Phototaxis refers to an organism's movement toward a light source, while photophobotaxis involves movement into illuminated regions. Although phototaxis in cyanobacteria has been widely studied, photophobotaxis has been investigated in only a few species. In this study, we examined photophobotaxis of 7 single-celled and 11 filamentous cyanobacterial species, among them 3 Nostocales (filaments with heterocysts) and 5 Oscillatoriales and 1 Desertifiliales member. All single-celled species and all Oscillatoriales/Desertifiliales exhibited photophobotaxis, whereas no evidence of photophobotaxis was found for the Nostocales and two other species. A pilus-free mutant of Synechocystis sp. PCC 6803 did not display this behavior. The photosystem II inhibitor DCMU disrupted photophobotaxis in single-celled and filamentous cyanobacteria at a concentration of 10 μM; only the filamentous Phormidium lacuna (P. lacuna) required 100 μM DCMU for inhibition. This points to PS II as a sensor of photophobotaxis. The widespread occurrence of photophobotaxis aligns with the universality of photosystems. Previous studies on spectral sensitivity and the cyanobacteriochrome PixJ in P. lacuna identified PixJ as a negative regulator of photophobotaxis. In pixJ mutants, light sensitivity was increased compared with the wild-type. Dual-wavelength experiments confirmed that yellow light induces PixJ to downregulate photophobotaxis. Our experiments also show that P. lacuna moves faster in darkness than in light and that a temporal change of light intensity from light to dark can induce a change of movement direction. Both findings support the light trap model which is based on random movement and a change of movement direction at the light-dark border.

Previous murine studies have implicated acid sphingomyelinase (aSMase)-generated subcellular microvesicle particles (MVP) in photosensitivity. Objective: The current double-blinded placebo-controlled studies examined if a single localized ultraviolet B radiation (UVB) treatment generated more MVP in human subjects with self-identified photosensitivity versus normal controls. A topical 4% formulation of the aSMase inhibitor imipramine applied immediately after UVB blocked the MVP release and erythema responses. Erythema responses at 24 and 72 h in response to multiple UVB fluences and minimal erythema doses (MED) at 24 h and effects of imipramine were also tested. Small cohorts of 10 adult self-identified photosensitive subjects and 12 controls were enrolled in these pilot studies which revealed increased levels of skin MVP in UVB-treated photosensitive subjects over controls which correlated with MED values. Moreover, post-UVB application of imipramine blunted UVB-induced MVP responses as well as tended to diminish erythema levels at 4 h but not at 24 or 72 h in photosensitive patients. Though limited by low numbers of self-identified subjects, these pilot studies provide some support for the hypothesis that MVP could be involved in multiple types of human photosensitivity responses and suggest aSMase inhibition as a potential therapeutic strategy.

Cyclobutane pyrimidine dimers (CPDs) are the major photoproducts of DNA produced by direct absorption of UV light but can also be produced indirectly by photosensitization and chemiexcitation. Deamination of C-containing CPDs is responsible for the majority of C to T mutations caused by UV, which have been linked to skin cancer. Another frequent mutagenic photoproduct of DNA is the (6-4) photoproduct (64PP). Because of their roles in causing mutations, NextGen sequencing methods have been developed to determine the location and frequency of these photoproducts in chromosomal DNA. All these methods, however, rely on enzyme-coupled methods that can only detect one photoproduct at a time. There is evidence, however, that the 64PP and certain oxidized bases can photosensitize CPD formation to produce compound lesions. We propose that such rare but possibly important compound lesions can be detected by single-molecule sequencing using nanopores. Herein, we show that site-specific TT CPD and 64PP photoproducts cause a large current drop when sequenced by an Oxford Nanotechnologies R10-based sequencing device. Furthermore, we demonstrate that both single and multiple photoproducts can be detected in UVB-irradiated DNA substrates containing T- and (PuTT)Pu-tracts. We also provide a simple 9mer kmer model that can simulate the nanopore current data.

