J. L. Sanders

Radiation produces breaks in L cell and mouse liver DNA characterized by 5′ phosphoryl termini

Abstract Using the polynucleotide kinase method, we were able to demonstrate the repair of radiation induced DNA breaks in mouse liver DNA and in L cells. The specificity of the enzyme indicates the breaks to have 5′ phosphoryl termini.

Effects of Radiation on Asynchronous and Synchronized L Cells under Energy Deprivation

The uncoupler of oxidative phosphorylation, 2,4-dinitrophenol (DNP) has been shown to decrease the radiosensitivity of L cells in spite of producing a severe depression of DNA, RNA, protein, and AT...

Radiation induced breaks increase the priming activity of rat sarcoma DNA in the DNA polymerase reaction

Abstract Radiation produces large numbers of DNA breaks which are characterized by 5′ termini. The presence of these breaks is accompanied by an increase in the ability of the DNA to serve as a primer in the DNA polymerase reaction. Since DNA polymerase adds nucleotides from the 3′ end of the molecule, and since a 3′ OH terminus is required, our results provide additional evidence that some radiation induced DNA breaks are characterized by 5′PO43′OH termini. DNA ligase is very likely responsible for rejoining this type of break.

The Relation of DNA Degradation to the Repair of Radiation Injury by L Cells

Experiments with bacteria suggest that extensive DNA degradation is an important step in the repair of radiation injury. Because of the potential importance, similar experiments with cultured mamma...

Energy dependent nucleolytic processes are responsible for the production of many post-irradiation breaks in L cell DNA.

Abstract L cells irradiated while in growth medium or in a balanced salts solution showed a rapid appearance of DNA breaks characterized by 5′ phosphoryl termini. Following irradiation, the number of breaks quickly reached a maximum, after which they were rapidly repaired. Dinitrophenol, an inhibitor of aerobic oxidative phosphorylation, prevented the DNA breaks from appearing.

Radiation alters the ability of mammalian cell DNA to compete in a DNA:DNA hybridization system

Abstract Five thousand rads of X-rays destroyed the ability of L5178Y DNA to compete in a DNA:DNA hybridization system.

In situ repair by human malignant cells of radiation-induced DNA breaks.

Abstract The rejoining of radiation-induced DNA breaks, characterized by 5′ termini, was measured by the polynucleotide kinase method. This method has potential clinical value because DNA damage can be measured for cells within solid tissue. Following irradiation of a human squamous-cell carcinoma, DNA rejoining occurred, but at a slower rate than observed for mammalian cells in culture. The results of the study indicate that cells within solid tumors, in situ, are able to repair at least some radiation-induced DNA damage. The importance of this type of repair to tumor response following therapeutic radiology is not known at present.

Evidence for a cyclic 32P labeling of deoxyribonucleic acid in irradiated L cells.

Mouse L cells show a cyclic32 P labeling of DNA following relatively low doses of x-rays. This effect appeared for cells which had been starved or treated with 2,4-dinitrophenol (DNP) but not for cells irradiated in growth medium. The response consisted of a rapid uptake and loss of label. Changes in ATP metabolism paralleled the cyclic labeling of DNA. This behavior possibly explains the enhanced repair of radiation injury previously described for DNP treated cells.

Radiation Increases the Solubility of L Cell DNA in a Detergent-Based Lysing System

Summary Treatment of L cells with a detergent-based lysing solution caused the formation of a precipitate which contained DNA and protein. Increasing doses of X-rays decreased the amount of DNA which precipitated; at the same time, the amount of DNA which remained in solution increased. Inclusion of EDTA in the lysing solution prevented the formation of the precipitate.

Cyclic Labeling of Mammalian Cell DNA after X-Irradiation Labeling with Specific Precursors

Summary Starved L cells show a radiation-induced cyclic labeling of the acid-insoluble fraction when adenosine and deoxyadenosine are used as labeled precursors. The response consisted of a rapid uptake and loss of label. A similar effect has also been reported for 32P labeling of DNA. These findings support the idea that X-irradiation of mammalian cells produces increased action of an enzyme which rejoins single-strand breaks in DNA. The enzyme mechanism involves formation of a transient DNA-adenylate complex. In such a reaction, labeled adenylate should enter and then leave the DNA fraction. The results reported here agree with such a mechanism.