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NONRECIPROCAL SYNERGISTIC LETHAL INTERACTION BETWEEN 365‐nm and 405‐nm RADIATION IN WILD TYPE and uvrA STRAINS OF ESCHERICHIA COLI *
Author(s) -
Webb Robert B.,
Brown Mickey S.,
Ley Ronald D.
Publication year - 1982
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1982.tb02632.x
Subject(s) - photolyase , pyrimidine dimer , irradiation , strain (injury) , escherichia coli , wild type , dna damage , chemistry , oxygen , radiochemistry , microbiology and biotechnology , materials science , dna , photochemistry , dna repair , mutant , biology , physics , biochemistry , gene , organic chemistry , anatomy , nuclear physics
— Lethality by 405‐nm radiation in three repair‐proficient and two uvrA strains of Escherichia coli that belong to two isogenic series was greatly enhanced by prior exposures to 365‐nm radiation at fluences greater than 1 times 10 6 Jm ‐2 . Fluences at 365 nm that yielded a surviving fraction of 0.10 (>1 times 10 6 Jm ‐2 ) in the 5 strains tested resulted in the following 405‐nm fluence enhancement factors (FEF, ratio of the 405‐nm F 37 in the absence of a prior 365‐nm irradiation to that in the presence): strain K.12 AB1157 (wild type), 8.7; strain B/r (wild type), 52; strain WP2 (wild type), 25; strain WP2s (uvrA) , 13; strain K.12 AB1886 (uvrA) , 15. The maximal 405‐nm FEF value obtained after a prior 365‐nm irradiation at greater fluences was 83 in the wild‐type strain B/r. Enhancement of anoxic 405‐nm radiation after a prior aerobic 365‐nm exposure was not detectable, suggesting that prior aerobic irradiation at 365‐nm increased the effects of damage produced at 405 nm by means of an oxygen‐dependent process. Single‐strand breaks (or alkali‐labile bonds) were produced by 405‐nm radiation at 3.0 times 10 ‐5 breaks per 2.5 times 10 9 daltons per Jm ‐2 in the polA strain P3478; pyrimidine dimers were not detected by biological assay (photoreactivation) at 405 nm. Although the introduction of different DNA lesions produced by 365‐ and 405‐nm radiations cannot be ruled out, we propose that the strong synergistic effect of 365‐nm irradiation on 405‐nm lethality is the consequence of pronounced inhibition by 365‐nm radiation of components of the DNA‐repair systems that can mend or bypass damage produced by 405‐nm radiation.