Solar ultraviolet (UV) radiation and atmospheric ozone are critical determinants of ecosystem dynamics and human health. This study aimed to assess the terrestrial profile of solar UV radiation and its genotoxic risk in the South American subtropical region (29° S 53° W). From 2005 to 2021, ground-based physical sensors showed an increase of approximately 50% in UVB (280-315 nm; +0.28 kJ/m per year), but no significant trend in UVA (315-400 nm). Despite the existence of four defined climatic seasons, simultaneous measurements using UVA, UVB, and DNA-based sensors revealed two distinct UV seasons: a high-UV season encompassing spring and summer, and a low-UV season encompassing winter and autumn. Notably, spring sunlight was found to be as genotoxic as summer sunlight, and even winter and autumn sunlight may pose a genotoxic risk on cloudless days, as indicated by measurements of cyclobutane pyrimidine dimers and oxidized bases. Given the rising UVB levels without an increase in UVA, we investigated satellite-derived ozone data from NASA's ozone monitoring instrument (OMI) and total ozone mapping spectrometer (TOMS) sensors across South America and Antarctica. Overall, analysis from 1979 to 2021 showed negative ozone trends at 2° S 54° W (Santarém), 23° S 46° W (São Paulo), and 29° S 53° W (Santa Maria) even after the onset of the Montreal Protocol, while positive trends were observed at 53° S 70° W (Punta Arenas) and 62° S 58° W (Brazilian Antarctic Station) following the protocol. Strikingly, the UVB and ozone trends observed across seasons suggest that ozone is being transported poleward persistently rather than seasonally, possibly driven by a climate change-induced acceleration of the Brewer-Dobson Circulation. This persistent pattern demonstrates that ozone depletion at low and mid-latitudes is not limited to springtime but persists throughout the year. Our findings indicate that low- and mid-latitudes in South America are experiencing climate changes, stratospheric ozone depletion, and increased UVB incidence, resulting in heightened genotoxic risks, highlighting the urgent need for monitoring and mitigation strategies.

In this paper, we investigated the response of the larvae of the sea urchin Centrostephanus rodgersii to unpolarized halogen light, darkness as well as polarized (linear, circular and elliptical) halogen light presented in side view to observation chambers. The larvae exhibited positive phototaxis when exposed to unpolarized, horizontally polarized, elliptically polarized, and circularly polarized light. However, they did not respond to vertically polarized light. In fact, larval swimming behavior after exposure to vertically polarized light was the same as keeping them in the dark. These findings indicate that not only may the larvae of C. rodgersii have photoreceptors capable of detecting light in the visible spectrum but they may also possess the capacity to differentiate between horizontally and vertically polarized light, which might help them navigate. These findings suggest the possibility of aligned photoreceptors in these larvae. In addition, we found that the larvae respond to circularly polarized light. This result is notable as there are few documented cases of circular polarization sensitivity in animals. As they did not appear to have a preference between the left- and right-handed polarizations, one would need to study their photoreceptor cells to determine the mechanism by which they can detect circular polarization. This could pave the way to the development of new polarization detectors based on biological mechanisms.

P-glycoprotein (P-gp, ABCB1)-mediated multidrug resistance (MDR) remains a significant barrier to successful chemotherapy outcomes for cancer patients. While photoactivation of verteporfin (VP), a photosensitizer, has demonstrated success for overcoming MDR through direct protein aggregation upon photoactivation and through adenosine triphosphate (ATP) depletion, the impact of VP's formulation on P-gp function and cellular energetics has not been fully characterized in this context. In this study, we screened four well-established VP formulations-liposomal VP (L-VP), lysophosphatidylcholine-conjugated VP (lysoPC VP), liposomal formulation of lysoPC VP (L-lysoPC VP), and a self-assembled VP nanoaggregate (NanoVP), with a free form of VP as a control-for their ability to inhibit P-gp. Using a combination of in vitro intracellular VP accumulation assays, P-gp substrate retention experiments, and Seahorse-based metabolic profiling, we identified NanoVP as the lead formulation for P-gp modulation in cancer cells. NanoVP effectively depleted ATP in drug-resistant cancer cells, while being recognized as a P-gp substrate. Photodynamic priming with NanoVP at sub-cytotoxic light doses enhanced P-gp substrate retention within the cells without damaging P-gp protein, indicating ATP depletion as the primary mode of functional inhibition. These findings highlighted NanoVP's clinical potential to enhance chemotherapeutic efficacy via photoactivation-based modulation of P-gp's function in multidrug-resistant cancers.

