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Author (up) Burton, P.; Holland, I.B. file  url
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  Title Two pathways of division inhibition in UV-irradiated E. coli Type Journal Article
  Year 1983 Publication Molecular & General Genetics : MGG Abbreviated Journal Mol Gen Genet  
  Volume 190 Issue 2 Pages 309-314  
  Keywords Bacterial Proteins/metabolism; Cell Division/drug effects/*radiation effects; DNA Replication; DNA, Bacterial/radiation effects; Escherichia coli/drug effects/*radiation effects; Genes, Bacterial; Nalidixic Acid/pharmacology; Rec A Recombinases; Rifampin/pharmacology; Ultraviolet Rays  
  Abstract We have investigated the mechanism of division inhibition in E. coli following UV-irradiation or nalidixic acid treatment. After UV, two separate mechanisms, both dependent upon recA+, appear to block division. One mechanism is dependent upon sfiA and sfiB, is inhibited by low levels (4 micrograms/ml) of rifamycin and is expressed in tif mutants at 42 degrees C. The second mechanism is independent of sfiA, and sfiB, is resistant to rifamycin and does not occur in cells lacking DNA replication forks. We suggest that this second mechanism is the result of the failure to terminate DNA replication in inhibited cells. Nalidixic acid inhibition of cell division also appears to involve both mechanisms but as found previously replication forks are also necessary to induce the sfi pathway.  
  Call Number Serial 416  
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Author (up) Doudney, C.O. file  url
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  Title Chloramphenicol effects on DNA replication in UV-damaged bacteria Type Journal Article
  Year 1973 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 17 Issue 1 Pages 1-12  
  Keywords Chloramphenicol/*pharmacology; DNA Repair/drug effects; DNA Replication/drug effects; DNA, Bacterial/*biosynthesis; Escherichia coli/drug effects/radiation effects; Radiation Effects; Ultraviolet Rays  
  Abstract Increasing UV-doses to cultures of Escherichia coli strain B/r decreased progressively the amount of DNA which was formed in the presence of chloramphenicol (160 μg/ml) from the amount formed in unirradiated control cultures in chloramphenicol-containing medium. This is attributed to the progressive inactivation of active sites of DNA replication by UV. In order to form DNA the bacteria must then replicate from the chromosomal fixed origin, an activity which requires protein synthesis and thus cannot occur in the presence of chloramphenicol. Such damage was shown to be subject to photoreactivation after lower UV-doses and thus is the pyrimidine dimer. After higher doses non-photoreversible lesions began to accumulate so that all such damage became non-photoreversible after 96 erg/mm2. The rate of synthesis of DNA in the presence of chloramphenicol was shown to be very close to the rate shown by bacteria incubated in the absence of chloramphenicol, indicating that all active sites of replication remaining after UV-damage remain active in the presence of chloramphenicol, as expected if the limiting effect of chloramphenicol is on initiation at the chromosomal origin and not due to reduction in rate of DNA replication.

A much lower concentration of chloramphenicol (2 μg/ml) blocking only the chloramphenicol-sensitive event in control of DNA replication described by Ward and Glaser15, imposed a limitation in DNA accumulation in the culture of somewhat less than a doubling, as would be expected if the antibiotic at this concentration does not block the chloramphenicol-resistant control event. DNA degradation occured with incubation of bacteria given a UV-dose sufficient to inactivate all active DNA replication sites on their chromosomes, when in medium containing chloramphenicol concentrations (above 20 μg/ml) sufficient to block the chloramphenicol-resistant control event. Such breakdown resulted in death. The damage responsible for such death and DNA breakdown was not photoreversible after this dose, supporting the hypothesis that breakdown results from non-photoreversible inactivation of active DNA replication sites. This was in contrast to increased death in UV-damaged bacteria promoted by nalidixic acid, a specific inhibitor of DNA replication, which could be prevented in part by light exposure after the same UV-dose.
 
  Call Number Serial 536  
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Author (up) Imlay, J.A.; Chin, S.M.; Linn, S. file  url
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  Title Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro Type Journal Article
  Year 1988 Publication Science (New York, N.Y.) Abbreviated Journal Science  
  Volume 240 Issue 4852 Pages 640-642  
  Keywords Bacteriophage lambda; Chemical Phenomena; Chemistry; *DNA Damage; DNA Repair; DNA, Bacterial/*drug effects; Escherichia coli/drug effects/*genetics; Ferrous Compounds; Free Radicals; Hydrogen Peroxide/administration & dosage/*pharmacology; Hydrogen-Ion Concentration; Hydroxides; Hydroxyl Radical; Oxidation-Reduction  
  Abstract Exposure of Escherichia coli to low concentrations of hydrogen peroxide results in DNA damage that causes mutagenesis and kills the bacteria, whereas higher concentrations of peroxide reduce the amount of such damage. Earlier studies indicated that the direct DNA oxidant is a derivative of hydrogen peroxide whose formation is dependent on cell metabolism. The generation of this oxidant depends on the availability of both reducing equivalents and an iron species, which together mediate a Fenton reaction in which ferrous iron reduces hydrogen peroxide to a reactive radical. An in vitro Fenton system was established that generates DNA strand breaks and inactivates bacteriophage and that also reproduces the suppression of DNA damage by high concentrations of peroxide. The direct DNA oxidant both in vivo and in this in vitro system exhibits reactivity unlike that of a free hydroxyl radical and may instead be a ferryl radical.  
