Mutagenesis by chemical agents in V79 Chinese hamster cells: A review and analysis of the literature

Bradley, Matthews O.; Bhuyan, Bijoy K.; Francis, Mary C.; Langenbach, Robert; Peterson, Andrew R.; Huberman, Eliezer

doi:10.1016/0165-1110(81)90029-4

Cited by 264 publications

(65 citation statements)

References 113 publications

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“…The ability of 6-thioguanine (6-TG)-resistant cells to replicate DNA and thus allowing cell multiplication in the presence of 6-TG is a reliable indicator of Hprt mutation [32,33]. For mutant frequency analysis, the sense or antisense oligonucleotide-treated V79 cells were subcultured into 100-mm dishes (5×10 5 cells/dish) in the growth medium containing 6-TG (7 µg/ml).…”

Section: Screening Of Hprt Mutantsmentioning

confidence: 99%

“…Experiments were repeated 4 to 5-times to identify presumptive mutants. Plating efficiencies were determined in the absence of the 6-TG [27,32,33]. In parallel experiments, sense or antisense oligonucleotide-treated cells were mock treated or treated with glucose oxidase (GO) to induce oxidative stress.…”

Section: Screening Of Hprt Mutantsmentioning

confidence: 99%

“…Colonies of 6-TGresistant cells grown for 6 to 8 days were fixed in 3.7% formalin, and stained with 0.1% crystal violet. The Hprt mutant frequency was calculated from the number of 6-TG-resistant colonies relative to the total number of colonies in non-selecting medium [32,33]. A549 cells at 60% confluency (~3 × 10 6 ) were treated with NEIL1 antisense or sense oligonucleotide four times in a 30 h time period.…”

Section: Screening Of Hprt Mutantsmentioning

confidence: 99%

“…Because of the ease in scoring its forward mutations [32,33] the single copy, X-linked Hprt locus has been widely used to evaluate the genotoxicity of various chemical and physical agents, as well as the impact of altered levels of DNA repair proteins, [37,38]. Fig 3 shows that NEIL1 downregulation increased the HPRT mutant frequency by about 3-fold in both V79 and A549 cells relative to treatment with the sense (control) oligonucleotide, or to the untreated cells.…”

Section: Increased Mutation Frequency In Neil1-downregulated Cellsmentioning

confidence: 99%

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Mutator phenotype of mammalian cells due to deficiency of NEIL1 DNA glycosylase, an oxidized base-specific repair enzyme

et al. 2008

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The recently characterized NEIL1 and NEIL2 are distinct from the previously characterized mammalian DNA glycosylases (OGG1 and NTH1) involved in repair of oxidized bases because of the NEILs' preference for excising base lesions from single-stranded DNA present in bubble and fork structures. OGG1 and NTH1 are active only with duplex DNA. This raises the possibility that NEILs function in the repair of base lesions during DNA replication and/or transcription. S-phasespecific activation of only NEIL1 suggests its preferential involvement in repair during DNA replication. Here we show that antisense oligonucleotides specific for human or Chinese hamster NEIL1 decreased in vivo NEIL1 levels by 70-80%, concomitant with increased oxidative damage in the genome. Moreover, NEIL1 downregulation enhanced spontaneous mutation in the HPRT locus by about 3-fold in both Chinese hamster V79 and human bronchial A549 cell lines. The mutant frequency was further enhanced (7-to 8-fold) under oxidative stress. The majority of both spontaneous and induced mutations occurred at A•T base pairs, indicating that oxidized A and/or T are NEIL1's preferred in vivo substrates. NEIL1 thus plays a distinct and important role in repairing endogenous and induced mutagenic oxidized bases, and hence in maintaining the functional integrity of mammalian genomes.

