Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 28
Filter
Add more filters










Publication year range
1.
Bull Exp Biol Med ; 158(6): 789-93, 2015 Apr.
Article in English | MEDLINE | ID: mdl-25894779

ABSTRACT

PT/Y mice used for studies of the effects of mutagens are characterized by the absence of spontaneous tumors of the liver, but often develop these tumors in response to chronic oaminoazotoluene treatment. The level of glucocorticoid induction of adaptive hepatic enzyme tyrosine aminotransferase decreases by more than 70% 24 h after acute injection of o-aminoazotoluene to these animals. These mice can serve as a model for studies of the relationship between the effect of carcinogens on the regulation of activity of adaptive hepatic enzymes and their capacity to induce the development of liver tumors.


Subject(s)
Glucocorticoids/pharmacology , Liver/metabolism , Tyrosine Transaminase/metabolism , o-Aminoazotoluene/toxicity , Animals , Mice
2.
Biofizika ; 59(3): 527-32, 2014.
Article in Russian | MEDLINE | ID: mdl-25715596

ABSTRACT

It is found that after administration of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB,) which was hepatocarcinogenic to rats, in suckling mice, the number of neoplastic lesions in the liver of mice was 3 times higher than after analogous administration of equimolar dose of ortho-aminoazotoluene (OAT)). However, in the Ames test (TA-98 strain of Salmonella typhimurium) with activation by hepatic enzymes (S-9 fraction) of both intact and Aroclor-1254-induced mice and rats OAT contributed by an order of magnitude to revertant colonies compared to 3'-Me-DAB. In vivo inhibition of sulfotransferase activity, the enzyme which catalyzes the final stage of the mutagenic activation of aminoazo dyes, had no effect on carcinogenicity of 3'-Me-DAB but more than 4 times elevated that of OAT. It was concluded that the mechanism of carcinogenic action of aminoazo dyes studied is not genotoxic and that the carcinogenic potential of OAT is lost in the process of mutagenic activation.


Subject(s)
Carcinogens/toxicity , Coloring Agents/toxicity , Liver Neoplasms, Experimental , Methyldimethylaminoazobenzene/toxicity , Mutagens/toxicity , o-Aminoazotoluene/toxicity , Animals , Carcinogens/pharmacology , Coloring Agents/pharmacology , Liver/enzymology , Liver/pathology , Liver Neoplasms, Experimental/chemically induced , Liver Neoplasms, Experimental/enzymology , Liver Neoplasms, Experimental/genetics , Liver Neoplasms, Experimental/pathology , Methyldimethylaminoazobenzene/pharmacology , Mice , Mice, Inbred CBA , Mice, Inbred ICR , Mutagens/pharmacology , Rats , Salmonella typhimurium/genetics , Salmonella typhimurium/metabolism , o-Aminoazotoluene/pharmacology
3.
Bull Exp Biol Med ; 154(5): 664-8, 2013 Mar.
Article in English | MEDLINE | ID: mdl-23658894

ABSTRACT

Pentachlorophenol (aromatic amine and azo stain metabolic stimulation inhibitor) reduced the hepatocarcinogenic activity of 4-aminoazobenzene and reduced that of ortho-aminoazotoluene in suckling mice. Both 4-aminoazobenzene and ortho-aminoazotoluene exhibited mutagenic activity in Ames' test in vitro on S. typhimurium TA 98 strain with activation with liver enzymes; this mutagenic activity was similarly suppressed by adding pentachlorophenol into activation medium. Induction of xenobiotic metabolism enzymes, stimulating the mutagenic activity of ortho-aminoazotoluene, suppressed its carcinogenic effect on mouse liver. Hence, ortho-aminotoluene (the initial compound), but not its mutagenic metabolites, was the direct active hepatocarcinogen for mice.


