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Biomedical subjects

L G Silvestri

Publications and source records attributed to L G Silvestri.

At least 19 recordsLinked to original sources
PubMed1977

The mechanism of action of nitro-heterocyclic antimicrobial drugs. Primary target of 1-methyl-2-nitro-5-vinylimidazole is DNA.

The antimicrobial drug 1-methyl-2-nitro-5-vinylimidazole (MEV) preferentially blocked DNA synthesis, was mutagenic and induced coliphage lambda in Escherichia coli. The antibacterial effects of MEV are the consequences of repairable damage to DNA, as shown by hypersensitivity of recA and uvr strains to MEV and related drugs, stimulation by MEV of DNA turnover which was dependent on the product of the uvrA gene, and the presence of cross-links in DNA from MEV-treated bacteria.

Anti-Bacterial Agents↗
PubMed1977

The mechanism of action of nitro-heterocyclic antimicrobial drugs. Metabolic activation by micro-organisms.

Although the target of the antimicrobial drug 1-methyl-2-nitro-5-vinylimidazole (MEV) has been shown to be DNA (Goldstein et al., 1977) the drug was ineffective in cell-free systems because it was not activated. Both the rate of metabolic activation of MEV and its antibacterial activity were increased when bacteria were grown in limiting oxygen. Mutants of Escherichia coli which were conditionally resistant to nitroimidazoles and nitrofurans were defective in drug activation. The activities of these drugs against E. coli correlated with their rates of metabolism. The antimicrobial spectrum of the drugs appeared to be related to their reducibility by different species.

Aerobiosis↗
PubMed1976

IgE antibodies in patients allergic to rifampicin.

In sera of patients treated with rifampicin, who had episodes ascribable to rifampicin sensitization, IgE antibodies were found. These antibodies cross-react with rifamycin SV and with the chromophoric moiety of rifamycins, but not with the side chain of rifampicin.

Antibodies↗
PubMed1976

Gardimycin, a new antibiotic from Actinoplanes. III. Biological properties.

The new antibiotic gardimycin has an interesting in vitro antibacterial activity against Gram-positive bacteria and Neisseria gonorrhoeae. Parenteral administration gives a high degree of protection against experimental infections in mice. It also shows some chemotherapeutic activity when given rectally.

Actinomycetales↗
PubMed1975

Mechanism of action of rifamazine, a member of a new class of (dimeric) rifamycins.

1. Rifamazine (AF/RP) a dimeric rifamycin, is active against bacterial DNA-dependent RNA polymerase and against viral RNA-dependent DNA polymerase. 2. Rifamazine is active also against DNA-dependent RNA polymerase extracted from rifampicin-resistant mutants of Escherichia coli. It does not interfere with enzyme-template interaction or with RNA elongation. It blocks initiation. 3. A comparison is made between the mechanism of action of rifamazine and that of rifampicin, and of AF/013 (octyloxime of 3-formylrifamycin SV), a C-class rifamycin. Our results show that the mechanism of action of rifamazine is more similar to that of rifampicin than to that of the octyloxime derivative. 4. Activity of rifamazine against RNA polymerase from rifampicin-resistant mutants is thought to be due to binding of the dimer to both the rifamycin-specific binding site and to a second weak site.

Coliphages↗
PubMed1975

Lack of effect of rifampin on the antibody response to a viral antigen in patients with tuberculosis.

Twenty-three volunteer patients with pulmonary tuberculosis were studied for the effect of rifampin on humoral immunity. The patients were matched for age and body weight with other patients not on rifampin treatment. Antibodies to influenza virus were measured 18 days after immunization. At the clinical doses used and for the periods of treatment between 3 and 8 months no difference in humoral immune response was observed between patients treated with rifampin and the control subjects. All but one treated patient showed an increase of antibody titers after vaccination.

Adult↗
PubMed1973

Relationships between curing of the F episome by rifampin and by acridine orange in Escherichia coli.

Subinhibitory doses of rifampin cured F(+)Escherichia coli cells from the episome. The target of the drug was transcription because E. coli mutants with a ribonucleic acid polymerase resistant to rifampin were not cured. The experimental conditions required for optimal curing with rifampin very closely resembled those required for curing with acridine orange. Mutants were found which are more resistant to curing by both acridine orange and rifampin. Probably the two drugs affect a common metabolic step, or alternatively they may inhibit the synthesis of a factor which is necessary for the replication of the episome.

Acridines↗
PubMed1971

Mechanism of action of rifampin on Mycobacterium smegmatis.

Deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase (EC 2.7.7.6) isolated from a rifampin-sensitive strain of Mycobacterium smegmatis was 90% inhibited by 1 mug of rifampin per ml; enzyme from a rifampin-resistant mutant was not affected by this concentration of antibiotic. Inhibition of phenylalanine-1-(14)C incorporation by rifampin in growing cultures was complete about 6 min after addition of antibiotic. Under the same conditions, uracil-2-(14)c incorporated was blocked after 1.5 to 2 min. Rifampin kills M. smegmatis very slowly. When rifampin-inhibited cultures were transferred to a rifampin-free medium, there was a partial resumption of uracil-2-(14)C incorporation, even in the presence of chloramphenicol. We conclude that a primary event in the inhibition of M. smegmatis by rifampin is the block of DNA-dependent RNA polymerase.

Adenosine Monophosphate↗