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S Wolff

Publications and source records attributed to S Wolff.

At least 145 records · Page 8Linked to original sources
PubMed1982

12-O-tetradecanoylphorbol-13-acetate (TPA) induces sister-chromatid exchanges and delays in cell progression in Chinese hamster ovary and human cell lines.

The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induced a 20-45% increase in sister-chromatid exchange (SCE) frequency in Chinese hamster ovary cells (CHO) and in 2 SV40-transformed human fibroblast cell lines (GM637 and XP12RO) at concentrations up to 1 microgram/ml. The increase was independent of the time at which the cells were fixed after treatment and was not due to an impurity in the TPA preparation or to increased incorporation of bromodeoxyuridine into the DNA. There was no synergistic effect on SCE induction when CHO cells were simultaneously exposed to TPA and the carcinogens mitomycin C or ultraviolet light, but there was when TPA and benzo[a]pyrene were used. In addition to its weak SCE-inducing effects in CHO cells, TPA caused slight delays in cell cycle progression and greatly enhanced the cell cycle delay induced by benzo[a]pyrene.

Animals↗
PubMed1982

Activity of nitro-polynuclear aromatic hydrocarbons in the sister chromatid exchange assay with and without metabolic activation.

Nitro-polynuclear aromatic hydrocarbons are found in diesel particulates. These compounds are potent mutagens in the Ames test. To determine whether nitro-polynuclear aromatic hydrocarbons are active in a mammalian cell assay, 1-nitropyrene, 1,8-dinitropyrene, 2-nitrofluorene, and 4-nitrobiphenyl were incubated with cultures of Chinese hamster ovary cells. The frequency of sister chromatid exchange (SCE) was measured in the presence and absence of rat liver S-9 mix. The addition of S-9 mix resulted in a large increase in the SCEs induced by all four compounds.

Animals↗
PubMed1982

Sister chromatid exchange induced by short-lived monoadducts produced by the bifunctional agents mitomycin C and 8-methoxypsoralen.

To see if DNA crosslinks are involved in the induction of sister chromatid exchange (SCE), Chinese hamster ovary cells were exposed to two bifunctional alkylating agents, mitomycin C and 8-methoxypsoralen, and their monofunctional derivatives, decarbamoyl mitomycin C and angelicin. The data indicate that monoadducts, rather than crosslinks, are responsible for SCE formation. Furthermore, all agents but angelicin produced short-lived lesions that led to SCEs in the first period of DNA replication after treatment (twin SCEs), but not in the second (single SCEs). In contrast, angelicin, like methyl methanesulfonate and N-acetoxyacetylaminofluorene, produced lesions that lasted more than one cycle, indicating that several different types of DNA lesions are capable of SCE induction.

Animals↗
PubMed1982

Difficulties in assessing the human health effect of mutagenic carcinogens by cytogenetic analyses.

The analysis of induced chromosome aberrations in the peripheral lymphocytes of irradiated people is a reliable method for determining exposure to ionizing radiations. The system should also work for S-independent chemicals. For the majority of chemical clastogens, which are S-dependent, however, the utility of the system is far less certain because DNA repair can remove many of the adducts before the cells enter S. Sister chromatid exchanges are sensitive indicators of S-dependent mutagens; however, because of DNA repair, great interpersonal variability of response, and variability of reference populations, it has not yet been proved that they can be used to monitor populations for low-level chronic exposure. In any case, these cytogenetic tests can only be used to estimate the risk to the population as a whole. They cannot be used to predict whether a given person will suffer any particular form of ill health.

Carcinogens↗
PubMed1982

Increased induction of sister chromatid exchange by diethylstilbestrol in lymphocytes from pregnant and premenopausal women.

Cultures of whole blood from pregnant women (4 to 6 months), premenopausal women, postmenopausal women, and normal men were grown in the presence of varying concentrations (1 x 10(-5) M, 2 x 10(-5) M, and 4 x 10(-5) M) of diethylstilbestrol (DES), a synthetic estrogen and known carcinogen, to see if it had sex-related cytogenetic effects. DES induced sister chromatid exchanges in lymphocytes from pregnant and premenopausal women but had only a small effect at the highest concentration (4 x 10(-5) M) in lymphocytes from men and postmenopausal women. At all concentrations, the average number of sister chromatid exchanges was higher in lymphocytes from pregnant women than in those from premenopausal women. In lymphocytes from both a man and a pregnant woman, DES strongly inhibited cell proliferation in vitro. When lymphocytes from a man and a pregnant woman were cocultured in the presence of DES, only the lymphocytes of the woman responded with an increase in sister chromatid exchanges. This indicated that there is no interaction between DES and a factor present in the blood but that DES acts directly on each cell.

