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S Wolff

Publications and source records attributed to S Wolff.

34 records · Page 2Linked to original sources
PubMed1978

Molecular suicide studies of 125I and 3H disintegration in the DNA of Chinese hamster cells.

The shape of the survival curve for cells inactivated by tritium decay in DNA is modified by the presence of halogenated pyrimidines in the DNA in a manner analogous to their effect on X-ray induced reproductive death. The large shoulder found for tritium suicide is removed completely by coincorporation of 10(-6) M IUdR. The oxygen enhancement ratio for 125I and tritium disintegrations in unsynchronized Chinese hamster cells was determined for cells permitted to accumulate damage from these events at 4 degrees C. The oxygen enhancement ratio for 125I induced damage is 1.4. This is much smaller than the OER found for tritium decay which is similar or more than that found for X-ray exposure under the same conditions. These results suggest that the nature of the lesions produced by 125I decay in DNA are analogous to those produced by high LET radiation while those lesions produced by tritium are similar to lesions produced by roentgen rays. In synchronous V79 cells the effects of 125I induced damage in different regions of the mammalian cell DNA was examined taking advantage of the fact that DNA replication in hamster nuclei follows a time-dependent three dimensional pattern. The experiments indicate that 125I decays accumulated in the G2-period of the cell cycle have different efficiences for the induction of reproductive death depending on the region of the DNA which is labeled. The efficiency for the induction of reproductive death appears to be a maximum in DNA that replicates in V79 cells near the end of the DNA replication cycle. Electron capture events are dramatically efficient in the production of lethal chromosome aberrations. In CHO cells synchronized in the G1-stage of the cell cycle stored in the frozen state the efficiency for the induction of dicentric and ring chromosomes is 0.03. The dose response curve for the induction of these aberrations is linear in contrast to the curvilinear response found for roentgen ray exposure under the same conditions. Data on this kind suggest that there may exist "critical" regions within mammalian cell nuclei where chromatin fibers from two different chromosomes are in close proximity to each other and both are damaged non-repairably by a single electron capture event.

Animals↗
PubMed1976

Sister chromatid exchange as an assay for genetic damage induced by mutagen-carcinogens. I. In vivo test for compounds requiring metabolic activation.

An in vivo system has been devised in which chemical mutagen-carcinogens injected into an animal induce sister chromatid exchanges that can be observed when the animal's peripheral lymphocytes are subsequently cultured and then stained with the FPG technique. Chemicals requiring metabolic activation, as well as those that do not, produce significant increases in SCE frequency one day after exposure. The frequency then returns to control level within two weeks. This in vivo system is a highly sensitive assay for the ability of chemical agents to damage chromosomes.

Animals↗
PubMed1976

Sister chromatid exchange as an assay for genetic damage induced by mutagen-carcinogens. II. In vitro test for compounds requiring metabolic activation.

Sister chromatid exchanges (SCE's) which are easily seen by "harlequin chromosome" techniques can be readily induced in cultured Chinese hamster ovary (CHO) cells by low concentrations of mutagen-carcinogens that do not require metabolic activation. If the cells are simultaneously treated with cyclophosphamide which does require metabolic activation before it becomes mutagenic, and an activating system consisting of an extract of rat liver containing microsomes (S-9 Mix) then numerous SCE's are induced by the compound. This indicates that the induction of sister chromatid exchanges in such cells can be used as an in vitro assay for mutagens that require activation as well as those that do not. The method, which is very simple and quick, is more sensitive than is the usual cytogenetic assay in which chromosome aberrations are assayed.

Animals↗
PubMed1976

Cytological evidence for switches in polarity of chromosomal DNA.

From the types of ring chromosomes induced in x-irradiated Chinese hamster ovary (CHO) cells, we deduce the existence of switches in the polarity of chromosomal DNA; if there is a continuous DNA double helix along the full length of the chromosome then the polarity switches imply 3'-3' and 5'-5' phosphodiester linkages. The resolution of the method is such that we estimate that there is one polarity switch for every 10(9) normal 3'-5' phosphodiester bonds.