The direct introduction of ionic character in azoheteroarenes led to the generation of azopyridinium, azoimidazolium, and azopyrazolium photoswitches, which have previously garnered intriguing application prospects due to their varied Z-E thermal relaxation properties. We leveraged this foundation to design and synthesize three azoisoxazolium-based ionic photoswitches, aiming to expand their application scope and tailor their properties. The investigations on their photoswitching characteristics in different solvents, including water, revealed a solvent-dependent aggregation that competes with isomerization, although their thermal relaxations slow down the aggregation. Also, spectroscopic and dynamic light scattering (DLS) studies showed that the azoisoxazolium ionic photoswitches can exhibit negative photochromism, light-induced disaggregation at low concentrations in one of the derivatives, and significantly fluorescence emission in water. In addition, microscopic studies using scanning electron microscope (SEM), transmission electron microscope (TEM), polarized optical microscope (POM), and confocal microscope revealed the size and structural morphology and mesophase changes of the aggregates. Overall, our comprehensive investigation has positioned azoisoxazolium salts as a new class of ionic photoswitches characterized by several intriguing properties and a pronounced tendency to aggregate.

The use of 5-aminolevulinic acid (ALA)-induced protoporphyrin IX (PpIX) for tumor fluorescence imaging and photodynamic therapy (PDT) may be limited by intrinsic PpIX-reducing mechanisms including PpIX bioconversion and efflux transport. The effectiveness of targeting these PpIX-reducing mechanisms was evaluated in glioblastoma cell lines. Although either inhibiting PpIX bioconversion by an iron chelator deferoxamine (DFO) or suppressing PpIX efflux by an ABCG2 transporter inhibitor lapatinib (Lap) significantly increased ALA-PpIX and PDT effect in the A172 cell line with weak ABCG2 activity, DFO in combination with Lap led to significantly greater enhancement effects. However, DFO did not significantly enhance ALA in H4, U-87, and U-118 cell lines with robust ABCG2 activities, whereas Lap showed effective enhancement effects. The combination of DFO and Lap enhanced ALA-induced PpIX and PDT in these three cell lines. Not just increasing ALA-PpIX levels, Lap enhanced PpIX localization in the mitochondria and promoted mitochondria-mediated apoptosis after PDT in the H4 cell line with strong ABCG2 activities. Our results demonstrate that blocking ABCG2-mediated PpIX efflux is critical for the enhancement of ALA and, in tumor cells with ABCG2 activities, inhibiting PpIX bioconversion by DFO needs to be combined with PpIX efflux suppression for effective enhancement of ALA.

The in vivo transcriptional response of mouse skin to ultraviolet radiation (UV-R) exposure reveals key genomic alterations associated with UV-R-induced damage but it does not provide precise dose thresholds for these effects. These initial findings provided the impetus to advance dose-response characterization by integrating benchmark dose (BMD) modeling with transcriptomic data, aiming to identify biologically relevant points of departure for gene and pathway activation. To accomplish this, mice were exposed to five erythemally weighted UV-R doses (0-40 mJ/cm) emitted from a UV-emitting tanning device, across six post-exposure timepoints (0-96 h). Four analytical methods were used to estimate BMDs, with the lowest consistent response dose (LCRD) approach yielding the most sensitive estimates (1.21-3.44 mJ/cm). Transcriptomic responses revealed activation of shared pathways related to DNA damage and cancer, oxidative stress and metabolism, inflammation and immunity, and hormonal disruption. Notably, the majority of LCRD BMD estimates (1.21-3.44 mJ/cm) were lower than the International Electrotechnical Commission standard actinic exposure limit (3 mJ/cm (erythemally weighted)) for broadband UV-R (200-400 nm) for unprotected skin and the eye for an 8 h period. These findings suggest that transcriptomic BMD modeling can detect early biological responses to UV-R at doses lower than current exposure limits.

Interrelated secondary events occur within days and weeks following a spinal cord injury (SCI), constituting a major hurdle in providing both an effective and affordable treatment for spinal cord repair in that it requires a multifaceted approach. Photobiomodulation (PBM) therapy in the red/near-infrared spectrum holds promising reparative potential; however, there are no consistent or defined parameters for PBM delivery, which may explain the limited number of ongoing clinical trials and less-than-optimal reported outcomes. This review outlines the associated complexities of the secondary cascade after SCI, with insights on how and when red/near-infrared irradiation may alleviate these issues. The primary focus is to discuss limitations within the field that may be inhibiting our ability to characterize optimal guidelines and specifications. Ultimately, this review provides a call for action, as there is an urgent need for consensus and standardization of therapeutic preclinical methodologies if we hope to develop treatment protocols that provide a first-line minimally invasive therapy to (i) minimize injury sequelae and (ii) facilitate spinal cord repair. We recommend establishing a universal method to measure the therapeutic dose of light delivered to an injury site and employing standardized methodologies across all studies to assess the benefits of PBM therapy.