Adult↗
PubMed1981

Anti-receptor antibody-induced suppression of murine H-Y-specific delayed-type hypersensitivity responses.

A putative anti-H-Y receptor antiserum (ARA) was raised in C57BL/6 male mice against splenic T lymphocytes from syngeneic females immunized against H-Y antigen. When this antiserum is given i.v. to C57BL/6 females it prevents the expression of H-Y-specific delayed-type hypersensitivity (DTH). The suppressive activity in ARA was selectively retained on rabbit anti-mouse immunoglobulin columns, and could be absorbed by H-Y-immune spleen cells from C57BL/6 female mice. The abrogation of H-Y DTH reactivity was at least in part due to the generation of suppressor T cells which are generated by ARA in naive female mice. ARA-generated suppressor cells specifically inhibit the induction phase of DTH responses to the H-Y antigen, having no effect on (4-hydroxy-3-nitrophenyl)acetyl (NP)-specific cutaneous sensitivity responses or on DTH responses to minor histocompatibility antigens. Furthermore, there is a requirement for Igh gene homology between the strain producing the ARA and the strain in which the DTH response is induced. Thus, C57BL/6 ARA given to A.BY (H-2b, Igh-1e) or to B.C-8 (H-2b, Igh-1a) mice was unable to suppress homologous H-Y DTH responses in these strains. However, C57BL/6 ARA induced suppressor cells in B.C-8 mice which were capable of inhibiting H-Y DTH responses when adoptively transferred to C57BL/6 females.

Absorption↗
PubMed1981

X-ray sensitization of chromatids with unifilarly and bifilary substituted DNA.

When cells are grown for two rounds of DNA replication in the presence of the thymidine analogue 5-bromodeoxyuridine, chromosomes containing one chromatid with unifilarly substituted DNA and one with bifilarly substituted DNA are found. These can be distinguished by harlequin staining techniques that stain one chromatid dark and one light. When the degree of substitution is 60% or greater, 3 times as many X-ray-induced chromatid breaks are produced as in unsubstituted chromatids. This represents maximal sensitization. The unifilarly substituted (dark) chromatid is as sensitive as its bifilarly substituted (light) sister chromatid. If cells are grown in low concentrations of 5-bromo-deoxyuridine (BrdUrd), then the amount of substitution is less and the bifilarly substituted chromatid is more sensitive than the unifilarly substituted one. When large numbers of cells are grown in very low concentrations of BrdUrd, the analogue is almost completely depleted during the first round of replication leading to harlequin chromosomes containing one unsubstituted (dark) and one unifilarly substituted (light) chromatid. Under these conditions a maximal sensitization between light-staining and dark-staining chromatids can occur. This can be confused with the differential sensitivity between unifilarly and bifilarly substituted chromatids. The apparent discrepant results obtained by different investigators are most likely caused by the use of very low levels of BrdUrd in some of the experiments.

Animals↗
PubMed1981

Sister-chromatid exchanges: a report of the GENE-TOX program.

The effects of a number of chemicals on sister-chromatid exchange (SCE) frequencies in in vivo and in vitro systems are reviewed. Standardized protocols for future SCE testing in important systems, as well as for evaluation of test results, are presented. Data reported thus far suggest that SCE analysis may prove useful, especially at a secondary level, as a test of mutagenic carcinogens. Strengths and limitations of SCE analysis are summarized as a guide for future evaluation and use of this procedure.

Alkylating Agents↗
PubMed1981

Mammalian in vivo and in vitro cytogenetic assays: a report of the U.S. EPA's gene-tox program.