Cell Line↗
PubMed1975

Distribution of sister chromatid exchanges in the euchromatin and heterochromatin of the Indian muntjac.

The frequency of sister chromatid exchanges (SCEs) was determined for the chromosomes (except Y2) of the Indian muntjac stained by the fluorescence plus Giemsa (FPG) or harlequin chromosome technique. The relative DNA content of each of the chromosomes was also measured by scanning cytophotometry. After growth in bromodeoxyuridine (BrdU) for two DNA replication cycles. SCEs were distributed according to the Poisson formula in each of the chromosomes. The frequency of SCE in each of the chromosomes was directly proportional to DNA content. A more detailed analysis of SCEs was performed for the three morphologically distinguishable regions of the X-autosome composite chromosome. The SCE frequency in the euchromatic long arm and short arm were proportional to the amount of DNA. In contrast, the constitutive heterochromatin in the neck of this chromosome contained far fewer SCEs than expected on the basis of the amount of DNA in this region. A high frequency of SCE, however, was observed at the point junctions between the euchromatin and heterochromatin.

Animals↗
PubMed1975

The induction of chromatid deletions in accord with the breakage-and-reunion hypothesis.

In the present experiments it has been possible to study large numbers of X-ray induced chromatid deletions, or breads, in Chinese hamster chromosomes and to discern whether or not a sister chromatid exchange also occurs at the point of breadage. Chromatid deletions are only infrequently associated with a sister chromatid exchange. This is contrary to the expectations derived from the exchange hypothesis of Revell. Pn the basis of this hypothesis, in which chromatid deletions are considered to be incomplete exchanges that occur in the necks of little loops in the chromosomes, 40% of the chromatid breaks are expected to be associated with sister chromatid exchanges. The present data are in accord with the conclusions drawn from the earlier autoradiographic experiments of HEDDLE AND BODYCOTE, and show that chromatide breaks can be accounted for on the basis of the breakage-and reunion hypothesis, with the majority being simple breaks and some being incomplete exchanges between two such breaks.

Animals↗
PubMed1975

Estimation of the effects of chemical mutagens: lessons from radiation genetics.

Years of work with ionizing radiations have given us a wealth of data on radiation-induced mutations. These data, which have given insights regarding the mutational processes, should form the background for all mutagenesis work. In chemical mutagenesis, as in radiation mutagenesis, it is important to know the shape of the dose-effect curve in order to make further interpretations and calculations. It is also important to be on the constant alert for new relations that can be explored.

Animals↗
PubMed1975

Sister chromatid exchange in xeroderma pigmentosum cells that are defective in DNA excision repair or post-replication repair.

The formation of sister chromatid exchanges has been postulated to depend upon the action of DNA repair enzymes. Our experiments with various human cell lines show that the yield of sister chromatid exchanges is within normal limits in both excision-repair-defective and post-replication-repair-defective cells from the autosomal recessive disease, xeroderma pigmentosum. These results indicate that hypotheses invoking known DNA repair processes to acconnt for the recombination of sister chromatids are inadequate and that the exact enzymatic processes are as yet unknown.

Cell Line↗
PubMedDate not supplied

Re-analysis of radiation-induced specific locus mutations in the mouse.

A re-analysis of published data on mouse mutation rates induced by X and gamma rays suggests that the kinetics of induction can be analysed by fitting the data to a parabolic curve. We interpret this to mean that a substantial proportion of the induced mutations results from gross chromosomal changes such as deletions, some of which are one-track and some of which are two-track. This analysis is based on the assumption that the shape of the dose curve, which in the female is concave upward, reflects the manner in which the mutations are induced rather than representing a one-track (linear) curve whose shape has been modified by differential repair.

Animals↗