The subjects were given a self-administered questionnaire to evaluate symptoms, which included dryness of the mucous membranes, loss of appetite, nausea, vomiting, diarrhea, fatigue, headache, dizziness, feeling of inebriation, visual disturbances, tremor, muscular weakness, impairment of coordination or paresthesia. No symptoms associated with solvent exposure were observed. With a human expert panel, odor from liquid imaging copier emissions became weakly discernible at approximately 50 ppm. Numerous long-term exposures have been conducted in animals with only one major finding observed. Renal tubular damage has been found in kidneys of male rats upon repeated exposures to isoparaffins. It does not occur in mice or in female rats. This male rat nephropathy has been observed with a number of hydrocarbons, including wholly vaporized unleaded gasoline. The phenomenon has been attributed to reversible binding of hydrocarbon to α2μ-globulin. Since humans do not synthesize α2μ-globulin or a similar protein, the finding is not considered to be of biological significance to man. No clinically significant renal abnormalities have been found in refinery workers exposed to hydrocarbons. When evaluated for developmental toxicity in rats, isoparaffins were neither embryotoxic nor teratogenic. Isoparaffins were consistently negative on standard bacterial genotoxicity assays. They were also non-genotoxic in in vivo mammalian testing for somatic or germ cell mutations (mouse micronucleus test and rat dominant lethal assay, respectively).

Notes:

Cited By (since 1996): 14

Export Date: 12 March 2010

Source: Scopus

URL:

http://www.scopus.com/inward/record.url?eid=2-s2.0-0025351189&partnerID=40&md5=aece38bd7872cf41d34984aa94d111e3

Author Address:

Syntex Corporation, 3401 Hillview Avenue, Palo Alto, CA 94304, United States

Reference Type:

Journal Article

Record Number:

7606

Author:

L. Zhao, S. Yan and T. Jiang

Year:

1990

Title:

Inhibitory effect of liuwei dihuang decoction on induced mutation and spontaneous tumor

Journal:

Zhong xi yi jie he za zhi = Chinese journal of modern developments in traditional medicine / Zhongguo Zhong xi yi jie he yan jiu hui (chou), Zhong yi yan jiu yuan, zhu ban

Volume:

10

Issue:

7

Pages:

433-435, 390

Short Title:

Inhibitory effect of liuwei dihuang decoction on induced mutation and spontaneous tumor

Abstract:

Anti-mutagenic activity was evaluated with micronuclear test. It appeared to be same between the result of mice treated with 10 g/kg Liuwei Dihuang decoction (LWDHd) for 3 days and that with 34.5 g/kg for 10 days. All the permillages of micronuclear appearance of treated groups were less than that of controls. The intercept (A) value of dose-effect curve were 12.7 and 9.4 as treated with cyclophosphamide (Cy) alone, but 1.2 and 3.2 as orally administered with LWDHd before injecting Cy. It showed that LWDHd could inhibite mutagenic activity of Cy. The affection of LWDHd on spontaneous tumorigenesis was observed in LACA mice. The tumor incidence rate was 9.0% in the control mice observed for 60 weeks, but 5.0% in the animal feeding LWDHd in food. The tumor incidence rate of big dose group was 1.0% and the difference was significant between it and that of the control (P less than 0.01).

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Export Date: 12 March 2010

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URL:

http://www.scopus.com/inward/record.url?eid=2-s2.0-0025455429&partnerID=40&md5=20482468e9416b97a38f98bb57f4672b

Author Address:

Institute of Chinese Materia Medica, China Academy of TCM, Beijing.

Reference Type:

Journal Article

Record Number:

7607

Author:

C. G. Rogers, B. G. Boyes and E. Lok

Year:

1990

Title:

Comparative genotoxicity of 3 procarcinogens in V79 cells as related to glutathione S-transferase activity of hepatocytes from untreated rats and those fed 2% butylated hydroxyanisole

Journal:

Mutation Research

Volume:

244

Issue:

2

Pages:

163-171

Short Title:

Comparative genotoxicity of 3 procarcinogens in V79 cells as related to glutathione S-transferase activity of hepatocytes from untreated rats and those fed 2% butylated hydroxyanisole

Keywords:

AFB1

Antioxidant-induced enzymes

Chromosome effect

DMBA


DMN

Glutathione S-transferase activity of hepatocytes

GST activity

Hepatocytes



Abstract:

When 7,12-dimethylbenz[a]anthracene (DMBA) and aflatoxin B1 (AFB1) were activated by hepatocytes from Fischer 344 rats fed a diet containing 2% butylated hydroxyanisole (BHA), frequencies of mutation to 6-thioguanine resistance (TG(R)) at the HGPRTase gene locus and to ouabain resistance (Ou(R)) at the Na+, K+-ATPase gene locus in V79 cells were 30-70% less than those obtained with hepatocytes from untreated controls. A difference in the mutation frequency did not occur when dimethylnitrosamine (DMN) was activated by BHA induced-rather than control-hepatocytes. Analysis of hepatocytes from rats fed 2% BHA showed a small (1.5-fold), but significant, increase in glutathione levels over that in the controls but no change in activity of cytochrome P450. Cytosolic glutathione S-transferase (GST) activity was increased 2-3 fold in hepatocytes from rats fed the 2% BHA diet. These results suggest that mutagenic response to DMBA and AFB1 is reduced, at least in part, because of BHA-induction of hepatocyte GST activity; while activation of DMN can occur by pathway(s) unaffected by BHA-induction of these liver enzymes. In contrast to mutation frequencies, significant differences between BHA- and control-activation in the production of sister-chromatid exchange (SCE) and micronucleus formation (MN) were not detected with any of the genotoxins. It was concluded that the mechanism(s) by which SCE and MN occur are likely unrelated to the capacity of BHA to induced activity of hepatic enzyjes, e.g. the GSH S-transferases, that directly or indirectly affect mutation end-points.
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