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Biomedical subjects

M M Elkind

Publications and source records attributed to M M Elkind.

At least 91 records · Page 5Linked to original sources
PubMed1981

Recovery after exposure to near-ultraviolet light of cells containing 5-bromodeoxyuridine.

The survival of synchronized V79 Chinese hamster cells irradiated with near-ultraviolet light after a 1-h labeling with 5-bromodeoxyuridine (BrdUrd) is highly dependent upon the cell's position in the cell cycle at the time of irradiation (Hagan, M., and M. M. Elkind. Biophys. J. 1979. 27:75-86). In this report, we show that cells irradiated in the same S phase after BrdUrd incorporation demonstrate an ability to repair sublethal damage, in contrast to the lack of an increase in survival with dose fractionation in template-labeled cells (Ben-Hur, E., and M. M. Elkind. Mutat. Res. 1972. 14:236-245). In addition, we show that pulse-labeled cells in S phase can repair potentially lethal damage expressed by caffeine. The kinetics of these recovery processes and the absence of a caffeine effect on the repair of sublethal damage indicate that these two processes are to a large degree unrelated. We conclude that in template-labeled cells inadequate time to effect prereplicational repair precludes effective contributions to cell survival from other kinds of DNa repair processes.

Animals↗
PubMed1981

Spectral dependencies of killing, mutation, and transformation in mammalian cells and their relevance to hazards caused by solar ultraviolet radiation.

Using germicidal lamps and Westinghouse sunlamps with and without filtration, the effectiveness of ultraviolet and near-ultraviolet light in inducing molecular and cellular changes was measured. Cell survival and the induction of resistance to 6-thioguanine or to ouabain were measured with V79 Chinese hamster cells, cell survival and neoplastic transformation were measured with C3H mouse 10 T 1/2 cells, and the induction of pyrimidine dimers containing thymine was measured in both cell lines. The short-wavelength cutoff of the sunlamp emission was shifted from approximately 290 nm (unfiltered) to approximately 300 and approximately 310 nm by appropriate filters. Although it was found that the efficiency with which all end points were induced progressively decreased as the short-wavelength cutoff was shifted to longer wavelengths, the rates of decrease differed appreciably. For example, doses of near-ultraviolet light longer than approximately 300 nm that were effective in mutating or in transforming cells were ineffective in killing them. In respect to pyrimidine dimer induction, several but not all cellular end points were induced by dose ratios of sunlamp light (short-wavelength cutoff, approximately 290 nm) to germicidal lamp light (254 nm) in fairly close accord with the doses required to produce equivalent proportions of dimers. However, for near-ultraviolet light having cutoffs at longer wavelengths, the biological action observed was appreciably greater than what would be predicted from the proportion of dimers induced. From the latter observation, it is inferred that increasing intensities of short-wavelength ultraviolet light, as would be expected from reductions in stratospheric ozone around the earth, would result in smaller increases in biological action, e.g., skin cancer, compared to current levels of action than would be predicted from an action spectrum completely corresponding to that of a pyrimidine dimer induction spectrum in DNA.

Animals↗
PubMed1980

Enhanced near-ultraviolet light sensitivity induced by coal combustor effluents in cultured mammalian cells.

The cytotoxicity of radiation from Westinghouse sun lamps (principal emission 290-340 nm) was enhanced by treatment of cells with nontoxic concentrations of condensate from the gaseous effluent from a pressurized, fluidized-bed coal combustor. The effect was similar to the photoenhanced cell killing induced by nontoxic concentrations of 7,12-dimethylbenz[a]anthracene, a carcinogenic derivative of substances produced by incomplete combusion of fossil fuels. Furthermore, light-dependent cell killing requiring the presence of the condensate was observed even when the sun lamp emission was filtered (principal emission 300-340 nm) to eliminate cell killing due to near-ultraviolet light alone, or when a black light near ultraviolet source (emission maximum, 365 nm) was used. It is suggested that coal combustor effluents may act synergistically with the short-wavelength component of sunlight.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Repair of cell killing and neoplastic transformation at reduced dose rates of 60Co gamma-rays.

Using the C3H/10T1/2 mouse embryo-derived cell line, we measured the survival and incidence of neoplastic transformation following exposures of the cells to 60Co gamma-rays at an acute (100 rads/min) and at reduced (2.5, 0.5, and 0.1 rad/min) dose rates. Typical of what is generally observed with mammalian cells, at reduced dose rates, the survival of 10T1/2 cells increases as the dose rate is decreased due to the repair of sublethal damage during irradiation. The induction curve following acute exposures of 60Co gamma-rays is similar to that previously reported for 50-kV X-rays; the frequency initially rises rapidly, reaching a plateau of about 3 X 10(-3) transformants/survivor. The transformation induction curves for the reduced dose rates, while similar in shape to that for the high dose rate, exhibit a strong dependence on dose rate. All of the induction frequencies for reduced dose rates lie below those for 100 rads/min. In the low-dose region (i.e., 0 to 150 rads), our results are most extensive at 100 and at 0.1 rad/min. While each set of data in the low-dose region is fitted quite well by a linear dose dependence, the slope of the regression line at 0.1 rad/min is about one-half of that at 100 rads/min. We conclude that subeffective transformation damage, as well as sublethal damage, is repaired during low-dose-rate irradiation.

Animals↗
PubMed1979

Changes in repair competency after 5-bromodeoxyuridine pulse labeling and near-ultraviolet light.

Synchronized V79 Chinese hamster cells, pulse-labeled with 5-bromodeoxyuridine (BrdUrd), show marked changes in the sensitivity to near-ultraviolet light during the cell cycle. Cells are least sensitive during the remainder of the S-phase after the BrdUrd pulse. They become maximally sensitive in the next cell cycle when the BrdUrd-labeled DNA presumably serves as the template for replication. This is followed by a return to relative insensitivity during the remainder of the S-phase, the increase in survival does not occur until DNA synthesis progresses beyond the time when the DNA made during the second pulse serves as a template. Furthermore, cells in the resistant phases of the cell cycle are sensitized by 1-2 mM caffeine. Survival curves are shown for the various cell ages of interest and are discussed in relation to the observed changes in functional repair capacity. The data support the hypothesis that lesions in the BrdUrd-containing DNA are effectively repaired after semiconservative replication. The data indicate that saturation of repair capacity and not target multiplicity is responsible for the appearance of a shoulder on the survival curves.

Animals↗
PubMed1979

Transformation of mouse C3H/10T1/2 cells by single and fractionated doses of X-rays and fission-spectrum neutrons.

A mouse embryo-derived cell line, C3H/10T1/2, was used to measure the frequency of in vitro neoplastic transformation induced by 50-kVp X-rays and by fission-spectrum neutrons from the JANUS reactor at the Argonne National Laboratory. The transformation frequency after single X-ray doses rises exponentially, reaching a plateau at about 3 X 10(-3) transformant/survivor. The induction curve following single neutron doses, while qualitatively similar, initially rises more steeply and levels off at a maximum of about 6 X 10(-3) transformant/survivor. For both radiations, transformation frequency varies with changes in the number of viable cells per dish, showing about a 10-fold decrease in transformation frequency when the number of viable cells per 90-mm dish was increased from about 300 to about 1000. Fractionation of a total X-ray dose of 700 rads results in an approximately 6-fold increase in survival and reduction in transformation frequency over a 16-hr interval. Fractionation of the total neutron dose of 378 rads has no effect upon cell survival, and transformation frequency declines by a factor of only about 1.7 at most over a 24-hr period. Cells derived from transformed foci formed fibrosarcomas when injected into appropriately treated mice.

Animals↗