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J M Boyle

Publications and source records attributed to J M Boyle.

99 records · Page 6Linked to original sources
PubMed1971

Role of pyridine nucleotides in 5-fluorouracil-mediated reactivation of ultraviolet radiation damage.

Ultraviolet irradiation (520 ergs/mm(2) at 254 nm) causes the respiration of Escherichia coli B/r cells to cease after about 90 min postirradiation incubation in a minimal medium containing glycerol as the sole source of carbon. The cessation of respiration is associated with loss of pyridine nucleotides. Agents which interfere with postirradiation transcription and translation prevent cessation of respiration. We have studied the effects of one of these agents, 5-fluorouracil (FU), on respiration, pyridine nucleotide levels, viability, capacity to support phage growth, and the repair of irradiated deoxyribonucleic acid (DNA). Addition of FU to cells immediately after irradiation results in the continuance of respiration at a linear rate and the maintenance of high levels of pyridine nucleotides. Cellular viability increases dramatically during the first 60 min of postirradiation incubation in the presence of FU. The ability of irradiated cells to support the growth of phage T4 is also greatly increased. FU treatment has no effect on the kinetics of pyrimidine dimer excision or the degradation of DNA. However, treated cells repair single-strand breaks resulting from early steps in excision repair slightly more efficiently than do untreated cells. The results support the hypothesis that one of the causes of death in these irradiated cells is the disappearance of pyridine nucleotides, coenzymes of certain respiratory dehydrogenases, and, in the case of nicotinamide adenine dinucleotide, for polynucleotide ligase, the enzyme responsible for the final step in the repair of DNA.

Centrifugation, Density Gradient↗
PubMed1971

Ultraviolet- and X-ray-induced responses of a deoxyribonucleic acid polymerase-deficient mutant of Escherichia coli.

Escherichia coli K-12, polAl(-) is a mutant strain whose extracts are deficient in Kornberg deoxyribonucleic acid (DNA) polymerase activity. We have compared the mutant and parental strains on the basis of a number of responses to ultraviolet (UV) and X-irradiation. For both types of radiation, the mutant is more sensitive by approximately the same factor as measured by reduction in colony formation, depression of DNA synthesis, and enhancement of DNA degradation. The rate of repair of X-ray-induced single-strand breaks in the mutant is also slower, as is the repair of breaks after excision repair of UV damage. On the other hand, the mutant has a significant capability to reactivate UV-irradiated lambda phage, although it is almost totally deficient in the ability to carry out UV reactivation. The data indicate that the polAl mutation leaves the cells with some ability to perform excision and strand-rejoining repair but that an exonuclease, whose identity remains obscure, is the agent responsible for the extensive breakdown of the DNA in polAl(-) cells after irradiation.

Bacteriological Techniques↗
PubMedDate not supplied

Stimulation of UV-induced DNA excision repair by chemotherapeutic drugs in cancer patients.

We have used a monoclonal antibody specific for UV-induced 6-4 photoproducts in an ELISA assay to determine the kinetics of loss of antigenicity from the DNA of lymphocytes obtained from four groups of people; normal controls and cancer patients who had either received chemotherapy, hormone therapy or no treatment at all. This result was confirmed on a matched pairs analysis of 12 breast cancer patients sampled before and after chemotherapy. We conclude, that chemotherapeutic treatment with alkylating agents modulate the capacity of UV-induced DNA-repair in human lymphocytes in a yet unknown way.

Alkylating Agents↗