12 research outputs found
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Comparison of benzo(a)pyrene metabolism and mutation induction in CHO cells using rat liver homogenate (S9) or Syrian hamster embryonic cell-mediated activation systems
Mutagenesis in CHO cells has been studied by the addition of an ezymatically active liver homogenate (S9) fraction. However, the metabolism of procarcinogens, such as benzo(a)pyrene (B(a)P), by rat liver homogenate differs from that in intact cellular activation systems. Consequently, B(a)P-induced mutation frequencies in mammalian cells may vary when different activation systems are used. This study attempts to compare B(a)P metabolism and conjugation in rat liver homogenate (S9 preparation) and in Syrian hamster embryonic (SHE) cells. Furthermore, a CHO mutation assay incorporating either of the activation systems is being used to measure the mutation induction frequency
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Genotoxic effects of sunlight-activated waste waters
Natural sunlight induces a genotoxic response in cultured CHO cells pre-treated with shale oil retort process water. Near ultraviolet light (NUV) component of the solar spectrum is the apparent radiation responsible for photoactivation. Cultured human skin fibroblasts are acutely sensitive to the genotoxic effects of photoactivated process water. The mutagenic potential of photoactivated process water in human cells is the same as that witnessed for an equivalent killing dose of the potent skin carcinogen FUV. DNA repair processes are involved in modulating genotoxic effects of this photo-induced process. The exact magnitude of the potential health-related and environmental risks resulting from photoactivation of retort process waters and other oil shale by-products is unassessed at this time. Our demonstration that a significant rate of mutation occurs in cultured human cells exposed to high dilutions of process waters and fluences of NUV comparable to that encountered during nominal exposure to sunlight suggests that such assessment is a prerequisite to minimal risk development of our oil shale resources
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Effects of butylated hydroxyanisole on the metabolism and mutagenic and transformation potentials of benzo(a)-pyrene in cultured mammalian cells
The mechanism by which butylated hydroxyanisole (BHA) inhibits benzo(a)pyrene (BaP)-induced neoplasia in vivo and mutagenicity in vitro has been the subject of a number of investigations. In this study the effect of BHA on BaP metabolism in Syrian hamster embryonic (SHE) cells was studied. In addition, a SHE cell-mediated Chinese hamster ovary (CHO) cell mutagenesis and a SHE cell transformation assay have been used to study the biological effects of BHA. The results indicate that BHA reduces the metabolism of BaP in SHE cells, suppresses BaP-induced mutagenicity in target CHO cells and reduces morphological transformation by BaP in SHE cells. (ACR
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Alterations in the metabolism of benzo(a)pyrene in syrian hamster embryo (SHE) cells pretreated with phenolic antioxidants
Inhibition of chemical- or raddiation-induced neoplasia has been observed in animals whose diets were supplemented with antioxidants commonly used as food additives. Inhibition of the carcinogenicity of benzo(a)pyrene (BaP) or of 7,12-dimenthylbenz(a)anthracene (DMBA) - in rats has been achieved by the addition of the phenolic antioxidants butylated hydroxyanisole (BHA) or butylated hydroxytoluene (BHT) to the diet. Our data suggest that in SHE cells antioxidants inhibit the overall metabolism of BaP to its various oxidized moieties including 7,8-diol- and 7,8,9,10-tetrol-BaP. A plausible explanation for our results with SHE cells is that the antioxidants interact directly with AHH, thus inhibiting AHH metabolic capacity. From analysis of nuclear material from SHE cells (+- antioxidants) incubated for 36 hours with BaP at 1 ..mu..g/ml, it is calculated that 4.6, 2.4 and 2.9 pmol BaP are bound to the DNA isolated from 10/sup 7/ nuclei of control, BHA-(20 ..mu..g/ml) and p-MP-(10 ..mu..g/ml) treated cultures, respectively
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Sunlight activation of shale-oil byproducts as measured by genotoxic effects in cultured Chinese hamster cells
Activation of certain classes of promutagens/procarcinogens can be accomplished by exposure to various radiation sources. Retort processes currently in use in the production of shale oil generate significant quantities of process waters which contain a wide spectrum of uv-absorbing, organic material. Photoactivation of these waters with an artificial source of NUV results in genotoxic events in cultured mammalian cells. Since significant amounts (2 to 4%) of solar radiation reaching the earth's surface is NUV, we were concerned about potential biological effects resulting from solar-irradiated waste streams. This paper summarizes new and previously published data concerning the induction of both cytotoxicity and mutagenicity in cultured Chinese hamster cells (line CHO) after their exposure to a particular oil shale retort process water and natural sunlight
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Determination of direct-acting mutagens and clastogens in oil shale retort process water
Shale oil products contain various metabolically active and photoactive genotoxic components. In addition, preliminary observations indicated that retort process water contain direct-acting mutagens which cause significant increases in 6-thioguanine resistance (6TG/sup R/) mutants in Chinese hamster ovary (CHO) cells. However, we have been unable to demonstrate the occurrence of direct-acting mutagens in these process waters when tested in the standard Ames/Salmonella assay. In this report results are presented concerning the dose response of direct-acting mutagenicity in an above ground retort process (ARP) water and various fractions from it. Since many mutagenic agents are also clastogrenic, the cytogenetic and mutagenic effects of this process water under the same experimental conditions are compared