This report presents an assessment made by the U.S. Environmental Protection Agency Gene-Tox Program's Work Group on mammalian cytogenetics of the clastogenic effects of chemicals in in vivo and in vitro mammalian cell assays. This assessment is based on information provided by the Environmental Mutagen Information Center, Oak Ridge National Laboratory, with the proviso that the experimental protocol used in these papers was adjudged to be acceptable by standards outlined by the Work Group. Some data were accepted as "qualitative only" because the protocol used was fairly close to that proposed as suitable. Using these criteria, 177 papers were selected for review. 6 assays were reviewed: bone marrow (32 papers, 31 chemicals), spermatogonial (10 papers, 10 chemicals), spermatocyte (25 papers, 25 chemicals), oocyte or early embryo (18 papers, 19 chemicals), in vitro cell culture (30 papers, 66 chemicals), and leukocyte (66 papers, 53 chemicals). Each assay was considered separately, and comparisons were then made between them for their similarities or differences in producing a positive or negative clastogenic effect of a particular chemical or chemical class. A large proportion of the available cytogenetic data was not suitable for inclusion in the final data base because of poor experimental design or unsatisfactory reporting of the information. It was not possible to recommend any one assay for determining potential clastogenicity because each had its own particular advantages and limitations and provided unique information. For demonstrating in vivo effects, the bone-marrow assay is probably the simplest and most economical. If only in vitro exposures were considered, leukocytes or cultured mammalian cell lines would be suitable. However, there are advantages to using leukocytes because they are a synchronous population, at least through their cell division, and because of the ready availability of human cells. In general, there was good agreement between clastogenicity and carcinogenicity.

Animals↗
PubMed1980

Cell cycle kinetics in human lymphocyte cultures.

Short-term cultures of phytohaemagglutinin (PHA)-stimulated human lymphocytes are widely used to detect chromosome-damaging agents, possible human exposure to mutagenic carcinogens and the immune response of blood. Because the results are affected by the number of cell divisions before sampling, an accurate knowledge of lymphocyte proliferation in culture is essential for these studies. Unfortunately, the information available on the lymphocyte proliferative characteristics is quite conflicting. For instance, although after stimulation of blood lymphocytes with PHA the cultures soon contain cells that have divided different numbers of times: this heterogeneity has been explained variously as a difference in cell-cycle times or in the times when the cells start blastogenesis by responding to PHA. Prolonged treatment with high concentrations of 3H-thymidine (TdR) have often been used to investigate lymphocyte proliferation. Incorporated 3H-TdR can, however, affect cell kinetics. The differential staining of sister chromatids in cells dividing for different numbers of times in the presence of bromodeoxyuridine (BUdR) can be used to study cell kinetics. In experiments combining sister chromatid differential staining and autoradiography, we show here that 3H-TdR labelling at more than 0.1 microCi ml-1 slows lymphocyte cycling, and that the heterogeneity of different generations of cells is caused by a difference in the times when they start their first DNA synthesis in response to PHA.

Autoradiography↗
PubMed1980

Schizoid personality in childhood: a controlled follow-up study.

Twenty-two boys with schizoid personality were followed-up some 10 years later and compared with a matched control group with other diagnoses who had been referred to the same child psychiatry department. The diagnostic category is shown to have predictive validity. A start has been made towards an operational definition of the syndrome.

Adolescent↗
PubMed1980

Tests for DNA and chromosomal damage induced by nuclear magnetic resonance imaging.

Chinese hamster ovary (CHO) cells in culture were exposed in a nuclear magnetic resonance (NMR) imaging apparatus to a strong magnetic field, pulsed field gradients, and radio frequency emissions. No chromosomal aberrations were induced even after an exposure of approximately 14 hours. No sister chromatid exchanges were induced by four-hour exposures to either low (average 7.2 mW) or high (average 61.2 mW) radio frequency power. When HeLa cells were exposed for 16 hours to an average radio frequency power of 61.2 mW, no inhibition of DNA synthesis was detectable. These data indicate that the conditions used for NMR imaging do not cause genetic damage which is detectable by any of these methods.

Animals↗
PubMed1980

Increase of sister chromatid exchanges and perturbations of cell division kinetics in human lymphocytes by benzene metabolites.

Benzene, which has been associated with human cancers, is metabolized to produce several major metabolites that could be responsible for the biological effects. Tests have now been carried out on human lymphocytes in culture to determine if benzene or its metabolites, phenol, catechol, and hydroquinone, induce cytogenetic changes and affect the cell cycle. The results indicate that benzene itself does not induce sister chromatid exchanges or affect cell cycle kinetics over a wide range of doses. Phenol has an effect only at very high doses. On the other hand, catechol is a potent compound that induces sister chromatid exchanges and delays cell division very readily. Hydroquinone is also potent, but less so than catechol. Thus, the formation of catechol and hydroquinone is the most likely cause of benzene toxicity.

Benzene↗