4.6 Article

The antimicrobial action of polyaniline involves production of oxidative stress while functionalisation of polyaniline introduces additional mechanisms

Journal

PEERJ
Volume 6, Issue -, Pages -

Publisher

PEERJ INC
DOI: 10.7717/peerj.5135

Keywords

Polyaniline; Conducting polymer; Poly(3-aminobenzoic acid); Antimicrobial mechanism; Escherichia coli; Oxidative stress; Iron dysregulation; Uncoupler

Funding

  1. New Zealand Ministry of Business, Innovation and Employment (MBIE) [UOAX0812, UOAX1410]
  2. University of Auckland's Vice Chancellors Strategic Development Fund [23563]
  3. New Zealand Ministry of Business, Innovation & Employment (MBIE) [UOAX0812] Funding Source: New Zealand Ministry of Business, Innovation & Employment (MBIE)

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Polyaniline (PANT) and functionalised polyanilines (fPANI) are novel antimicrobial agents whose mechanism of action was investigated. Escherichia coli single gene deletion mutants revealed that the antimicrobial mechanism of PANI likely involves production of hydrogen peroxide while homopolymer poly(3-aminobenzoic acid), P3ABA, used as an example of a fPANI, disrupts metabolic and respiratory machinery, by targeting ATP synthase and causes acid stress. PANI was more active against E. coli in aerobic, compared to anaerobic, conditions, while this was apparent for P3ABA only in rich media. Greater activity in aerobic conditions suggests involvement of reactive oxygen species. P3ABA treatment causes an increase in intracellular free iron, which is linked to perturbation of metabolic enzymes and could promote reactive oxygen species production. Addition of exogenous catalase protected E. coli from PANI antimicrobial action; however, this was not apparent for P3ABA treated cells. The results presented suggest that PANI induces production of hydrogen peroxide, which can promote formation of hydroxyl radicals causing biomolecule damage and potentially cell death. P3ABA is thought to act as an uncoupler by targeting ATP synthase resulting in a futile cycle, which precipitates dysregulation of iron homeostasis, oxidative stress, acid stress, and potentially the fatal loss of proton motive force.

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