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A B Acton

Publications and source records attributed to A B Acton.

15 recordsLinked to original sources
PubMed1988

Chromosome aberrations in cultured central mudminnow heart cells and Chinese hamster ovary cells exposed to polycyclic aromatic hydrocarbons and sediment extracts.

1. Genotoxicity experiments were conducted with cultured fish cells to determine if the high frequency of epidermal papillomas observed in lemon sole from Sturgeon Bank, where a sewage treatment plant discharges, could be correlated with contamination of the sediments with chemicals such as 3,4-benzopyrene. 2. The frequency of chromosome aberrations was measured in cultured Umbra limi heart (U1-H) and Chinese hamster ovary (CHO) cells following exposure to the polycyclic aromatic hydrocarbons (PAH) 3,4-benzopyrene (BP), 1,2,5,6-dibenzanthracene (DBA), 1,2-benzanthracene (BA), and pyrene (PY), activated using S9 prepared from rainbow trout liver. 3. An increase in the chromosome aberration frequency was only observed following exposure to fish S9-activated BP in both cell lines. 4. Following exposure of the cells to both Sturgeon Bank and Spanish Bank sediment extracts, it was determined that a higher level of toxic and genotoxic activity was associated with the Sturgeon Bank sediments. 5. Since the detection of PAH genotoxicity requires the presence of S9, and since a higher level of genotoxic activity was noted following sediment extract exposures with no S9 present, this suggests that the extracts contain a complex mix of chemicals, some of which express genotoxic activity. 6. An assessment using the micronucleus test failed to indicate in vivo genotoxicity in fish collected from Sturgeon and Spanish Banks. 7. It was, therefore, difficult to associate the observed sediment genotoxicity with the previously noted high incidence of epidermal papillomas in lemon sole from this area.

Animals↗
PubMed1987

DNA repair synthesis in cultured fish and human cells exposed to fish S9-activated aromatic hydrocarbons.

Unscheduled DNA repair synthesis was measured autoradiographically in cultured rainbow trout gonad (RTG) and human fibroblast (HF) cells following exposure to aflatoxin B1 (AFB1), 3,4-benzopyrene (BP), 1,2,5,6-dibenzanthracene (DBA), 1,2-benzanthracene (BA) and pyrene (PY) activated with S9 prepared from rainbow trout liver. S9 from rainbow trout injected with Arochlor 1254 or an oil extract was compared with S9 from Fischer rats injected with Arochlor 1254 for the ability to activate AFB1 and cause DNA repair in RTG and HF cells. All three types of S9 activated AFB1, but the measured DNA repair response was greater in the HF cells. A significant grain count response was found following exposure of HF cells to fish S9-activated BP. Using assay conditions which enhance fish cell grain counts, a significant level of DNA repair was also found in RTG cells exposed to fish S9-activated BP. Marginal but statistically significant amounts of DNA repair were elicited in HF and RTG cells exposed to rainbow trout S9-activated BA and DBA, but no response was detected following PY exposure. Fish S9 was found to be able to activate a series of polycyclic aromatic hydrocarbons (PAH) and cause DNA repair synthesis in both fish and mammalian cells. The magnitude of the repair response roughly parallels the carcinogenic potential of the PAHs. These results elicit trans species and phyla comparisons which help to validate fish as models for aquatic carcinogenesis research, and also demonstrate PAH DNA-damaging effects on fish DNA, adding further credence for studying the effects of these chemicals on aquatic organisms.

Aflatoxin B1↗
PubMed1984

Comparison of DNA-repair synthesis, chromosome aberrations and induction of micronuclei in cultured human fibroblasts, Chinese hamster ovary and central mudminnow (Umbra limi) cells exposed to chemical mutagens.

In mammalian cells it has previously been observed that low DNA-repair activity is correlated with high chromosome-aberration frequency. Since fish cells typically express comparatively low amounts of DNA repair, the chromosome aberration test holds potential as a sensitive fish genotoxicity assay. A comparison of in vitro DNA-repair activity showed HF greater than CHO greater than Ul-H = Ul-F following exposure to MNNG and 4NQO. Although peak chromosome-aberration frequency varied CHO greater than Ul-H greater than HF, at comparable mutagen concentrations the relationship was Ul-H greater than HF greater than CHO following 4NQO exposure and Ul-H greater than HF = CHO after MNNG exposure. Analyzing for chromosome aberrations at high mutagen concentrations was not possible due to mitotic inhibition/toxicity which varied according to the mutagen and cell line. Micronuclei frequency varied CHO greater than Ul-H greater than HF = Ul-F. In CHO and Ul-H, a 10-15-fold increase over controls compares with only a 2-3-fold increase for HF and Ul-F. These differences are likely related, in part, to the cell-division rate of each line and the coincident repair of the damaged DNA. Reasons for the lack of negative correlation between DNA repair and chromosomal damage in fish cells are discussed.