Subject(s)
Carcinogenesis , Carcinogens/metabolism , Liver/drug effects , Liver/metabolism , Pentachlorophenol/pharmacology , o-Aminoazotoluene/metabolism , Animals , Carcinogenicity Tests , Carcinogens/toxicity , Male , Mice , Mice, Inbred C57BL , Mice, Inbred CBA , Mice, Inbred ICR , Mutagenicity Tests , Pentachlorophenol/chemistry , Pentachlorophenol/metabolism , o-Aminoazotoluene/chemistry , o-Aminoazotoluene/toxicity
4.
Cell Cycle ; 12(2): 353-64, 2013 Jan 15.
Article in English | MEDLINE | ID: mdl-23287475

ABSTRACT

One undisputed milestone of traditional oncology is neoplastic progression, which consists of a progressive selection of dedifferentiated cells driven by a chance sequence of genetic mutations. Recently it has been demonstrated that the overexpression of well-defined transcription factors reprograms somatic cells to the pluripotent stem status. The demonstration raises crucial questions as to whether and to what extent this reprogramming contributes to tumorigenesis, and whether the epigenetic changes involved in it are reversible. Here, we show for the first time that a tumor produced in vivo by a chemical carcinogen is the product of the interaction between neoplastic progression and reprogramming. The experimental model employed the prototype of ascites tumors, the Yoshida AH130 hepatoma and other neoplasias, including human melanoma. AH130 hepatoma was started in the liver by the carcinogen o-aminoazotoluene. This compound binds to and abolishes the p53 protein, producing a genomic instability that promotes both the neoplastic progression and the hepatoma reprogramming. Eventually this tumor contained 100% CD133(+) elements and pO(2)-dependent percentages of the three embryonic transcription factors Nanog, Klf4 and c-Myc. Once transferred into aerobic cultures, the minor cellular fraction expressing this triad generates various types of adherent cells, which are progressively substituted by non-tumorigenic elements committed to fibromuscular, neuronal and glial differentiation. This reprogramming appears to be accomplished stepwise, with the assembly of the triad into a sophisticated transcriptional, oxygen-dependent circuitry, in which Nanog and Klf4 antagonistically regulate c-Myc, and hence, cell hypoxia survival and cell cycle activation.


Subject(s)
Cell Dedifferentiation/physiology , Cell Transformation, Neoplastic/metabolism , Gene Expression Regulation, Neoplastic/physiology , Kruppel-Like Transcription Factors/metabolism , Proto-Oncogene Proteins c-myc/metabolism , Transcription Factors/metabolism , Animals , Cell Dedifferentiation/drug effects , Cell Line, Tumor , Cell Transformation, Neoplastic/drug effects , DNA Primers/genetics , Flow Cytometry , Genomic Instability/drug effects , Humans , Kruppel-Like Factor 4 , Liver Neoplasms, Experimental/chemically induced , Male , Microscopy, Electron , Nanog Homeobox Protein , Rats , Rats, Wistar , Real-Time Polymerase Chain Reaction , Tumor Suppressor Protein p53/metabolism , o-Aminoazotoluene/metabolism , o-Aminoazotoluene/toxicity
5.
Vopr Onkol ; 57(2): 216-20, 2011.
Article in Russian | MEDLINE | ID: mdl-21809668

ABSTRACT

Pentachlorophenol, an inhibitor of metabolic activation of aminoazo dyes was administered to suckling mice prior to o-aminoazotoluene (OAT). It was followed by formation of numerous preneoplastic nodules and tumors in the lungs and liver. At the same time, 2,3,7,8-tetrachlorodibenzo-p-dioxine treatment decreased their number in the liver while slightly increasing them in the lung. A possible mechanism of aminoazo dye carcinogenicity is suggested.


Subject(s)
Carcinogens/toxicity , Coloring Agents/toxicity , Liver/pathology , Lung/pathology , Polychlorinated Dibenzodioxins/pharmacology , Precancerous Conditions/chemically induced , o-Aminoazotoluene/toxicity , Animals , Biotransformation/drug effects , Liver/drug effects , Lung/drug effects , Male , Mice , Mice, Inbred CBA , Pentachlorophenol/pharmacology , Polychlorinated Dibenzodioxins/toxicity
6.
Toxicol Appl Pharmacol ; 255(1): 76-85, 2011 Aug 15.
Article in English | MEDLINE | ID: mdl-21672546

