Induction of Ouabain-resistant Mutation and Sister Chromatid Exchanges in Chinese Hamster Cells with Chemical Carcinogens Mediated by Human Pulmonary Macrophages

Hsu, Ih‐Chang; Harris, Curtis C.; Yamaguchi, Maria; Trump, Benjamin F.; Schafer, Paul W.

doi:10.1172/jci109579

Cited by 19 publications

(3 citation statements)

References 22 publications

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“…In our study, no mutagenic activity was observed in V79 cells exposed to the different types of asbestos whether or not human PAMs were added to the cultures to detect mutagens requiring metabolic activation. In contrast, increased levels of sister chromatid exchanges (SCEs) and formation of O r mutants were observed in V79 cells cocultivated with human PAMs as an activation source and B[a]P or its proximate mutagenic metabolite, the 7,8-dihydrodiol (Hsu et al, 1979). To further substantiate the lack of genotoxicity of asbestos, increased SCE was not observed in V79 cells following exposure to CA (Price-Jones et al, 1980).…”

Section: Discussionmentioning

confidence: 97%

“…Chinese hamster lung (V79) cells were cultured in DMEM supplemented with 10% FBS, 80 #g/ml gentamycin~ and 100 U/ml mycostatin. Ouabain resistance (O r) was determined according to the method of Hsu et al (1979). The asbestos was tested for mutagenicity at 10 and 50 #g/ml exposure for 24 h. Additionally, the asbestos was tested at 10/.tg/ml in the presence of PAMs as an activation source.…”

Section: Preparation Of Pamsmentioning

confidence: 99%

“…Since PAMs also express mixed function oxidase activity, their role in detoxification or activation of xenobiotics by methods other than phagocytosis is of even greater importance (Hocking et al, 1979;Hsu et al, 1979). The use of human PAMs for mutagenicity studies with mammalian (V79) cells, and originally reported by Hsu et al (1979) and Harris et al (1978), enables data to be accumulated regarding the potential acute human pulmonary health hazard from a variety of xenobiotics. In this study, PAMs were used to determine cytotoxicity and mutagenic activation of untreated and hydrophobicallytreated asbestos.…”

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In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

et al. 1986

Cell Biol Toxicol

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Human pulmonary alveolar macrophages were used to quantitate the cytotoxic effect of surface-altered chrysotile asbestos. Little difference was observed in mortality between chrysotile asbestos that was surface-treated to a 42% extent by a hydrophobic organosilane or untreated chrysotile. Little or no effect on mortality was observed when human pulmonary alveolar macrophages were cultured with untreated chrysotile or acid-leached asbestos in the presence of 10 mM dipalmitoyl lecithin. However, when human pulmonary alveolar macrophages were cultured with a hydrophobically-treated (to a 42% or 95% extent) chrysotile asbestos in the presence of 10 mM dipalmitoyl lecithin, a statistically significant decrease in mortality was observed compared to untreated chrysotile. No mutagenic activity was observed when V79 cells were cultured with acid-leached, or 42% hydrophobically-treated chrysotile asbestos, even when human pulmonary alveolar macrophages were included as an activation source. The 95% hydrophobically-treated and acid-leached chrysotile also exhibited decreased binding of benzo[a]pyrene compared to untreated chrysotile asbestos.

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Section: Discussionmentioning

confidence: 97%

Section: Preparation Of Pamsmentioning

confidence: 99%

mentioning

confidence: 99%

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In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

et al. 1986

Cell Biol Toxicol

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Genotoxic effects of five polycyclic aromatic hydrocarbons in human and rat mammary epithelial cells

Mane

Purnell

Hsu

1990

Environ and Mol Mutagen

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Five polycyclic aromatic hydrocarbons (PAHs) of different carcinogenic activities were evaluated for their effects on DNA synthesis (3HTdR labeling index (L.I.] of rat and human mammary epithelial cells (MEC) and for their effects on chromosomes in MEC-mediated sister chromatid exchange (SCE) assays. When compared with DMSO-treated cells, exposures of rat MEC to the two most potent carcinogens (5 micrograms/ml for 24 hr), i.e., 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene (B[a]P), resulted in a 45-62% reduction in the L.I. of rat MEC. Another carcinogen, 20-methylcholanthrene (MCA), produced a 35-48% reduction in L.I., while the noncarcinogenic PAHs, 1,2-benzanthracene (BA) and benzo(e)pyrene (B[e]P), showed no effect. Similarly, exposures of human MEC to DMBA and B[a]P resulted in a 50-90% depression in L.I. while BA was significantly less effective (30% reduction). When co-cultivated with Chinese hamster V-79 cells in the presence of PAH, both rat and human MEC can activate and release the active metabolites to induce SCE in V-79 cells. In the rat MEC-mediated assay for all 5 PAHs, the frequencies of SCE per chromosome in DMBA-, B[a]P-, MCA-, BA-, B[e]P-, and DMSO (solvent control)-treated groups were 6, 3, 1.4, 0.7, 0.4, and 0.3, respectively. DMBA was most effective in increasing SCE, while B[e]P was ineffective. In the human MEC-mediated assay, B[a]P was more effective than DMBA in inducing SCE, and the frequencies of SCE per chromosome were 4.5 and 3.6 in B[a]P- and DMBA-treated groups, respectively. Comparing depression of L.I., SCE, and in vivo carcinogenicity for the 5 PAHs, SCE mediated by rat MEC is better correlated with carcinogenicity in rat than L.I. depression.

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Peroxidatic Activation of Procarcinogens: A Role for Prostaglandin H Synthase in Initiation of Chemical Carcinogenesis

Zenser¹,

Davis²

1985

Biochemistry of Arachidonic Acid Metabolism

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Induction of Ouabain-resistant Mutation and Sister Chromatid Exchanges in Chinese Hamster Cells with Chemical Carcinogens Mediated by Human Pulmonary Macrophages

Abstract: A B S T R A C T Pulmonary macrophages (PAM)meta

Cited by 19 publications

References 22 publications

In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

Genotoxic effects of five polycyclic aromatic hydrocarbons in human and rat mammary epithelial cells

Peroxidatic Activation of Procarcinogens: A Role for Prostaglandin H Synthase in Initiation of Chemical Carcinogenesis

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