INACTIVATION BY MONOCHROMATIC NEAR‐UV RADIATION OF AN Escherichia coli hemA8 MUTANT GROWN WITH AND WITHOUT δ‐AMINOLEVULINIC ACID: THE ROLE OF DNA vs MEMBRANE DAMAGE

Abstract
Abstract— Escherichia coli strain RT8 hemA8 [blocked in biosynthesis of δ‐aminolevulinic acid (δ‐ALA), and unable to manufacture porphyrins unless exogenously supplied with δ‐ALA] is inactivated more efficiently by monochromatic 334‐ and 405‐nm radiations if the cells are grown with δ‐ALA supplementation. The fiuence enhancement factor for δ‐ALA sensitization is larger for light at 405 nm than at 334 nm. Both irradiation conditions (plus or minus δ‐ALA) showed prominent oxygen enhancement ratios, which were also larger at 405 nm than at 334 nm. At 334 nm, δ‐ALA supplementation did not affect the accumulation of DNA breaks, while at 405 nm, the induction of DNA breaks doubled for cells supplemented with δ‐ALA. Rubidium leakage caused by 405‐nm radiation occurred at a smaller fiuence in cells supplemented with higher concentrations of δ‐ALA than in cells supplemented with a lower concentration. The results suggest that (1) porphyrin derivatives may have a role in cell killing by near‐UV radiations, and (2) damage to cytomembranes may be a critical lesion produced by these events, whereas DNA breakage may not.