Izvorni znanstveni članak
Repair mechanism in irradiated cells
D. Krsmanović-Simić
; Laboratoire de Biopliysique et Radiobiologie, Faculte des Sciences, Unroersite Libre de Bruxelles
M. Errera
; Laboratoire de Biopliysique et Radiobiologie, Faculte des Sciences, Unroersite Libre de Bruxelles
Sažetak
Many aspects of bacterial mutations which lead to enhanced sensitivity to UV and X radiations have been studied. Radiosensitivity appears to result from a loss of the capacity to repair damaged DNA. The genetic map of these mutations in the chromosome of E. coli is shown. Sofar the best known DNA repair mechanisms are by excision repair (excision of pyrimidine dimers controlled by nonlinked uvr genes) and by recombination repair (elimination of similar damage as a result of genetic recombination between undamaged regions of the DNA). The understanding of the lethal and mutagenic effects of radiation on cells rests on the quantitative and qualitative identification of the various lesions in the DNA. Exposure to UV irradiation causes the production of many different types of photoproducts, but pyrimidine dimers appear to be the most important damage causing biological inactivation. The study of biochemical defects of UV sensitive mutants has allowed a partial understanding of the repair mechanisms. Generally, they consist in removing the UV induced-pyrimidine dimers by cellular enzyme systems (monomerization through photoreactivation, excision or recombination by the action of endo and exonucleases, polymerases and polynucleotides ligases). The X-ray induced lesions arc very heterogenous and not yet as well defined and the mechanisms of recovery are far less understood than in the case of U. V.
Ključne riječi
Hrčak ID:
175414
URI
Datum izdavanja:
21.6.1969.
Posjeta: 790 *