  Call Number Serial 1583  
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Author (up) Knothe, H.; Shah, P.; Krcmery, V.; Antal, M.; Mitsuhashi, S. file  url
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  Title Transferable resistance to cefotaxime, cefoxitin, cefamandole and cefuroxime in clinical isolates of Klebsiella pneumoniae and Serratia marcescens Type Journal Article
  Year 1983 Publication Infection Abbreviated Journal Infection  
  Volume 11 Issue 6 Pages 315-317  
  Keywords Cefamandole/*pharmacology; Cefotaxime/*pharmacology; Cefoxitin/*pharmacology; Cefuroxime/*pharmacology; Cephalosporins/*pharmacology; *Conjugation, Genetic; Escherichia coli/drug effects/genetics; Humans; Klebsiella pneumoniae/drug effects/*genetics; Proteus mirabilis/drug effects/genetics; *R Factors; Salmonella typhimurium/drug effects/genetics; Serratia marcescens/drug effects/*genetics  
  Abstract In conjugational crosses, three Klebsiella pneumoniae strains and one Serratia marcescens strain have been demonstrated to transfer resistance determinants to newer types of cephalosporins. While Klebsiella strains donated cefotaxime, cefamandole and cefuroxime resistance to Escherichia coli K-12 recipients, the genetic analysis of exconjugants after the transfer of plasmids from Serratia strains to Proteus or Salmonella recipients showed that the cefoxitin resistance determinant was also co-transferred. In subsequent transfer cycles of this plasmid, cefotaxime and cefoxitin resistance determinants segregated in contrast to the relative stability of plasmids derived from Klebsiella strains in subsequent transfer cycles. From results obtained in this study, it may be concluded that in some strains of nosocomial Enterobacteriaceae, resistance to newer cephalosporins could be transmissible and thus plasmid-located.  
  Call Number Serial 494  
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Author (up) Lapenda, J.C.; Silva, P.A.; Vicalvi, M.C.; Sena, K.X.F.R.; Nascimento, S.C. file  url
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  Title Antimicrobial activity of prodigiosin isolated from Serratia marcescens UFPEDA 398 Type Journal Article
  Year 2015 Publication World Journal of Microbiology & Biotechnology Abbreviated Journal World J Microbiol Biotechnol  
  Volume 31 Issue 2 Pages 399-406  
  Keywords Acinetobacter/drug effects; Anti-Bacterial Agents/chemistry/*pharmacology; Bacteria/*drug effects/growth & development; Disk Diffusion Antimicrobial Tests; Enterococcus faecalis/drug effects; Escherichia coli/drug effects; Prodigiosin/chemistry/*pharmacology; Pseudomonas aeruginosa/drug effects; Serratia marcescens/*chemistry; Spectrophotometry; Staphylococcus aureus/drug effects; Streptococcus pyogenes/drug effects  
  Abstract Prodigiosin is an alkaloid and natural red pigment produced by Serratia marcescens. Prodigiosin has antimicrobial, antimalarial and antitumor properties and induces apoptosis in T and B lymphocytes. These properties have piqued the interest of researchers in the fields of medicine, pharmaceutics and different industries. The aim of the present study was to evaluate the antimicrobial activity of prodigiosin against pathogenic micro-organisms. The red pigments produced by S. marcescens exhibited absorption at 534 nm, Rf of 0.59 and molecular weight of 323 m/z. Antimicrobial activity was tested against oxacillin-resistant Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, Enterococcus faecalis, Streptococcus pyogenes, Acinetobacter sp. and oxacillin-resistant S. aureus. The standard antibiotics employed were ampicillin, chloramphenicol, gentamicin and oxacillin. The disc-diffusion tests demonstrated significant inhibition zones for S. aureus (35 +/- 0.6), E. faecalis (22 +/- 1.0) and S. pyogenes (14 +/- 0.6). However, prodigiosin showed resistance to E. coli, P. aeruginosa and acinetobacter, where no significant formation of inhibitory halos were observed. We determined the inhibitory minimum concentrations and bactericidal for 20 strains of oxacillin-resistant S. aureus (ORSA). The pattern was the antibiotic oxacillin. The minimum inhibitory concentrations observed ranged from 1, 2 and 4.0 mug/mL, respectively, while the minimum bactericidal concentrations ranged from 2, 4, 8 and 16 mug/mL. The S. marcescens prodigiosin produced by showed bactericidal and bacteriostatic effect showing promising antimicrobial activity and suggesting future studies regarding its applicability in antibiotics therapies directed ORSA.  
  Call Number Serial 1672  
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