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Biomedical subjects

M M Elkind

Publications and source records attributed to M M Elkind.

At least 127 records · Page 7Linked to original sources
PubMed1972

Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinese hamster cells exposed to fluorescent light.

Illumination of Chinese hamster cells with fluorescent light after 5-bromodeoxyuridine incorporation leads to extensive single-strand breakage in the DNA of the exposed cells. The rate of production of single-strand breaks is dependent on the extent to which thymine is replaced by 5-bromouracil. At least some of the breaks observed with alkaline gradients are probably produced in vivo and are probably not contingent upon alkaline hydrolysis since breakage can be demonstrated with neutral gradients also. Cells are able to rejoin most of the single-strand breaks within 60 min; however, damage to the DNA-containing material (the "complex") initially released from cells is repaired more slowly. Cysteamine protects against single-strand breakage with a dose-modifying factor of 2.8. A comparison is made between the production of single-strand breaks by fluorescent light and X-rays, and the significance of such breaks relative to cell survival is discussed.

Animals↗
PubMed1971

Sedimentation of DNA released from Chinese hamster cells.

Under high pH and high salt conditions, Chinese hamster cells lyse and release a DNA-containing material of large molecular weight. With increasing lysis time, a smaller material is resolved from the large one. Relative to T4 DNA, the smaller is estimated to be approximately 2 x 10(8) daltons (number average). From a comparison of radiation data, the target size of the larger is about 15 times that of the smaller (probably a lower limit estimate). In addition to concentration of alkali, temperature, and time of lysis, the resolution of the smaller from the larger material is shown to be affected by other factors. Three of these are: fluorescent light exposure during lysis, X-irradiation before lysis, and incorporation of actinomycin D before lysis. All of these treatments result in degradation of the smaller molecules if large enough exposures are used. The sedimentation patterns of both DNA materials are strongly speed dependent. This probably results from changes in molecular conformation and concomitant increases in viscous drag with speed. The speed dependence differs qualitatively for the two materials, an observation which suggests that they differ in ways in addition to size.

Animals↗
PubMed1970

Two forms of repair of DNA in mammalian cells following irradiation.

When Chinese hamster cells are lysed on top of an alkaline sucrose gradient, in time a fairly discrete DNA-containing molecular species is released from an apparently more complex material. Small doses of X-radiation speed the resolution of this complex while large doses degrade the material released from it. Incubation after irradiation reverses both effects.

Animals↗
PubMed1969

X-rays and nitrogen mustard: independent action in Chinese hamster cells.

We have studied the combined effects of X-irradiation and nitrogen mustard treatment on the colony-forming ability of Chinese hamster cells. In contrast to X-irradiation, nitrogen mustard acting by itself yields an exponential dose-effect relationship. Moreover, whether delivered in immediate sequence or after varying intervals, nitrogen mustard treatment does not affect radiation survival and vice versa. These results, plus the lack of any indication of the repair of sublethal nitrogen mustard damage, are consistent with independent but different modes of action at the same site(s), or action at different sites.

Animals↗
PubMed1969

Cell killing by actinomycin D in relation to the growth cycle of chinese hamster cells.

Using Chinese hamster cells in culture, we have measured the effectiveness of actinomycin D to suppress division as a function of the position, or age, of a cell in its growth cycle. Cells were first exposed to millimolar concentrations of hydroxyurea in order to produce a synchronized population just before the onset of DNA synthesis. Thereafter, the survival response after 30 min exposures to actinomycin D was measured. Cells become resistant as they enter the S phase and then sensitive again in the latter part of S. When they reach G(2) (or G(2)-mitosis) they are maximally resistant; at 1.0 microg/ml, for example, the survival in G(2) is 30-fold greater than it is in G(1). These results, plus measurements reported earlier on the interaction of damage in S cells due to actinomycin D and X-irradiation, suggest that the age-response pattern of the toxic effects of this drug probably reflects both the functional capacity of DNA-actinomycin complexes and the ability of this antibiotic to penetrate chromatin and bind to DNA.

Animals↗