Abstract— The skin photosensitizing furocoumarins, 8‐methoxypsoralen (MOP) and 4,5′,8‐trimethylpsoralen (TMP), inactivate E. coli ribosomes in vitro, on UV irradiation at 313 nm. Purging the solutions with N2 protects the ribosomes considerably against photoinactivation (75% with MOP and 80% with TMP). In air, the ribosome photoinactivation is mainly due to singlet oxygen (1O2), since the presence of NaN3 and other 1O2 quenchers protects the system and the inactivation is enhanced in D2O. Although 1O2 dominates as the inactivating species, the possibility of additional (∼15%) minor mechanisms involving free radicals exists. However, O‐2 does not appear to be the damaging species, since superoxide dismutase does not provide any protection.
Photosensitization of the partially purified enzyme, phe‐tRNA‐synthetase with MOP or TMP shows inactivation and protection curves similar to those seen with the ribosomes. On the other hand, unfrac‐tionated tRNAphc is not photosensitized under similar conditions, although it shows self‐photosensitization. It is likely that in the furocoumarin‐sensitized ribosomes, the primary events of photoinactivation are associated with the proteins.
Chinese hamster V79 cells were exposed to 10(-5) moles/liter bromodeoxyuridine (BrdUrd) or iododeoxyuridine (IdUrd) for 16 or 29 hr and then tested for thermal sensitivity, radiosensitivity, and sensitivity to the combined treatments of heat and radiation. BrdUrd and IdUrd treatment of cells resulted in enhanced radiosensitivity which increased with exposure time but had little or no effect on thermal sensitivity. For 42.0 degrees C heating, no effect was observed, while for 45.0 degrees C heating, a small decrease in thermal sensitivity occurred for both 16- and 29-hr exposure times, in the combined treatment of heat and radiation, the presence of BrdUrd or IdUrd resulted in about the same thermal enhancement in radiosensitivity. BrdUrd and IdUrd uptake into cellular DNA were measured using high-pressure liquid chromatography and, after a 29-hr exposure to 10(-5) moles/liter of BrdUrd or IdUrd, approximately 40% of the thymidine was substituted.
Gamma-irradiated E coli ribosomes and tRNA, in aerated solutions, were inactivated with D37 doses of 144 and 77 Gy, respectively. Aminoacyl-tRNA-synthetases were only slightly inactivated under comparable conditions. Effects of additives to ribosome and tRNA solutions suggest that hydroxyl radicals were the major damaging species, that superoxide anions were not damaging and that radiolytically-formed hydrogen peroxide was also unimportant. Part of the damage by hydroxyl radicals is expressed through secondary radicals produced from additives and buffers. Results obtained with three different buffers suggest that (1) acetate ions provide protection by competing for hydroxyl radicals, (2) chloride ions are without effect and (3) inactivation of ribosomes and aminoacyl-tRNA-synthetases in Tris-HCl/MgCl2 and phosphate/MgCl2 buffered solutions was similar but the tRNA inactivation was lower in Tris-HCl/MgCl2 buffer.
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