Mutagenicity, sister chromatid exchange inducibility andin vitro cell transforming ability of particulates from Athens air

Athanasiou, Kyriacos A.; Arzimanoglou, Iordanis; Piccoli, C.; Yamasaki, Hiroshi

doi:10.1007/bf00117863

Cited by 14 publications

(8 citation statements)

References 18 publications

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“…DEPs are heterogeneous, consisting of more than 450 different organic compounds, including xenobiotics such as PAHs, halogenated aromatic hydrocarbons, and redox-active quinones (Athanasiou et al 1987; Li et al 2002; Whong et al 1981). Some of the individual components are cytotoxic and mutagenic in mammalian cells, but most are promutagens that require activation to electrophilic metabolites to exert their mutagenic or carcinogenic effects (Xue and Warshawsky 2005).…”

Section: Discussionmentioning

confidence: 99%

Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen

Bao

Tong

et al. 2009

Environ Health Perspect

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BackgroundDiesel exhaust [diesel exhaust particles (DEPs) and their extracts (DPE)] and ultraviolet A radiation (UVA) are two ubiquitous environmental factors that have been identified as essential risk factors for various benign or malignant human diseases, either alone or in combination with other agents.ObjectivesWe aimed to investigate the synergistic effects of DPE and UVA at low-dose exposures in human–hamster hybrid (AL) cells and their underlying mechanisms.MethodsWe exposed exponentially growing AL cells to DPE and/or UVA radiation with or without reactive oxygen species (ROS) quenchers and then assayed the cells for survival, mutation induction, apoptosis, and micronucleus generation. In addition, using a singlet oxygen (1O2) trapping probe, 2,2,6,6-tetramethyl-4-piperidone, coupled with electron paramagnetic resonance spectroscopy, we determined the production of 1O2.ResultsTreatment of AL cells with DPE + UVA induced significant cytotoxic and genotoxic damage. In contrast, we found no significant damage in cells treated with either UVA or DPE alone at the same doses. Mutation spectra of CD59− mutants showed that treatment with DPE + UVA easily induces multilocus deletions. Sodium azide significantly inhibited both cellular and DNA damage induced by DPE + UVA treatment, whereas other ROS inhibitors had little protecting effect. Furthermore, we found a significant increase of 1O2 in the cells that received DPE + UVA treatment.ConclusionThese findings suggest that UVA activated the genotoxicity and cytotoxicity of DPE in mammalian cells and that 1O2 played an important role in these processes.

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Section: Discussionmentioning

confidence: 99%

Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen

Bao

Tong

et al. 2009

Environ Health Perspect

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“…We have been using the BALB/c 3T3 cell transformation system in studies of the transforming potency of some genotoxic and nongenotoxic carcinogens and environmental pollutants [8,41] and have also adapted the protocol for detection of tumor promoters. The conceptual advantage of this assay is that transformed foci emerge from a confluent lawn of nontransformed cells; this therefore simulates in vivo promotion more closely than say the clonal SHE cell assay.…”

Section: Enhancement Of Cell Transformationmentioning

confidence: 99%

Tumor promotion: Models and assay systems

Yamasaki

1990

Teratog Carcinog Mutagen

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Tumor promotion is defined operationally from two-stage models of experimental carcinogenesis. It is, therefore, in a strict sense, possible to identify tumor promoters only from such models. The development and use of in vitro two-stage cell transformation assays was a logical extension toward in vitro short-term testing for tumor promoters. Another approach is to apply mechanistic knowledge of the tumor promotion process in developing end points for such assays. In this context, we have been examining the role of blocked gap-junctional intercellular communication (GJIC) in tumor promotion, using in vitro and in vivo systems. Many promoters have been shown to block GJIC in vitro; our studies support the idea that inhibition of GJIC does play an important role in the promotion stage of BALB/c 3T3 cell transformation. In animal studies, we have shown that the rat liver tumor promoter phenobarbital can decrease the level of expression of the 32 Kd gap junction protein gene specifically in liver upon systemic exposure in rats. Further examination of the role of GJIC in tumor promotion is indeed warranted. Also, deployment of in vitro GJIC and transformation assay systems should provide useful short-term tests for detecting tumor promoting activity of environmental chemicals.

