ULTRAVIOLET (193, 216 AND 254 NM) PHOTOINACTIVATION OF ESCHERICHIA-COLI STRAINS WITH DIFFERENT REPAIR DEFICIENCIES

Escherichia coli K12 bacteria strains AB1157 (repair-deficient wild-ty pe, uvrA(+) recA(+)), AB1886 (uvrA(-)), AB2463 (recA(-)) and AB2480 (u vrA(-) recA(-)) were exposed to 254 nm germicidal UV and 216 or 193 nm laser radiation. The mean lethal incident dose (D-37) for AB1157 does not change significantly with wavelength, whereas it increases for th e other strains on going from lambda(irr) = 254 to 193 nm, e.g. eightf old for AB2480. Quantum yields for inactivation, due to light absorbed by the chromosomal DNA, have been estimated from the D,, values. The large differences in D,, between uvrA(+) and uvrA(-) strains indicate a significant contribution of pyrimidine dimers and (6-4) photoproduct s to photodamage of DNA in the cells. The formation of dimers even wit h lambda(irr) = 193 nm is supported by the result that the photoreacti vable sector is larger than 63%. Inactivation of E. coli upon irradiat ion at 193 and 216 nm is therefore due to damage to intracellular DNA rather than to membrane or protein damage as is the case for mammalian cells. The ratio of the lethal doses for AB1157 vs AB2480 is approxim ate to 900 with lambda(irr) = 254 nm, but only 160 with lambda(irr) = 193 nm. We propose that this is due to the better repair of photodimer s and (6-4) photoproducts than of damage induced by photoionization vi a upper excited states. Irradiation at 193 nm inactivates AB1157 mainl y by damage due to photoionization and AB2480 by damage due to photodi mers in the chromosomal DNA. (C) 1995 by Radiation Research Society