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Section: Screening Of Hprt Mutantsmentioning

confidence: 99%

Section: Screening Of Hprt Mutantsmentioning

confidence: 99%

Section: Screening Of Hprt Mutantsmentioning

confidence: 99%

Section: Increased Mutation Frequency In Neil1-downregulated Cellsmentioning

confidence: 99%

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Mutator phenotype of mammalian cells due to deficiency of NEIL1 DNA glycosylase, an oxidized base-specific repair enzyme

et al. 2008

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“…In order to better understand the cytotoxic activity of manool, a normal cell line (V79, Chinese hamster lung fibroblasts) was used to compare its selectivity. The choice of V79 cells for comparison is due the fact it is a well characterized cell line and commonly used in cytotoxicity studies (Bradley et al 1981;Munari et al 2014). …”

Section: Introductionmentioning

confidence: 99%

Manool, a Salvia officinalis diterpene, induces selective cytotoxicity in cancer cells

et al. 2015

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Manool, a diterpene isolated from Salvia officinalis, was evaluated by the XTT colorimetric assay for cytotoxicity and selectivity against different cancer cell lines: B16F10 (murine melanoma), MCF-7 (human breast adenocarcinoma), HeLa (human cervical adenocarcinoma), HepG2 (human hepatocellular carcinoma), and MO59J, U343 and U251 (human glioblastoma). A normal cell line (V79, Chinese hamster lung fibroblasts) was used to compare the selectivity of the test substance. Manool exhibited higher cytotoxic activity against HeLa (IC 50 = 6.7 ± 1.1 lg/mL) and U343 (IC 50 = 6.7 ± 1.2 lg/mL) cells. In addition, in the used experimental protocols, the treatment with manool was significantly more cytotoxic for different tumor cell lines than for the normal cell line V79 (IC 50 = 49.3 ± 3.3 lg/mL), and showed high selectivity. These results suggest that manool may be used to treat cancer without affecting normal cells.

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Glutaraldehyde-containing dentin bonding agents are mutagens in mammalian cellsin vitro

Schweikl

Schmalz

1997

J. Biomed. Mater. Res.

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The mutagenic potential of glutaraldehyde-containing dentin bonding agents was shown in previous studies using a bacterial gene mutation assay, the Ames test. However, current strategies of genotoxicity testing and regulatory requirements for the biological evaluation of medical devices recommend a battery of tests that indicate induced mutations in prokaryotic and eukaryotic cells. Accordingly, the mutagenicity of three glutaraldehyde-containing bonding agents (Syntac adhesive, Prisma Universal Bond 3 adhesive, and Gluma 3) was investigated using a quantitative mammalian cell gene mutation assay (V79/HPRT test) in the present investigation. The materials were extracted in dimethyl sulfoxide (0.1 g/2 mL) for 24 h and original extracts were then serially diluted in cell culture medium before exposure to V79 cells. Cytotoxic and mutagenic effects were observed with identical concentrations of extracts of the different test materials. There was a moderate decrease of the number of surviving cells immediately after the end of exposure. Mutagenicity at the hprt locus in V79 cells was found with all materials tested, and the increases in the absolute numbers of mutants were dose dependent. The mutant frequencies were about 15- (Syntac adhesive and Gluma 3) to 20-fold (Prisma UB3 adhesive) higher than solvent control values. Since other substances than glutaraldehyde may be responsible for the mutagenic effects in mammalian cells in this study, work is currently in progress to identify the individual mutagenic compounds of dentin adhesives and related composite materials.

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Mutagenesis by chemical agents in V79 Chinese hamster cells: A review and analysis of the literature

Cited by 264 publications

References 113 publications

Mutator phenotype of mammalian cells due to deficiency of NEIL1 DNA glycosylase, an oxidized base-specific repair enzyme

Mutator phenotype of mammalian cells due to deficiency of NEIL1 DNA glycosylase, an oxidized base-specific repair enzyme

Manool, a Salvia officinalis diterpene, induces selective cytotoxicity in cancer cells

Glutaraldehyde-containing dentin bonding agents are mutagens in mammalian cellsin vitro

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