ABSTRACT

2'-3-dimethyl-4-aminoazobenzene (ortho-aminoazotoluene, OAT) is an azo dye and a rodent carcinogen that has been evaluated by the International Agency for Research on Cancer (IARC) as a possible (class 2B) human carcinogen. Its mechanism of action remains unclear. We examined the role of the xenobiotic receptor Constitutive Androstane Receptor (CAR, NR1I3) as a mediator of the effects of OAT. We found that OAT increases mouse CAR (mCAR) transactivation in a dose-dependent manner. This effect is specific because another closely related azo dye, 3'-methyl-4-dimethyl-aminoazobenzene (3'MeDAB), did not activate mCAR. Real-time Q-PCR analysis in wild-type C57BL/6 mice revealed that OAT induces the hepatic mRNA expression of the following CAR target genes: Cyp2b10, Cyp2c29, Cyp3a11, Ugt1a1, Mrp4, Mrp2 and c-Myc. CAR-null (Car(-/-)) mice showed no increased expression of these genes following OAT treatment, demonstrating that CAR is required for their OAT dependent induction. The OAT-induced CAR-dependent increase of Cyp2b10 and c-Myc expression was confirmed by Western blotting. Immunohistochemistry analysis of wild-type and Car(-/-) livers showed that OAT did not acutely induce hepatocyte proliferation, but at much later time points showed an unexpected CAR-dependent proliferative response. These studies demonstrate that mCAR is an OAT xenosensor, and indicate that at least some of the biological effects of this compound are mediated by this nuclear receptor.


Subject(s)
Receptors, Cytoplasmic and Nuclear/drug effects , o-Aminoazotoluene/toxicity , Animals , Aryl Hydrocarbon Hydroxylases/genetics , Cell Proliferation/drug effects , Constitutive Androstane Receptor , Cytochrome P450 Family 2 , Hep G2 Cells , Hepatocytes/drug effects , Hepatocytes/physiology , Humans , Liver/drug effects , Liver/metabolism , Male , Mice , Mice, Inbred C57BL , Proto-Oncogene Proteins c-myc/genetics , RNA, Messenger/analysis , Receptors, Cytoplasmic and Nuclear/physiology , Steroid Hydroxylases/genetics
7.
Bull Exp Biol Med ; 152(1): 101-4, 2011 Nov.
Article in English, Russian | MEDLINE | ID: mdl-22803052

ABSTRACT

Transcription factors of the FoxA family (forkhead box A) regulate cell metabolism and differentiation and maintain specificity of liver cell proteome and phenotype of mature hepatocytes. The relationship between hepatocarcinogenicity of azo compounds o-aminoazotoluene (OAT) and 3'-methyl-4-dimethylaminobenzene (3'MeDAB) for GR mice and one of the early events, modulation of the DNA-binding activity of FoxA transcription factor, was studied. Single injection of 3'MeDAB to 12-day-old mice caused liver tumors in 100% males and females similarly as OAT, a well-known mouse hepatocarcinogene. The DNA-binding activity of FoxA in the liver decreased 2.5-3 times by OAT, this resulting in a 40% reduction of glucocorticoid induction of tyrosine aminotransferase (liver-specific gene). In contrast to these, 3'MeDAB did not modify FoxA protein activities or the degree of glucocorticoid induction of tyrosine aminotransferase.


Subject(s)
Azo Compounds/toxicity , Benzene Derivatives/toxicity , Hepatocyte Nuclear Factors/metabolism , Liver Neoplasms/chemically induced , o-Aminoazotoluene/toxicity , Animals , Azo Compounds/pharmacology , Benzene Derivatives/pharmacology , Female , Glucocorticoids , Liver/drug effects , Liver/metabolism , Liver Neoplasms/metabolism , Male , Mice , Protein Binding , Proto-Oncogene Proteins c-ets/metabolism , Transcriptional Activation/drug effects , o-Aminoazotoluene/pharmacology
8.
Mol Carcinog ; 44(4): 223-32, 2005 Dec.
Article in English | MEDLINE | ID: mdl-16267830

ABSTRACT

The effects of rat-specific hepatocarcinogen 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB), mouse-specific hepatocarcinogen ortho-aminoazotoluene (OAT), non-species-specific hepatocarcinogen diethylnitrosamine (DENA), and non-carcinogenic 4'-methyl-4-dimethylaminoazobenzene (4'-MeDAB) on glucocorticoid induction of tyrosine aminotransferase (TAT) and DNA-binding activity of hepatocyte nuclear factor 3 (HNF3) family of transcription factors were investigated with carcinogen-susceptible and -resistant animals. Species-specific hepatocarcinogens 3'-MeDAB and OAT strongly inhibited glucocorticoid induction of TAT in the liver of susceptible but not resistant animals. DENA, which is highly carcinogenic for the liver of both rats and mice inhibited glucocorticoid induction of TAT in both species, while non-carcinogenic 4'-MeDAB was absolutely ineffective both in rats and mice. The inhibition of TAT activity by the carcinogens was due to reduced levels of TAT mRNA, which is most likely to be a result of the reduced rate of transcription initiation of the TAT gene. In all cases, the TAT inhibition was accompanied by significant reduction of DNA-binding activity of the HNF3 transcription factor, which is known to be critical to glucocorticoid regulation of TAT gene. We also demonstrated that the described species-specific effects of OAT and of 3'-MeDAB on HNF3 DNA-binding activity may be initiated not only by administration in vivo, but also by their direct administration to homogenate, intact nuclei or nuclear lysate, but not to nuclear extract fraction, obtained by precipitation with 0.32 g/mL of ammonium sulfate (Fraction I). We showed, that a factor responsible for this effect might be precipitated in 0.32-0.47 g/mL interval of ammonium sulfate concentration. In contrast, non-specific hepatocarcinogen DENA was effective upon being added directly to Fraction I, implying a different mechanism of its action.