Animals↗
PubMed1984

DNA repair synthesis following exposure to chemical mutagens in primary liver, stomach, and intestinal cells isolated from rainbow trout.

DNA repair synthesis was autoradiographically measured in liver, stomach, and intestinal cells isolated from rainbow trout which were exposed in vitro to the chemical mutagens, N-methyl-N'-nitro-N-nitrosoguanidine, 4-nitroquinoline 1-oxide, and aflatoxin B1. The level of repair was greatest in primary hepatocytes which responded to all three mutagens. Only nominal amounts of repair were detected in stomach cells following N-methyl-N'-nitro-N-nitrosoguanidine and 4-nitroquinoline 1-oxide exposures and in intestinal cells following 4-nitroquinoline 1-oxide exposure. In comparison with cultured rainbow trout cells, the quantity of DNA repair found in primary cells is significantly less.

4-Nitroquinoline-1-oxide↗
PubMed1983

DNA repair synthesis in cultured mammalian and fish cells following exposure to chemical mutagens.

Unscheduled DNA repair synthesis (UDS) was measured autoradiographically in HF, CHO, RTG, RTO, CH and FHM cells given a 3-h exposure to MNNG, 4NQO, NA2AAF and AFB1. All the chemicals produced a dose-response, the magnitude of which varied with the particular chemical and cell line. HF produced the greatest response, CHO less and the fish cell lines the least. The response of all fish cell lines was approximately equal for a particular chemical. A number of factors were investigated to account for the comparative differences in UDS response. The time course of repair in HF, CHO and RTG following a 3-h exposure to MNNG or 4NQO was the same. As S-phase nuclei were observed in control slides and the amount of repair following UV exposure varies HF greater than CHO greater than RTG, neither 3HTdR nor mutagen uptake is limiting. The observed results are discussed.

Animals↗
PubMed1980

Mutagenicity of fecal extracts from carnivorous and herbivorous animals.

Extracts of the feces of 3 carnivorous animals (dog, river otter and sea gull) and 5 herbivorous animals (cow, horse, sheep, chicken and goose) induced chromosome aberrations (breaks and exchanges) in cultured CHO cells. The addition of CuII (10(-4)M) enhanced the clastogenic effect of fecal extracts of the examined animals with the exceptiion of 1 dog and 3 cow samples. Catalase reduced the chromosome-breaking and mitosis-inhibiting capacities of fecal extracts. These results indicate the presence of hydrogen peroxide-forming compounds. The possibility must be considered that animal and human excreta may be a major source of mutagens entering man's environment.

Animals↗
PubMed1979

Can mutation theories of carcinogenesis set priorities for carcinogen testing programs?

The recent activity in designing, validating and implementing short-term tests for carcinogens has been spurred by the fairly convincing correlation between the carcinogenicity and mutagenicity of chemicals and by the assumption that mutations are somehow involved in neoplastic transformation. Moreover, it has been tacitly assumed that the mutagenic capacity alone of compounds would induce regulatory agencies to pass rules for their removal from man's environment, and would lead the public to avoid them. The actual response, however, is quite different. Government departments shy away from making any decisions on the basis of in vitro test systems, the public at large is becoming irritated by daily announcements that many of their cherished habits could adversely affect their health, and industries feel threatened and may reduce their search for new beneficial chemicals. The reluctance to accept wholeheartedly the mutagenicity tests for the detection of carcinogens is partly due to the uncertainty about the involvement of mutations in the formation of benign and malignant tumors. Following the initial rapid advances in the detection of environmental chemicals with carcinogenic and mutagenic properties, we seem to have arrived at the cross roads: we must now set new priorities for future research, and must make an unbiased assessment of the actual hazard of a compound to man and the human population.

Animals↗
PubMed1976

Carcinogens in estuaries, their monitoring and possible hazard to man.

Bottom-dwelling flatfish and their skin tumors can be used as an early-warning-system for the pollution by chemical carcinogens in sub- and inter-tidal waters. A trial in British Columbia and the State of Washington showed a link between tumor prevalence and urban activity. The possible use of marine accumulator organisms (mussels) in the estimation of benzo(a)pyrene levels of harbours is considered. The combination of biological and chemical assays could provide the basis for a large-scale routine surveillance of the marine environment.

Age Factors↗