Photodynamic therapy (PDT) is a photochemistry-based treatment modality that synergizes with traditional agents and can overcome chemoresistance. Eighty percent of ovarian cancer patients develop chemoresistant disease, highlighting the need to identify sources of treatment failure and develop rational combinations. Studies have shown that perfluoroalkyl substances (PFAS) induce chemoresistance in a duration-dependent manner in OVCAR-3 cells. PFAS are widespread drinking water contaminants present in the blood of nearly all Americans. The present study evaluated the ability of photodynamic priming (PDP), a sub-cytotoxic variant of PDT, in combination with chemotherapy to overcome chemoresistance in two OVCAR-3 cell cohorts: PFAS chronically-exposed and outgrown (allowed to "recover" from chronic PFAS exposure). Effectiveness of benzoporphyrin derivative- (BPD-) or aminolevulinic acid-induced protoporphyrin IX-PDP (ALA-PpIX-PDP) was assessed in combination with carboplatin and doxorubicin. In PFAS chronically-exposed cells, BPD-PDP + carboplatin reduced survival fraction compared to carboplatin alone. Mitochondrial membrane potential also decreased significantly in both cohorts following ALA-PpIX-PDP-based combinations. PDP + doxorubicin also successfully overcame chemoresistance arising from chronic PFAS exposure but was less effective than PDP + carboplatin. Together, these findings demonstrate the efficacy of PDP-based combinations in overcoming chronic PFAS exposure-induced chemoresistance and should be explored in pre-clinical models of ovarian cancer.

6-Thioguanine (6-TGua) is one of the thiopurines used as a cytostatic drug. When internalized by cells, 6-TGua is metabolized through the purine salvage pathway and readily incorporated into DNA. Patients treated with these thiopurines are more prone to develop squamous cell carcinoma of the skin. The absorbance spectrum of 6-TGua, in contrast to guanine (Gua) or any other canonical base, has a maximum absorbance at 342 nm. Therefore, 6-TGua undergoes photoexcitation upon exposure to UVA radiation, with maximum absorption at 340 nm. In this study, the used approach unequivocally demonstrates the generation and quenching of O by 6-TGua via the direct spectroscopic detection of O monomol light emission at 1270 nm. Chemiluminescence-based methods were employed for the determination of the O generation quantum yield (ΦO) and the total O quenching rate constant (k). For the O quantum yield, we found values of 0.22 ± 0.03 for 6-TGua and 0.12 ± 0.03 for 2'-deoxy-6-thioguanosine (6-TdGuo). These compounds presented k values of 1.5 × 10 L mol s and 1.1 × 10 L mol s, respectively. Through the comparison of these values with the ones obtained for 2'-deoxyguanosine (dGuo) and its oxidation product 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo), we aim to provide new insights into the 6-TGua-containing DNA (DNA-6-TGua) reactivity towards O in a biological context.

Light pollution from widespread artificial illumination affects photosensitive organisms, including humans. Prolonged exposure to artificial light at night (ALAN), particularly blue light, is associated with melatonin suppression and circadian disruption, both implicated in carcinogenesis. This systematic review investigated the relationship between extended ALAN exposure and malignant neoplasms, identifying associated cancer types and biological mechanisms. A search was conducted in PubMed/Medline and Scopus using PRISMA guidelines. Original studies evaluating associations between ALAN, light pollution, or blue light and cancer in humans were included. Eighteen studies demonstrated a positive link between ALAN and breast cancer, with mechanisms involving interference in the cell cycle, DNA repair, oxidative stress, and activation of oncogenic pathways. Night-shift work correlated with increased breast cancer risk, reduced melatonin levels, and hormonal dysregulation. Exogenous melatonin showed oncostatic potential, reversing epigenetic changes induced by ALAN and reducing tumor burden. Melatonin suppression may promote tumor progression through circadian gene disruption and hormonal imbalance. While findings support a consistent link between ALAN exposure and oncogenesis-especially breast and prostate cancers-methodological variability and confounding factors, such as genetic predisposition and lifestyle, limit generalization. Further studies are needed to clarify mechanisms and explore preventive strategies, including light pollution control and melatonin-based interventions.