Subject(s)
Carcinogens/toxicity , Hepatocyte Nuclear Factor 3-alpha/biosynthesis , Liver Neoplasms, Experimental/chemically induced , Liver/drug effects , Methyldimethylaminoazobenzene/toxicity , Tyrosine Transaminase/biosynthesis , o-Aminoazotoluene/toxicity , Animals , Cell Nucleus/metabolism , Diethylnitrosamine/toxicity , Enzyme Induction , Glucocorticoids/pharmacology , Hepatocyte Nuclear Factor 3-alpha/genetics , Liver/metabolism , Liver Neoplasms, Experimental/metabolism , Male , Mice , RNA, Messenger/metabolism , Rats , Rats, Wistar , Species Specificity , Tyrosine Transaminase/genetics , p-Dimethylaminoazobenzene/toxicity
9.
Toxicology ; 211(1-2): 132-8, 2005 Jul 01.
Article in English | MEDLINE | ID: mdl-15863256

ABSTRACT

The objective of this study was to investigate the CYP1A1 and CYP1A2 mRNAs and enzyme activities in mouse liver during induction with o-aminoazotoluene (OAT) as well as the capability of the hepatic S9-fraction from OAT-treated mice to induce its own activation to mutagens in the Ames test using S. typhymurium strain TA98. The data obtained indicate that when used at appropriate doses, OAT is a PAH-type inducer of mouse hepatic microsomal monooxygenases, which activity is not less than that of the known inducer 3,4-benzo[alpha]pyrene. In the absence of S9-fraction enzymes no OAT-mediated mutagenicity was observed in the Ames test. In the presence of the S9-fraction from OAT-pretreated mice, OAT induced as high revertant numbers, as it did in the presence of the S9 fraction from the liver of Aroclor 1254-treated mice. Thus, OAT does induce the enzymes of its own mutagenic activation in mouse liver.


Subject(s)
Enzyme Induction/drug effects , Liver/enzymology , Mutagens/metabolism , Mutagens/toxicity , o-Aminoazotoluene/pharmacology , Animals , Benzo(a)pyrene/metabolism , Biotransformation/drug effects , Cytochrome P-450 CYP1A1/biosynthesis , Cytochrome P-450 CYP1A2/biosynthesis , DNA, Complementary/biosynthesis , DNA, Complementary/isolation & purification , Hydroxylation , Liver/drug effects , Male , Mice , Mice, Inbred C57BL , Mutagenicity Tests , RNA/biosynthesis , RNA/isolation & purification , Reverse Transcriptase Polymerase Chain Reaction , Subcellular Fractions/drug effects , Subcellular Fractions/enzymology , o-Aminoazotoluene/metabolism , o-Aminoazotoluene/toxicity
10.
Tsitologiia ; 46(4): 301-11, 2004.
Article in Russian | MEDLINE | ID: mdl-15346788

