<p>Antimicrobial photodynamic therapy (aPDT) is a promising non-pharmacological approach for managing biofilm-associated fungal infections. In this study, we investigated the antifungal efficacy of a double-agent aPDT system combining bisdemethoxycurcumin (BDMC) as a photosensitizer and potassium iodide (KI) as a photodynamic enhancer against <i>Candida albicans</i> biofilms, with particular emphasis on the underlying reactive oxygen species (ROS)–mediated mechanisms. Mature <i>C. albicans</i> biofilms were treated with BDMC alone (20, 40, and 80 µM), KI alone (100 mM), or their combination, followed by dental blue LED irradiation (430 ± 10&#xa0;nm LED, 200 mW/cm², 0–100&#xa0;J/cm²). Biofilm viability was assessed, and ROS generation quantified using fluorescence-based assays and electron paramagnetic resonance spectroscopy. The contribution of specific ROS to antifungal activity was evaluated through Spearman correlation analyses. The combined BDMC–KI aPDT system produced significantly greater biofilm inactivation than single-agent treatments. Enhanced antifungal activity was strongly associated with increased singlet oxygen (<sup>1</sup>O₂) generation, while hydroxyl radicals contributed to a lesser extent. These findings support a double-mode photodynamic mechanism in which BDMC-derived ROS are chemically amplified by iodide, yielding longer-lived reactive iodine species and oxidative intermediates that enhance biofilm disruption. Overall, this study demonstrates that KI functions as an effective photodynamic potentiator rather than a photosensitizer, significantly augmenting BDMC-mediated aPDT against <i>C. albicans</i> biofilms. The mechanistic insights gained here support the further development of double-agent photodynamic strategies for the management of drug-resistant fungal biofilm infections. Clinical relevance: Bisdemethoxycurcumin+potassium iodide act as a photosensitizer in PDT to inhibit <i>Candida albicans</i> biofilms.</p>

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Photodynamic therapy-induced anticandidal effects via reactive oxygen species generation from bisdemethoxycurcumin and potassium iodide

  • Monique Ravago,
  • Waranuch Pitiphat,
  • Noppawan Phumala Morales,
  • Teerasak Damrongrungruang

摘要

Antimicrobial photodynamic therapy (aPDT) is a promising non-pharmacological approach for managing biofilm-associated fungal infections. In this study, we investigated the antifungal efficacy of a double-agent aPDT system combining bisdemethoxycurcumin (BDMC) as a photosensitizer and potassium iodide (KI) as a photodynamic enhancer against Candida albicans biofilms, with particular emphasis on the underlying reactive oxygen species (ROS)–mediated mechanisms. Mature C. albicans biofilms were treated with BDMC alone (20, 40, and 80 µM), KI alone (100 mM), or their combination, followed by dental blue LED irradiation (430 ± 10 nm LED, 200 mW/cm², 0–100 J/cm²). Biofilm viability was assessed, and ROS generation quantified using fluorescence-based assays and electron paramagnetic resonance spectroscopy. The contribution of specific ROS to antifungal activity was evaluated through Spearman correlation analyses. The combined BDMC–KI aPDT system produced significantly greater biofilm inactivation than single-agent treatments. Enhanced antifungal activity was strongly associated with increased singlet oxygen (1O₂) generation, while hydroxyl radicals contributed to a lesser extent. These findings support a double-mode photodynamic mechanism in which BDMC-derived ROS are chemically amplified by iodide, yielding longer-lived reactive iodine species and oxidative intermediates that enhance biofilm disruption. Overall, this study demonstrates that KI functions as an effective photodynamic potentiator rather than a photosensitizer, significantly augmenting BDMC-mediated aPDT against C. albicans biofilms. The mechanistic insights gained here support the further development of double-agent photodynamic strategies for the management of drug-resistant fungal biofilm infections. Clinical relevance: Bisdemethoxycurcumin+potassium iodide act as a photosensitizer in PDT to inhibit Candida albicans biofilms.