Investigations of genotoxic activity of antimicrobial/antiviral agent FS-1 in human lymphocytes and tumor cell

Nersesyan, Armen; Il’in, A. I.; Kulmanov, Marat

doi:10.3103/s0095452711020101

Cited by 3 publications

(5 citation statements)

References 12 publications

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“…Concerning genotoxic activity of FS-1, it should be indicated that the coumpund is not mutagenic in the Salmonella/microsome test (unpublished data), MN, and the comet assays in vitro in human and mouse cancer cells lines (6,7). In addition, our in vivo experiments in mice and rats using MN and comet assays confirmed the absence of FS-1 genotocxicity.…”

Section: Discussionsupporting

confidence: 67%

“…Completely negative results were obtained (Prof. S. Knasmüller, Medical University of Vienna, a manuscript in preparation). FS-1 was studied for its ability to induce DNA damage and micronuclei (MN) frequency in human tumor cell lines HeLa and Caco-2 and mouse lymphoma cell line L5178Y at concentrations of 200, 500, and 1000 µg/ ml without exogenous metabolic activation (6,7). The compound was additionally tested for DNA damaging ability in human lymphocytes at concentrations of 200, 400 and 800 µg/ml.…”

Section: Introductionmentioning

confidence: 99%

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Investigations of genotoxic activity of the antimicrobial/antiviral agent FS-1 in rodents by means of the micronucleus and the comet assays

Nersesyan¹,

Il’in²,

Kulmanov³

et al. 2011

Arch Oncol

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Background: FS-1 is a complex of iodine and synthesized polysaccharides and it is very effective against a number of microbe and virus strains. The aim of the study was to evaluate possible genotoxic properties of FS-1. Methods: The compound was studied in rat and mouse bone marrow micronucleus (MN) assay and the comet assay in murine peripheral blood leukocytes, hepatocytes, and kidney cells. Two treatment protocols were applied, namely acute and subacute ones. In the first protocol, the compound was administered orally once and in subacute treatment two times, 24 h apart. The animals were sacrificed 24 h after the last treatment, and appropriate cells were used to assess DNA damage and MN induction. Results: In none of the tests (MN and comet assays) significant increase compared with respective negative controls was observed. Conclusion: The fact that the compound neither induces DNA damage in various organs of mice nor is effective in the induction of MN in bone marrow cells of rats and mice is important for future genotoxicity studies of FS-1, which can be used in clinical medicine after additional testing of safety for humans

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Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Investigations of genotoxic activity of the antimicrobial/antiviral agent FS-1 in rodents by means of the micronucleus and the comet assays

Nersesyan¹,

Il’in²,

Kulmanov³

et al. 2011

Arch Oncol

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“…A series of studies indicate similar results in terms of genotoxic potential and MN induction for: Strychnos pseudoquina , a Brazilian medicinal plant with novel antiulcerogenic activity, that was shown to give rise to MN in blood cells (Santos et al, 2006), West African plant Cryptolepis sanguinolenta which contains an anti-malarial herbal alkaloid, cryptolepine, that induces MN in hamster fibroblast cells (Ansah et al, 2005), anti-obesity drugs sibutramine and fenproporex that induce MN in Swiss mice (da Silva et al, 2010), and some antibacterial/antiviral drugs possessing clastogenic and aneugenic properties (Abou-Eisha et al, 2004; Balakrishnan and Eastmond, 2006; Nersesyan et al, 2011). …”

Section: Micronuclei and Genotoxic Agentsmentioning

confidence: 99%

Micronuclei in genotoxicity assessment: from genetics to epigenetics and beyond

Luzhna¹,

Kathiria²,

Kovalchuk³

2013

Front. Genet.

362

203

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Micronuclei (MN) are extra-nuclear bodies that contain damaged chromosome fragments and/or whole chromosomes that were not incorporated into the nucleus after cell division. MN can be induced by defects in the cell repair machinery and accumulation of DNA damages and chromosomal aberrations. A variety of genotoxic agents may induce MN formation leading to cell death, genomic instability, or cancer development. In this review, the genetic and epigenetic mechanisms of MN formation after various clastogenic and aneugenic effects on cell division and cell cycle are described. The knowledge accumulated in literature on cytotoxicity of various genotoxins is precisely reflected and individual sensitivity to MN formation due to single gene polymorphisms is discussed. The importance of rapid MN scoring with respect to the cytokinesis-block micronucleus assay is also evaluated.

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“…FS-1 consists of synthesized polysaccharide micellar units containing triiodide complexes coordinated by metal ions and integrated into a dextrin-polypeptide moiety resulting in a 30–300 kDa complex [ 89 ]. The polysaccharides act as solubilizing agents and aid in the release of free iodine when mixed with water [ 90 ]. The released free iodine causes oxidative stress in the bacterial cell, a mechanism that drug-resistant mutants are more susceptible to [ 89 , 91 ].…”

Section: Susceptibility Reversionmentioning

confidence: 99%

“…FS-1 also prevents recurrence of infection, which is commonly observed with antibiotics within 30 days of recovery time [ 89 ]. Studies in human lymphocytes and tumor cell lines (HeLa and Caco2) show no DNA damaging action [ 90 ]. Moreover, it has been observed in animal models that FS-1 reduces the hepatotoxicity caused by some antimycobacterial agents [ 89 ].…”

Section: Susceptibility Reversionmentioning

confidence: 99%

MmpL3 Inhibition: A New Approach to Treat Nontuberculous Mycobacterial Infections

Sethiya

Sowards

Jackson

et al. 2020

IJMS

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Outside of Mycobacterium tuberculosis and Mycobacterium leprae, nontuberculous mycobacteria (NTM) are environmental mycobacteria (>190 species) and are classified as slow- or rapid-growing mycobacteria. Infections caused by NTM show an increased incidence in immunocompromised patients and patients with underlying structural lung disease. The true global prevalence of NTM infections remains unknown because many countries do not require mandatory reporting of the infection. This is coupled with a challenging diagnosis and identification of the species. Current therapies for treatment of NTM infections require multidrug regimens for a minimum of 18 months and are associated with serious adverse reactions, infection relapse, and high reinfection rates, necessitating discovery of novel antimycobacterial agents. Robust drug discovery processes have discovered inhibitors targeting mycobacterial membrane protein large 3 (MmpL3), a protein responsible for translocating mycolic acids from the inner membrane to periplasm in the biosynthesis of the mycobacterial cell membrane. This review focuses on promising new chemical scaffolds that inhibit MmpL3 function and represent interesting and promising putative drug candidates for the treatment of NTM infections. Additionally, agents (FS-1, SMARt-420, C10) that promote reversion of drug resistance are also reviewed.

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Investigations of genotoxic activity of antimicrobial/antiviral agent FS-1 in human lymphocytes and tumor cell

Cited by 3 publications

References 12 publications

Investigations of genotoxic activity of the antimicrobial/antiviral agent FS-1 in rodents by means of the micronucleus and the comet assays

Investigations of genotoxic activity of the antimicrobial/antiviral agent FS-1 in rodents by means of the micronucleus and the comet assays

Micronuclei in genotoxicity assessment: from genetics to epigenetics and beyond

MmpL3 Inhibition: A New Approach to Treat Nontuberculous Mycobacterial Infections

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