ABSTRACT

A most convenient model to study mechanisms of live organism response to chemical carcinogens is tumor induction in murine liver by aminoazodyes, in particular by ortho-aminoazotoluene (OAT). We studied both early and late stages of hepatocarcinogenesis on several lines of inbred mice differing in sensibility to OAT. By means of autoradiography, we examined proliferative activity of hepatocytes obtained from the liver of sensitive (A/He, DD, SWR) and resistant to OAT AKR, CC57Br, BALB/c lines of mice, which were injected carcinogen. The level of p53, p21Cip1, bax, mdm2, cyclin G, gadd45 genes expression in the liver of mice of different lines given OAT injection was studied by multiplex PCR method. Carcinogen caused a decrease of hepatocyte proliferative activity induced by partial hypatectomy (PHE), and an increase in p53, p21Cip, bax, mdm2, and cyclin G genes within mice of A/He, DD and SWR lines. Cell fusion experiments on hepatocytes obtained from regenerating murine liver sensitive to A/He line carcinogen and given long-time OAT administrations with resting and proliferating fibroblasts of NIH 3T3 mice revealed no obvious suppression of DNA synthesis in heterokaryons. Unlike, in fusion experiments on serum-stimulated fibroblasts with hepatocytes obtained from the liver of BALB/c line mice also given OAT suppression of DNA synthesis in stimulated fibroblasts in heterokaryons was observed 15 days following PHE. These results enable us to conclude that OAT administrations break negative endogenous mechanisms of hepatocyte proliferation control in the liver of mice sensitive to carcinogenes.


Subject(s)
Carcinogens/toxicity , Hepatocytes/drug effects , Liver Neoplasms, Experimental/chemically induced , o-Aminoazotoluene/toxicity , 3T3 Cells , Animals , Cell Cycle Proteins/metabolism , Cell Division/drug effects , Cell Fusion , Cyclin G , Cyclin G1 , Cyclin-Dependent Kinase Inhibitor p21 , Cyclins/metabolism , Hepatectomy , Liver/drug effects , Liver/metabolism , Liver Neoplasms, Experimental/metabolism , Male , Mice , Mice, Inbred Strains , Nuclear Proteins/metabolism , Proto-Oncogene Proteins/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , Proto-Oncogene Proteins c-mdm2 , Time Factors , Tumor Suppressor Protein p53/metabolism , bcl-2-Associated X Protein
12.
Toxicol Sci ; 73(1): 108-13, 2003 May.
Article in English | MEDLINE | ID: mdl-12700417

ABSTRACT

The objective of this study was to investigate cytochrome P4501A1 and 1A2 mRNA, protein, and enzyme activity in the liver of male mice differing in the aryl hydrocarbon receptor (AhR) genotype during treatment with the carcinogenic compounds 3-methylcholanthrene (MC) and o-aminoazotoluene (OAT). The basal levels of the CYP1A1 and CYP1A2 enzyme activities were comparable among the mouse strains examined. Significant interstrain variations were observed after treatment by the inducers: EROD and MROD activities were considerably increased in C57BL and A/Sn mice, but not in AKR, SWR, and DBA mice. Western blot analysis did not detect CYP1A1 in the liver of untreated mice. Treatment of mice with MC or OAT caused CYP1A1 accumulation in the liver of C57BL and A/Sn mice, but not in AKR, SWR, and DBA mice. CYP1A2 was detected in all studied mouse strains in both untreated and inducer-treated livers. The results of multiplex RT-PCR showed that the CYP1A1 mRNA in the liver of untreated mice was hardly detectable while constitutive expression of the CYP1A2 gene was rather high. After treatment with MC and OAT the CYP1A1 mRNA level dramatically increased in all strains examined while the increase in the CYP1A2 mRNA level was not striking. This finding did not correlate with the data on the enzyme activity. Our results demonstrated a discrepancy between the transcription of CYP1A1 and CYP1A2 genes and the inducibility of these enzymes in the liver of mice, suggesting a posttranscriptional mechanism of cytochrome P4501A regulation. This comparison between aromatic hydrocarbon-responsive and -nonresponsive strains could contribute to understanding of cytochrome P4501A gene regulation in the liver under the influence of environmental factors.


Subject(s)
Carcinogens/toxicity , Cytochrome P-450 CYP1A1/genetics , Cytochrome P-450 CYP1A2/genetics , Gene Expression Regulation, Enzymologic/drug effects , Liver/enzymology , Methylcholanthrene/toxicity , Polycyclic Aromatic Hydrocarbons/toxicity , o-Aminoazotoluene/toxicity , Animals , Blotting, Western , DNA, Complementary/biosynthesis , DNA, Complementary/genetics , Electrophoresis, Polyacrylamide Gel , Genotype , Liver/drug effects , Male , Mice , Mice, Inbred AKR , Mice, Inbred C57BL , Mice, Inbred DBA , RNA, Messenger/biosynthesis , Reverse Transcriptase Polymerase Chain Reaction , Species Specificity
14.
Mutat Res ; 491(1-2): 211-20, 2001 Apr 05.
Article in English | MEDLINE | ID: mdl-11287313

