DNA-repair mechanisms : symposium, Schloss Reinhartshausen/Rhein, Oct. 4th/5th, 1971 / chairman H. Altmann.

Date:
[1972]
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Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: DNA-repair mechanisms : symposium, Schloss Reinhartshausen/Rhein, Oct. 4th/5th, 1971 / chairman H. Altmann. Source: Wellcome Collection.

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    Averbeck: During the 8th Annual Meeting of the European Society for Radiation Biology in Basko Polje, Yugoslavia, H. S. Kaplan gave a paper concerning »Chemical inhibitors of the repair of X-ray induced single-strand breaks in cellular DNA «. Using the method of alkaline sucrose gradient centri fugation described by McGrath and Williams it was demonstrated that there are three types of repair of single-strand breaks in E. coli. 1. The first type of repair can take place in complete growth medium, not in buffer. Recombination-deficient strains of E. coli (rec~) are unable to carry out this type of repair. This recombination or post-replication repair is a very slow repair process. More than 30 minutes are needed in E. coli. Hydroxyurea (impure, i.e. contaminated with an unknown compound) can act as an inhibitor [Kapp, D. S. and K. Smith: The chemical inhibition of the repair of single-strand breaks in DNA: post-irradiation sensitization to X-rays. Int. J. Radiat. Biol. 19: 255 (1971)]. 2. The second type of repair is faster than the first type. It can take place in buffer and is complete in about 15 minutes. This type of repair is absent in E. coli polA mutants which are lacking the Kornberg polymerase I. In wild-type cells it can be inhibited by NaCN and EDTA. It is also tempera ture-dependent. 3. The third type of repair is an »ultrafast« repair process. It is inhibited in air-irradiated cells. Heat, cold, oxygen, N-ethyl-maleimide and hydroxyurea can act as inhibitors. It was suggested that this type of repair is dependent on a DNA ligase. This repair process can take place in less than 2 minutes. Since it has been suggested by H. S. Kaplan (8th Annual Meeting of the European Society for Radiation Biology in Basko Polje, Yugoslavia, 1971) that there exists a third repair process (perhaps related to the DNA ligase) which is very fast in wild-type cells but inefficient in cells irradiated in oxy genated conditions, it can be assumed that oxygen can act (directly or indirect ly) as an inhibitor of the activity of repair enzymes. Perhaps in this aspect the oxygen effect can be interpreted in terms of equal lesions but different repair ability of X-irradiated cells in oxygenated or hypoxic conditions. Boyle: May we now turn to the scheduled discussion which concerns the influence of drugs and environmental factors on repair mechanisms. I would like to make a few general comments at the outset. This subject can be dis cussed, of course, at a number of different levels, depending on the type of ap proach one wishes to use. For example, the biologist studying the effect of tem perature on the shape of radiation survival curves of cells may find a completely different value for the temperature optimum to that of the biochemist studying