The search for natural alternatives to synthetic sunscreens has driven interest in marine compounds with antioxidant and UV-protective properties. The present study expands our understanding of the potential of gadusol by evaluating the photochemoprotective and antioxidant effects of extracts from an underexploited marine by-product: the roes of yellowtail amberjack fish (Seriola lalandi). UVB-mediated responses were studied in vitro and in vivo using HaCaT keratinocytes and Caenorhabditis elegans worms, respectively. Additionally, several antioxidant assays were conducted to evaluate the antioxidant capacity and thermal stability over time. We also tested the docking binding of gadusol to the Nrf2-binding domain of Keap1 to better understand its potential chemoprotective role. Overall, the gadusol-containing extracts exhibited remarkable stability over time, offering effective protection against UVB radiation in both in vitro and in vivo models. This information contributes to a better characterization of the functional role of gadusol in crude extracts and its relevance for the design of innovative applications in various pharmaceutical and cosmetic industries.

The SKH-1 mouse model is commonly used to assess the effects of ultraviolet light exposure on skin using visual and biological endpoints. Although skin bi-fold thickness is a well-established quantitative measure of edema, evidence characterizing its use to evaluate skin responses in the UVC range remains limited. This study evaluated skin bi-fold thickness measurements made using a digital caliper. Hairless SKH-1 mice were exposed using the narrow bandwidth output from a monochromator with wavelengths from 200 to 270 nm. Post-exposure thickness measurements were normalized against pre-exposure thickness measurements to determine the fold change. These findings were compared with qualitative visual assessments of changes to the skin. The results indicate that quantitative measures of increases in skin thickness are correlated with subjective visual scoring measures. The observed magnitude of the bi-fold change following UVC exposures was limited in this study because exposures were at doses close to the threshold dose for causing a visually observed change to the skin. The results support using skin bi-fold measurements for quantifying skin responses to ultraviolet light exposure.

Phototherapy approaches include photodynamic therapy (PDT), which utilizes chemically stable photocatalysts to sensitize the conversion of endogenous molecules such as oxygen (O) to form transient reactive species such as O, and photopharmacology, a complementary approach that relies on molecules that undergo self-modifying photochemistry, such as bond cleavage reactions or isomerization, for the creation of biologically active products. While Ru(II) polypyridyl systems have demonstrated utility for both approaches, related organometallic systems are relatively less explored. Here, the photochemistry and photobiological responses were compared for five Ru(II) arene compounds containing photolabile monodentate azine ligands and the π-expansive bidentate ligands dipyrido[3,2-a:2',3'-c]phenazine (dppz), 4,5,9,16-tetraaza-dibenzo[a,c]naphthacene (dppn), and α-terthienyl-appended imidazo[4,5-f][1,10]phenanthroline (IP-3T). The compounds demonstrated significant light-mediated photocytotoxicity in lung cancer and melanoma cell lines, with up to 6000-fold increases in cytotoxicity upon irradiation. The arene systems were capable of partitioning between different excited state relaxation pathways, both releasing the monodentate ligand and generating O, but with notably low yields that did not correlate with the photocytotoxicity of the systems. The organometallic compounds exhibit less mixing of the metal-associated and ligand-centered excited states than analogous polypyridyl coordination compounds, providing a structurally, photochemically, and photobiologically distinct class of compounds that can support both metal- and ligand-centered reactivity.

Exposure to the ultraviolet (UV) spectrum of sunlight poses a threat to terrestrial species. Nearly all species possess the nucleotide excision repair (NER) machinery, which can repair the helix-distorting DNA lesions induced by UV light. However, many species also have photolyase enzymes, which use near-UV and visible wavelengths of sunlight to directly reverse major classes of UV photoproducts. In eukaryotic cells, both of these repair pathways must efficiently locate and repair UV photoproducts present in chromatin. While genome-wide damage mapping methods have been used to extensively characterize how chromatin and ongoing transcription impact NER, much less is known about how photolyase enzymes navigate these obstacles to repair UV damage. Here, we highlight a recent article from our laboratory that used genome-wide sequencing methods to characterize how yeast photolyase repairs UV damage, both in NER-proficient and -deficient cells, and prevents UV-induced mutations.