ABSTRACT

The o-aminoazotoluene (AAT) has been evaluated as a possible human carcinogen by the International Agency for Research on Cancer. In rodents, it is carcinogenic mainly in the liver, and also in lung following long term administration. We previously examined in lambda/lacZ transgenic mice for the induction of lacZ mutations in liver, lung, urinary bladder, colon, kidney, bone marrow, and testis. AAT induced gene mutations strongly in the liver and colon. In the present report, we reveal the molecular nature of mutations induced by AAT in the lambda cII gene (the cII gene, a phenotypically selectable marker in the lambda transgene, has 294bp, which makes it easier to sequence than the original target, the 3kb lacZ gene). The cII mutant frequency in liver and colon was five and nine times higher, respectively, in AAT-treated mice than in control mice. Sequence analysis revealed that AAT induced G:C to T:A transversions, whereas spontaneous mutations consisted primarily of G:C to A:T transitions at CpG sites.


Subject(s)
Lac Operon , Mutagens/toxicity , Mutation , Transcription Factors/genetics , o-Aminoazotoluene/toxicity , Animals , Base Sequence , DNA Primers , Male , Mice , Mice, Transgenic , Viral Proteins
15.
Mutat Res ; 471(1-2): 113-26, 2000 Nov 20.
Article in English | MEDLINE | ID: mdl-11080667

ABSTRACT

o-Aminoazotoluene (AAT) has been evaluated as a possible human carcinogen (Class 2B) by the International Agency for Research on Cancer (IARC). The Ames test found it to be mutagenic in the presence of a metabolic activation system, whereas it has little clastogenicity either in vitro or in vivo in the chromosomal aberration assay. AAT is also carcinogenic in the lung or liver of mice and rats given long-term administrations. Therefore, metabolites generated in the liver etc. may have gene mutation activity, and carcinogenesis would occur. We examined the mutagenicity of AAT in a gene mutation assay, using lacZ transgenic mice (MutaMice) and a positive selection method. AAT showed positive results for organs with metabolic functions, such as liver and colon and other organs. Positive results were also seen in an Ames test in the presence of metabolic activation and negative results seen in a chromosomal aberration test. Therefore, AAT had the potential to cause gene mutation in the presence of metabolic activation systems in vitro and the same reaction was confirmed in vivo with organs with metabolic function, such as liver and colon, but little clastogenicity in vitro or in vivo. Thus, metabolites with gene mutation activity may be responsible for the carcinogenicity of AAT. The transgenic mouse mutation assay proved to be useful for concurrent assessment of in vivo mutagenicity in multiple organs and to supplement the standard in vivo genotoxicity tests, such as the micronucleus assay which is limited to bone marrow as the only target organ.


Subject(s)
Carcinogens/toxicity , Coloring Agents/toxicity , Mutagenicity Tests , Mutagens/toxicity , o-Aminoazotoluene/toxicity , Animals , Animals, Newborn , Cells, Cultured , Chromosome Aberrations , Cricetinae , Cricetulus/genetics , Lac Operon/drug effects , Mice , Mice, Inbred BALB C , Mice, Inbred DBA , Mice, Transgenic , Point Mutation/genetics , Rats , Salmonella typhimurium/drug effects , Salmonella typhimurium/genetics
19.
Gig Sanit ; (5): 15-8, 1998.
Article in Russian | MEDLINE | ID: mdl-9816778

ABSTRACT

The impact of transport vibration on the mutagenic effect (ME) of asbestos, benzo(a)pyrene (BaP), benzene, ortho-aminotoluene, and quinoline was studied. There was a decrease in ME of all the substances when they influenced erythrocytes simultaneously with 24-hour vibration. Decreased ME of BaP was seen during 2-month vibration, and ME increased during 3-day vibration.


Subject(s)
Mutagens , Vibration/adverse effects , Animals , Asbestos/toxicity , Benzene/toxicity , Benzo(a)pyrene/toxicity , Bone Marrow/drug effects , Carcinogens/toxicity , Coloring Agents/toxicity , Data Interpretation, Statistical , Erythrocytes/drug effects , Male , Mice , Micronucleus Tests , Quinolines/toxicity , Solvents/toxicity , Time Factors , o-Aminoazotoluene/toxicity
SELECTION OF CITATIONS
SEARCH DETAIL
...