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“…The results of mutagenicity testing of air samples collected before the war indicated that, in general, the level of air pollution by potentially carcinogenic agents was relatively low in Saudi Arabian cities compared to the data obtained with urban air of major industrial countries (Tokiwa et al 1977, Athanasiou et al 1987). However, there was a clear indication that the histidine revertants/m 3 of air varied considerably with air samples from different areas of Saudi Arabia depending on the presence or absence of industrial sites, oil refineries, automobile traffic and construction activities.…”

Section: Discussionmentioning

confidence: 93%

“…Air-borne toxic agents are produced by industrial and automobile emissions as well as by burning of various organic substances (Suess et al, 1985). As the potential carcinogenic effects of air pollutants are of major concern, attempts have been made to determine and monitor genotoxic properties of air particulates in various cities of the industrialized countries (Sutou et al, 1980, Athanasiou et al, Downloaded by [New York University] at 10:21 05 November 20141986, 1987, Crebelli et al, 1988, Hoyer et al, 1992, Nardini and Clonfero 1992, Nardini et al, 1994. These studies have demonstrated the usefulness of Ames' histidine reversion assay in suitable tester strains of Salmonella typhimurium for screening organic extracts of air samples showing mutagenic activity.…”

Section: Introductionmentioning

confidence: 99%

A comparative analysis of mutagenic activities of air samples collected from Riyadh before, during and after the Gulf War

Al‐Khodairy¹,

Al-Dakan²,

Akel³

et al. 1998

International Journal of Environmental Health Research

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1998) A comparative analysis of mutagenic activities of air samples collected from Riyadh before, during and after the Samples of air particulates were collected from the city of Riyadh in 1988 before the Gulf War, a few months after the torching of oil wells in Kuwait during 1991 and several months (in 1992) after the burning oil wells were fully capped. The air samples were collected on fibre glass filters (GF-A, pore size 1.6 m m) by using a RADECO air sampler. Filters were shredded, soaked and sonicated in acetone to dissolve the organic contents. The solid residues obtained after evaporation of acetone were redissolved in 5 ml volumes of fresh acetone and tested for mutagenic activity in the Ames Salmonella assay using the tester strain TA98 for histidine reversion (Ames 1979, Maron andAmes 1983). The mutagenicity assay was performed with and without metabolic activation provided by the S-9 fraction of an Aroclor-induced rat liver homogenate and co-factors. The results of this study showed that the pre-war samples of air particulates from Riyadh induced 11 histidine revertants/10 m 3 of air analyzed, while the 1991 samples (during war) induced 40 -50 revertants/10 m 3 of air (4 -5 times higher). However, the number of histidine revertants induced by the post-war (1992) samples came down to 10 -11/10 m 3 of air. These data, thus, strongly suggested that there was an increase in air particulate mutagenicity due to the atmospheric pollution of Gulf areas caused by the burning oil wells in Kuwait. This notion is supported by the fact that the mutagenic activity of air samples collected months after the burning oil wells were capped assumed the pre-war level. In view of the strong correlation between mutagenicity and carcinogenicity (McCann and Ames 1976) it would be expected that air pollution with mutagenic agents enhanced by the Gulf War would increase the carcinogenic risk for upper aerodigestive tracts in the exposed population in Kuwait and the surrounding areas. Such adverse health effects of mutagenic air pollutants generated by the burning oil wells in Kuwait should be assessed by proper epidemiologic studies.

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Mutagenicity, sister chromatid exchange inducibility andin vitro cell transforming ability of particulates from Athens air

Cited by 14 publications

References 18 publications

Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen

Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen

Tumor promotion: Models and assay systems

A comparative analysis of mutagenic activities of air samples collected from Riyadh before, during and after the Gulf War

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