Ultraviolet (193, 216 and 254 nm) photoinactivation of Escherichia coli strains with different repair deficiencies.

Escherichia coli K12 bacteria strains AB1157 (repair-deficient wild-type, uvrA{sup +} recA{sup +}), AB1886 (uvrA{sup {minus}}), AB2463 (recA{sup {minus}}) and AB2480 (uvrA{sup {minus}} recA{sup {minus}}) were exposed to 254 nm germicidal UV and 216 or 193 nm laser radiation. The mean lethal incident dose (D{sub 37}) for AB1157 does not change significantly with wavelength, whereas it increases for the other strains on going from {lambda}{sub irr} = 254 to 193 nm, e.g., eightfold for AB2480. Quantum yields for inactivation, due to light absorbed by the chromosomal DNA, have been estimated from the D{sub 37} values. The large differences in D{sub 37} between uvrA{sup +} and uvrA{sup {minus}} strains indicate a significant contribution of pyrimidine dimers and (6-4) photoproducts to photodamage of DNA in the cells. The formation of dimers even with {lambda}{sub irr} = 193 nm is supported by the result that the photoreactivable sector is larger than 63%. Inactivation of E. coli upon irradiation 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 {approx}900 with {lambda}{sub irr} = 254 nm, butmore » only 160 with {lambda}{sub irr} = 193 nm. We propose that this is due to the better repair of photodimers and (6-4) photoproducts than of damage induced by photoionization via upper excited states. Irradiation at 193 nm inactivates AB1157 mainly by damage due to photoionization and AB2480 by damage due to photodimers in the chromosomal DNA. 51 refs., 3 figs., 5 tabs.« less