ArticleBMC microbiology2025
Zinc pyrithione impairs iron-sulfur cluster biogenesis in Mycobacterium tuberculosis.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- A conjugated polymer antimicrobial agent triggers metabolic cascade-mediated killing of carbapenem-resistantFrontiers in cellular and infection microbiology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundTuberculosis remains a major global health threat, especially with the increasing prevalence of drug-resistant Mycobacterium tuberculosis (Mtb). There is an urgent need to develop new antibiotics with novel mechanisms of action. Zinc pyrithione (ZnPT), a bidentate metal-chelating agent, displays potent in vitro activity against bacteria and fungi. This study aimed to evaluate the antimycobacterial activity of ZnPT and to explore its potential mechanisms.
methodsThe bactericidal activity of ZnPT against Mtb strains was evaluated using minimum inhibitory concentration and minimum bactericidal concentration assays. The role of copper was assessed through metal chelator supplementation studies, while intracellular metal accumulation was quantified using inductively coupled plasma mass spectrometry (ICP-MS). Mechanistic analyses included transcriptomic profiling, enzyme activity assays, and targeted metabolomics to assess effects on iron-sulfur (Fe-S) cluster biogenesis and energy metabolism.
resultsZnPT demonstrated potent bactericidal activity against both drug-sensitive and drug-resistant Mtb strains. Copper supplementation significantly enhanced the efficacy of ZnPT, and ICP-MS confirmed elevated intracellular copper levels. Transcriptomic analysis revealed disruption of multiple pathways, including the copper ion stress response, sulfur metabolism, Fe-S cluster biogenesis, siderophore biosynthesis, and intermediary metabolism. Notably, ZnPT induced upregulation of the sulfur mobilization (SUF) operon while repressing electron transfer ferredoxins, indicating disturbed Fe-S cluster homeostasis. Enzyme assays showed marked inhibition of cysteine desulfurase activity, a key step in Fe-S cluster assembly. Targeted metabolomics revealed depletion of tricarboxylic acid (TCA) cycle intermediates and accumulation of metabolic bottlenecks, indicating impaired Fe-S enzyme activity. ZnPT treatment further led to dysfunction of the electron transport chain, reduced proton motive force, and ATP depletion.
conclusionsZnPT exhibits antimycobacterial activity by disrupting Fe-S cluster biogenesis and impairing energy metabolism in Mtb.
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Registered trials
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