Inhibition and enhancement of phleomycin-induced DNA breakdown by aromatic tricyclic compounds.
AUTOR(ES)
Grigg, G W
RESUMO
Cationic aromatic tricyclic compounds including triphenylmethane dyes, phenazines, phenoxazines, acridines, phenothiazines, phenanthridinium compounds, anthracenes and xanthene dyes, which amplify cell killing in phleomycin-treated Escherichia coli B cells also modified phleomycin-induced breakdown of DNA to acid-soluble fragments. A plot of DNA breakdown as a function of concentration was bell-shaped for each of the active compounds, i.e. as the concentration increased, DNA breakdown was enhanced initially, but above a certain concentration, the proportion of DNA degraded declined, often to zero. One of the compounds, acriflavine, when tested also inhibited DNA breakdown following ultraviolet irradiation. A study, by sedimentation methods, of DNA single-strand breakage in phleomycin-treated E. coli cells, using 3 representative compounds, Crystal Violet, 3,6-diaminoacridine and Methylene Blue, revealed a consistent increase in DNA strand breaks as concentration of compound increased. In similar experiments with ethidium bromide the breakage yield/concentration curve exhibited a maximum. In general, however, it seems that the inhibition of DNA-breakdown observed at higher concentrations of these amplifying compounds is not explicable by an effect on the primary breakage event, but is due to suppression of exonucleolytic activity in the cells.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=320439Documentos Relacionados
- Effects of Coumarin, Thiopurines, and Pyronin Y on Amplification of Phleomycin-Induced Death and Deoxyribonucleic Acid Breakdown in Escherichia coli
- Phleomycin-Induced Solubilization of Deoxyribonucleic Acid in Uninfected and T Bacteriophage-Infected Escherichia coli B
- Inhibition of antigen- and mitogen-induced human lymphocyte proliferation by gold compounds.
- Trichloroethylene metabolism by microorganisms that degrade aromatic compounds.
- Inhibition of Clostridium botulinum by antioxidants, phenols, and related compounds.