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1.
Biophysics (Oxf) ; 67(5): 761-767, 2022.
Article in English | MEDLINE | ID: mdl-36567970

ABSTRACT

This study demonstrates a bacteriostatic effect of binuclear dinitrosyl iron complexes with glutathione on Escherichia coli TN300 cells. It has been quantified by the colony formation assay. The bacteriostatic effect exerted by these complexes increases considerably in the presence of diethyldithiocarbamate. Our results suggest that this effect is caused by the intense release of nitrosonium cations, NO+, from the complexes, which decompose under the action of diethyldithiocarbamate. A similar effect is observed when E. coli cells are treated with diethyldithiocarbamate 40 min after the addition of sodium nitrite or S-nitrosoglutathione. Notably, the level of dinitrosyl iron complexes observed in the bacterial cells due to the effects of sodium nitrite or S-nitrosoglutathione is almost the same as that obtained after treatment with glutathione-containing complexes. The bacteriostatic effects of the NO molecules released from nitrite or S-nitrosoglutathione during their brief interaction with bacteria were significantly smaller than the bacteriostatic effect of NO+. We deduce therefrom that the nitrosonium cations released from DNICs are responsible for the observed bacteriostatic effect of these complexes in E. coli cells.

5.
Biochemistry (Mosc) ; 69(8): 883-9, 2004 Aug.
Article in English | MEDLINE | ID: mdl-15377268

ABSTRACT

Nitrosyl-iron complexes used as aqueous preparations of binuclear dinitrosyl-iron complex with glutathione (DNICglu), initially polycrystalline preparations of binuclear tetranitrosyl-iron complex with thiosulfate (TNICthio), and also binuclear tetranitrosyl-iron complex with aminotriazole (TNICatria) and mononuclear dinitrosyl-iron complex with triazole (DNICtria) in the concentration to 0.1 mM activated expression of the soxS and sfiA genes in Escherichia coli. Higher concentrations of polycrystalline preparations of low stability in aqueous solutions were cytotoxic, whereas DNICglu, which is more stable in water (up to two days), increased the gene expression on increase in its concentration to 0.5 mM. The iron chelating agent o-phenanthroline completely inhibited the gene expression induced by all compounds studied. The genetic signal transduction seemed to be realized not by nitric oxide molecules and/or iron ions released in solutions but directly by the complexes themselves, which activate transcriptional proteins by transfer onto them of nitrosyl-iron groups [Fe+(NO+)2].


Subject(s)
Escherichia coli/drug effects , Escherichia coli/genetics , Gene Expression Regulation, Bacterial/drug effects , Iron/pharmacology , Nitrogen Oxides/pharmacology , Electron Spin Resonance Spectroscopy , Escherichia coli/metabolism , Escherichia coli Proteins/genetics , Iron/chemistry , Iron/metabolism , Iron Chelating Agents/pharmacology , Molecular Structure , Nitrogen Oxides/chemistry , Nitrogen Oxides/metabolism , Phenanthrolines/pharmacology , SOS Response, Genetics/drug effects , Solutions/chemistry , Trans-Activators/genetics , Water/chemistry
6.
Biochemistry (Mosc) ; 65(6): 690-5, 2000 Jun.
Article in English | MEDLINE | ID: mdl-10887288

ABSTRACT

An induction of the SOS DNA repair response by physiological nitric oxide donors (dinitrosyl iron complexes (DNIC) with thiols and S-nitrosothiols (RSNO)) was studied in E. coli cells. DNIC with thiols were the most effective SOS-inducers. Being more toxic, RSNO mediated a similar response at 10-100 microM, but they were inactive at concentrations above 0.5 mM. Pretreatment of the cells with chelating agents, o-phenanthroline and picolinic acid, prevented induction of the SOS response by all NO-donors used and led to a decrease in the DNIC-type EPR signal that appeared after incubation of the cells with DNIC or S-nitrosoglutathione (GSNO). Analysis of these effects revealed a dual role of iron ions in reactivity and toxicity of the NO-donating agents. On one hand, they could stabilize GSNO in the form of less toxic DNIC, and, on the other hand, they took part in the formation of the SOS-inducing signal by NO-donating agents.


Subject(s)
DNA Repair/physiology , Escherichia coli/genetics , Iron/physiology , Nitric Oxide/physiology , SOS Response, Genetics , Escherichia coli/physiology , Nitric Oxide Donors/pharmacology
7.
FEBS Lett ; 454(3): 177-80, 1999 Jul 09.
Article in English | MEDLINE | ID: mdl-10431802

ABSTRACT

The ability of nitric oxide (NO) donor compounds to induce the SOS DNA repair response in Escherichia coli is reported. Dinitrosyl iron complexes with glutathione and cysteine (DNIC) are the most potent SOS-inducers. S-Nitrosothiols (RSNO) mediate a similar response at 10-100 microM, but the response decreases sharply at concentrations above 0.5 mM. Pretreatment of the cells with the chelating agent o-phenanthroline (OP) prevents induction of the SOS response by all agents used. On the other hand, the toxicity of S-nitrosothiols is higher than that of DNIC. The EPR study shows the appearance of an EPR DNIC-type signal after incubation of the cells with S-nitrosoglutathione because of mutual transformation between RSNO and DNIC in the presence of accessible iron inside the cells. Pretreatment of the cells with OP leads to a decrease in this signal. Analysis of NO donor effects reveals a dual role of the iron ions in reactivity and toxicity of the compounds studied, i.e. (i) stabilization of the cytotoxic RSNO and (ii) generation of the SOS signal.


Subject(s)
DNA Repair/drug effects , Escherichia coli/genetics , Mercaptoethanol , Nitric Oxide Donors/pharmacology , Nitric Oxide/metabolism , S-Nitrosothiols , DNA, Bacterial/genetics , DNA, Bacterial/metabolism , Escherichia coli/metabolism , Iron/metabolism , Ligands , Nitroso Compounds/metabolism
8.
Mutat Res ; 192(2): 95-8, 1987 Oct.
Article in English | MEDLINE | ID: mdl-3309648

ABSTRACT

p-Aminobenzoic acid (PABA) exhibited antimutagenic activity toward N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)-induced mutagenicity in the Ames assay in Salmonella typhimurium. The antimutagenic effects were associated with an increased rate of decomposition of MNNG in the presence of PABA. The participation of other mechanisms, such as the alteration of cellular processes by PABA, however, cannot be excluded.


Subject(s)
4-Aminobenzoic Acid/pharmacology , Aminobenzoates/pharmacology , Methylnitronitrosoguanidine/antagonists & inhibitors , Salmonella typhimurium/drug effects , Mutagenicity Tests
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