• Iron Chelating Clioquinol In Drug Resistant Infection

    From ironjustice@21:1/5 to All on Tue Apr 17 20:16:29 2018
    Clioquinol, an alternative antimicrobial agent against common pathogenic microbe.
    You Z1, Ran X1, Dai Y2, Ran Y3.
    J Mycol Med. 2018 Apr 10. pii: S1156-5233(17)30417-1.
    doi: 10.1016/j.mycmed.2018.03.007.

    Skin and soft tissue infections (SSTIs) are very common in dermatology and the use of antimicrobial formulations are important in treating these diseases. With the increasing of drug-resistant strains, researchers need to find ways to enhance the
    effectiveness and/or reduce the drug resistance. Clioquinol was one of antiseptics that can inactivate microbes. It was lack of data of antimicrobial activity; meanwhile it was infrequently used in infection. In order to research the antimicrobial
    spectrum and activity of topical 3% clioquinol cream among common pathogenic microorganisms compared with other common topical pharmaceuticals, we used modified agar diffusion assay to judge drug susceptibility and compared with broth microdilution assay.
    Thirty strains of pathogenic fungi belonging to 14 species and 5 strains of pathogenic bacterium belonging to 4 species from clinic or standard strains were enrolled into the experiment. The inhibition zone around 3% clioquinol cream for all experiment
    isolates was observed. It could inhibit the growth of most fungal species with different strength, but the antibacterial activity was weak. For Candida tropicalis, Candida guilliermondii, Aspergillus terreus, Fusarium solani and Trichoderma harzianum,
    the inhibition zone was biggest among all the tested drugs. The antifungal activity for Dermatophytes and Candida albicans was moderate. Two assays had a degree of consistency. Based on results above, we identified the antifungal spectrum of 3%
    clioquinol cream was broad. The antimicrobial strength of 3% clioquinol cream depended on the species but it can act on most of the species.

    3% clioquinol; Drug susceptibility; Modified agar diffusion assay; Topical pharmaceuticals

    PMID: 29650464 DOI: 10.1016/j.mycmed.2018.03.007


    A novel method for assessing the role of iron and its functional
    chelation in fibrin fibril formation: the use of scanning electron
    Posted online on April 19, 2013.
    Etheresia Pretorius1, Natasha Vermeulen1, Janette Bester1, Boguslaw
    Lipinski2, and Douglas B. Kell3
    1Department of Physiology, Faculty of Health Sciences, University of
    Pretoria, Arcadia, South Africa,
    2Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA, and
    3School of Chemistry and Manchester Institute of Biotechnology,
    University of Manchester, Manchester, UK
    Address for correspondence: Etheresia Pretorius, Department of
    Physiology, Faculty of Health Sciences, University of Pretoria,
    Private Bag x323, Arcadia 0007, South Africa. Tel: +27 12 420 2864.
    Fax: +27 12 420 4482. E-mail: resia.p...@up.ac.za

    Aims: Inflammatory diseases associated with iron overload are
    characterized by a changed coagulation profile, where there is a
    persistent presence of fibrin-like material of dense-matted deposits
    (DMDs). It is believed that one source of such material is a result of
    the activation of blood coagulation without the generation of
    thrombin, causing clots to become resistant to fibrinolytic
    dissolution. The aim of the current manuscript therefore is to apply a
    novel scanning electron microscopy method for assessing the role of
    functional chelation in the prevention or reversal of iron-induced
    fibrin formation.

    Methods and results: Purified fibrinogen and platelet-rich plasma were
    exposed to chelating agents followed by iron, to determine the
    chelating effects. We show that there is another, pathological pathway
    of fibrin formation initiated by free iron (initially as Fe (III)),
    leading to the formation of highly reactive oxygen species such as the hydroxyl radical that can oxidize and insolubilize proteins, a process
    that might be inhibited by iron-chelating compounds. The final product
    of such a pathway is a fibrin-like material, termed DMDs that are
    remarkably resistant to proteolytic degradation.

    Conclusions: Scanning electron microscopy shows that iron-chelating
    agents are effective inhibitors of DMD formation. The most active
    inhibitors of DMD formation proved to be Desferal, Clioquinol and
    Curcumin, whereas Epigallocatechin gallate and Deferiprone were less effective. The functional model we describe may point the clinical
    utility of various substances in iron-mediated degenerative diseases.


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