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Updated: Feb 19, 2026
Rose Bengal-Mediated Photodynamic Therapy to Inhibit Candida albicans
Published on: March 24, 2022
Photodynamic damage predominates on different targets depending on cell growth phase of Candida albicans
Alessandra Baptista1, Caetano P Sabino2, Silvia C Núñez3
1Center for Lasers and Applications, Nuclear and Energy Research Institute, IPEN - CNEN/SP, São Paulo, SP, Brazil; Biomedical Engineering Post-Graduation Program, Universidade Brasil, São Paulo, SP, Brazil.
Abstract:
Photodynamic inactivation (PDI) has been reported to be effective to eradicate a wide variety of pathogens, including antimicrobial-resistant microorganisms. The aim of this study was to identify the potential molecular targets of PDI depending on growth phase of Candida albicans. Fungal cells in lag (6h) and stationary (48h) phases were submitted to PDI mediated by methylene blue (MB) combined with a (662±21) nm-LED, at 360mW of optical power. Pre-irradiation time was 10min and exposure times were 12min, 15min and 18min delivering radiant exposures of 129.6J/cm2, 162J/cm2 and 194.4J/cm2, respectively, on a 24-well plate of about 2cm2 at an irradiance of 180mW/cm2. Scanning electron microscopy (SEM), transmission electron microscopy (TEM), atomic force spectroscopy (AFS) and Fourier transform infrared spectroscopy (FT-IR) were employed to evaluate the photodynamic effect in young and old fungal cells following 15min of irradiation. Morphological analysis revealed wrinkled and shrunk fungal cell membrane for both growth phases while extracellular polymeric substance (EPS) removal was only observed for old fungal cells. Damaged intracellular structures were more pronounced in young fungal cells. The surface nanostiffness of young fungal cells decreased after PDI but increased for old fungal cells. Cellular adhesion force was reduced for both growth phases. Fungal cells in lag phase predominantly showed degradation of nucleic acids and proteins, while fungal cells in stationary phase showed more pronounced degradation of polysaccharides and lipids. Taken together, our results indicate different molecular targets for fungal cells in lag and stationary growth phase following PDI.
Insights
Photodynamic inactivation (PDI) targets different molecules in Candida albicans based on its growth phase. Young cells show nucleic acid and protein damage, while older cells exhibit polysaccharide and lipid degradation.
Area of Science:
- Microbiology
- Biophysics
- Photochemistry
Background:
- Photodynamic inactivation (PDI) is a promising method for pathogen eradication, including drug-resistant strains.
- Understanding PDI's molecular targets is crucial for optimizing its efficacy.
- Candida albicans exhibits distinct physiological states during its growth cycle.
Purpose of the Study:
- To investigate the differential molecular targets of PDI in Candida albicans based on its growth phase (lag vs. stationary).
- To analyze the impact of PDI on fungal cell morphology, surface properties, and molecular composition.
Main Methods:
- Fungal cells in lag (6h) and stationary (48h) phases were treated with methylene blue-mediated PDI using a 662nm LED.
- Morphological and ultrastructural changes were assessed using Scanning Electron Microscopy (SEM) and Transmission Electron Microscopy (TEM).
- Surface properties were analyzed by Atomic Force Spectroscopy (AFS), and molecular composition changes were evaluated using Fourier Transform Infrared Spectroscopy (FT-IR).
Main Results:
- PDI induced cell membrane shrinkage and wrinkling in both growth phases.
- Extracellular polymeric substance (EPS) removal was observed in stationary phase cells.
- Young cells showed more pronounced intracellular damage, while older cells had greater polysaccharide and lipid degradation; nucleic acid and protein degradation was dominant in young cells.
Conclusions:
- PDI affects Candida albicans differently depending on its growth phase, targeting distinct molecular components.
- Lag phase cells are primarily affected in nucleic acids and proteins.
- Stationary phase cells show greater susceptibility in polysaccharides and lipids, indicating phase-specific PDI mechanisms.
