Synergism between 365- and 254-nm Radiations for Inactivation of Escherichia coli

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Abstract
The lethal interaction between radiations at 254 and 365 nm was studied in strains of E. coli K12 that differ in repair capability. Increased sensitivity to 254-nm radiation was produced by a prior exposure to large fluences of 365-nm radiation for both stationary-phase and exponential-phase cells of strains K12 AB1157 (wild type) and K12 AB1886 (excision deficient). Results presented support the hypothesis that damage by 365-nm radiation to recombination and excision repair is a major cause of synergism between 365- and 254-nm radiations and a major factor in 365-nm inactivation of strains proficient in postreplication and/or excision repair. The interaction between 365- and 254-nm radiations in the postreplication repair-deficient strain (K12 AB2463) was complex. The 254-nm sensitivity decreased at relatively low fluences of 365-nm radiation (< 8 .times. 105 J m-2), but increased relative to the minimum value at greater fluences. The decrease in 254-nm sensitivity after a low fluence at 365 nm reflects the phenomenon of photoprotection, while the increase in 254-nm sensitivity at high 365-nm fluences supports the previous reports of 365-nm damage to the excision-repair system. The strong lethal synergism of 365- and 264-nm radiations was much greater in the radiation-resistant organism Micrococcus radiodurans than in E. coli.