Ethidium bromide inhibition of dark repair processes in ultraviolet- irradiated T$sub 1$ bacteriophage and bacteria

Journal Article · Mon Jan 01 04:00:00 EST 1973 · Stud. Biophys., v. 36-37, pp. 235-244

OSTI ID:4421613

Shankel, D M; Molholt, B

From international conference on the bases of the biological effects of ultraviolet radiation; Brno, Czechoslovakia (2 Oct Ethidium bromide (EB), an intercalating dye, was shown to be a potent inhibitor of the host cell reactivation of ultraviolet (uv)treated bacteriophage T/sub 1/, and of the dark repair of premutational damage produced by low dosages of uv-administered to Escherichia coli. Incorporation of 5 mu g/ml EB in the plating medium completely inhibits the host cell reactivation of the phage T/sub 1/, in E. coli B, but shows no effect in E. coli B/sub s-1/. At lower concentrations the degree of host cell reactivation is proportional to the concentration of the dye. For studies on inhibition of dark repair of premutational damage two mutations were employed, the forward mutation to high level streptomycin resistance and the reverse mutation from tryptophane requiring (try/sup -/) to tryptophane independence (try/sup +/). For both types of mutations a strong mutation enhancement effect was observed in E. coli strains possessing the host cell reactivation system (hcr/sup +/) when EB was included in the post-irradiation expression medium in concentrations of 1-5 mu g/ml. Conversely, in cells lacking the system (hcr-) an antimutagenic effect results from the presence of the dye. The presence of low concentrations of the dye also influences post-UV survival in the hcr+ strain, but not in the hcr/sup -/ strain. Pretreatment of the cells with EB does not affect the survival of either strain. EB in concentrations above 5-10 mu g/ml is normally lethal for these strains of E. coli. A mutant strain resistant to high levels (500 mu g/ml) of the dye has been developed. Survival curves show that the mutant has the same uv resistance as the parent. Greatly increased concentrations of the dye are required to inhibit dark repair in the mutant. (auth)

• Research Organization: Univ. of Kansas, Lawrence
• NSA Number: NSA-29-000575
• OSTI ID: 4421613
• Journal Information: Stud. Biophys., v. 36-37, pp. 235-244, Journal Name: Stud. Biophys., v. 36-37, pp. 235-244; ISSN STBIB
• Country of Publication: Country unknown/Code not available
• Language: English

Related Subjects

*BACTERIOPHAGES-- BIOLOGICAL REPAIR
*DYES-- BIOLOGICAL EFFECTS
*ESCHERICHIA COLI-- BIOLOGICAL REPAIR
BIOLOGICAL RADIATION EFFECTS
INHIBITION
MUTATIONS
N48310* --Life Sciences--Radiation Effects on Microorganisms- -Basic Studies
PHOTON BEAMS
STREPTOMYCIN
SURVIVAL TIME
TRYPTOPHAN
ULTRAVIOLET RADIATION