Exposure to UVR is well understood to accelerate symptoms of photoaging such as wrinkling and loss of skin elasticity. Sunscreen formulations containing titanium dioxide (TiO) and zinc oxide (ZnO) UV filters can therefore be used as an effective photoprotective measure to prevent the induction of signaling pathways in skin that contribute to photoaging. The aim of this study is to provide a broad investigation on the photoprotective impact of TiO, ZnO, and inorganic-only (ZnO + TiO) sunscreen formulations in human dermal fibroblasts at a gene and protein level. The study focused on genes involved in UV-only and complete solar light-induced MMP production, prostanoid biosynthesis for inflammation, and cell cycle arrest, as previously identified through RNA-seq analysis. Three inorganic formulations were prepared at commercially applicable active levels and varying particle sizes: (1) F(TiO ), (2) F(ZnO), and (3) an inorganic-only (ZnO + TiO) formulation F(ZnO/TiO ). The three formulations significantly alleviated the irradiation-induced expression of MMP1, MMP3, PTGS1, PTGES, MDM2, CDKN1A, and CCNE2, with the latter most alleviated by up to 77% (p ≤ 0.05). The inorganic-only (ZnO + TiO) formulation, containing both inorganic UV filters, exhibited the greatest mean or maximum alleviation in 75% of the genes investigated. Protein analyses of MMP1, PTGES, and p21, by immunocytochemistry and Western blot, also showed positive translation of alleviation at a protein level. The study provides further academic and commercial insights on the photoprotective impact of inorganic particles in sunscreens, based on relevant signaling pathways, genes, and proteins that are induced by UV to accelerate photoaging.

This study investigated the synergistic effects of resveratrol and antimicrobial photodynamic therapy (aPDT) on peri-implant bone repair in a type 2 diabetes model. Forty-eight rats were allocated into four groups: normoglycemic, normoglycemic + resveratrol, type 2 diabetes (T2D), and T2D + resveratrol. Diabetes was induced using a cafeteria diet and streptozotocin (35 mg/kg). Resveratrol (100 mg/kg) was administered systemically beginning 7 days later. After 14 days, maxillary molars were extracted, and surgical drilling was performed. Half of the animals in each group received aPDT (methylene blue and 660 nm diode laser) before immediate implant placement. Animals were euthanized 28 days post-surgery for biomechanical, RT-PCR, and confocal microscopy analyses. Resveratrol improved glycemic control and body weight. In T2D animals, aPDT significantly enhanced implant removal torque. Gene expression analyses revealed downregulation of bone resorption markers and upregulation of bone mineralization genes in T2D and T2D + resveratrol groups treated with aPDT. Confocal microscopy demonstrated increased mineral apposition rates in animals treated with resveratrol and/or aPDT. These findings suggest that the combination of systemic resveratrol and local aPDT enhances peri-implant bone healing under diabetic conditions, highlighting a potential therapeutic approach to improve implant osseointegration in compromised metabolic states.

We aimed to compare the anticandidal effect among different preirradiation times, measure singlet oxygen levels, and investigate the correlation between candidal reduction and singlet oxygen formation in erythrosine + KI photodynamic therapy. Candida albicans (ATCC10231) biofilms were treated with 100/200 μM erythrosine + 100 mM KI for 1, 3, or 5 min before light-emitting diode (520 ± 10 nm, 250 mW/cm, 20 J/cm) irradiation. Phosphate-buffered saline, and nystatin were negative and positive controls, respectively. Candidal cells were quantified using a drop plate assay. Singlet oxygen was measured using a 9,10-dimethylanthacene probe at 375/436 nm emission/excitation wavelengths. Median candidal counts and singlet oxygen formation were compared using Kruskal-Wallis with Dunn test. A p-value <0.05 was considered significant. Spearman's correlation was used to correlate candidal reduction and singlet oxygen formation. All preirradiation times for 200 μM erythrosine + 100 mM KI decreased candidal cells by 7.59 (IQR = 0.33) logCFU/mL. At a 1-min preirradiation, this group significantly generated higher singlet oxygen than the positive control (p < 0.001). Singlet oxygen levels correlated mildly with candidal reduction in the lower erythrosine group but not the higher group, likely due to singlet oxygen saturation. A 1-min preirradiation with 200 μM erythrosine + 100 mM KI generates singlet oxygen to inhibit C. albicans biofilms and shows potential for clinical oral candidiasis treatment.