Search Results (3,040)

Mycotoxigenic fungi, particularly species of Aspergillus, Fusarium, and Penicillium, contribute substantially to food contamination through the production of chemically diverse mycotoxins. Plant-derived essential oils (EOs) and extracts have therefore attracted increasing interest as potential alternatives or complements to conventional antifungal strategies. The genus Artemisia, which comprises several aromatic species with extensive biological properties, may constitute a promising source of such natural agents. This review critically examines the available data on the use of EOs and extracts from four Artemisia species (A. absinthium, A. campestris, A. herba-alba, and A. judaica) against mycotoxigenic fungi, with an emphasis on chemical composition, antifungal efficacy, mechanisms of action, and safety. Across the available studies, evidence suggests that Artemisia preparations frequently inhibit fungal growth, but their efficacy varies substantially according to species, geographical origin, plant part, harvesting conditions, extraction method, chemical composition, fungal species, and experimental assay. Importantly, evidence for direct inhibition of mycotoxin biosynthesis remains considerably more limited than evidence for fungal growth inhibition. Proposed antifungal mechanisms include disruption of the fungal cell wall and plasma membrane, altered mitochondrial function, and interference with cellular transport processes, although mechanistic evidence specifically for Artemisia preparations remains limited. Available toxicological data further indicate that efficacy and safety must be evaluated together, particularly for chemotypes containing potentially hazardous constituents such as thujone. Overall, Artemisia EOs and extracts may represent promising but not yet sufficiently validated candidates for food-associated mycotoxin control. Future studies could prioritize chemical standardization, mechanistic characterization, mycotoxin-specific endpoints, food-matrix validation, and integrated efficacy–safety assessment. Full article

The general objective of this study was to evaluate Eucalyptus globulus bark extract as a candidate component of wood preservatives with a reduced load of synthetic biocides. Extraction conditions were screened using a 2³ full factorial design with a center point, identifying 75 °C, 60% ethanol and 1 h as the highest-yielding conditions (5.94%) within the tested ranges. In four-week laboratory wood-block assays, the extract alone did not exceed 40% inhibition of wood-staining fungi, whereas hinokitiol reached complete inhibition at 0.4%. Combining the extract (5%) with hinokitiol (0.4%) achieved 95–100% inhibition, similar to the synthetic reference; because hinokitiol alone reached complete inhibition at this concentration, the extract’s contribution could not be isolated, and formulations in which the extract or hinokitiol was used instead of chlorothalonil and carbendazim alongside a copper-8-quinolinolate product retained 97–100% inhibition at half, and 90–93% at a quarter, of the copper-product dose (87% and 93% reductions in synthetic active ingredients), although the copper product alone was also fully effective at 2% and the contribution of the natural components could not be isolated at that dose. On a per-mass basis, the extract (48 h LC₅₀ 27,500 ppm) was approximately 710-fold less acutely toxic than the copper-8-quinolinolate product used as synthetic reference (38.71 ppm) in Daphnia magna bioassays. On the basis of its composition and the literature, the extract may contribute multi-target antifungal mechanisms, including metal chelation, enzyme inhibition and membrane disruption, that could complement the more stable action of hinokitiol; these mechanisms were not measured here. This work supports eucalyptus bark extract, a residue that is abundant in Chile and in other eucalypt-pulp-producing countries, as a candidate component of reduced-synthetic (hybrid) wood-protection formulations; the aquatic toxicity of the final formulations was not tested, and leaching, penetration and field-durability testing are required before practical or environmental benefits can be claimed. Full article

Antibiotic resistance limits infected-wound treatment and motivates the search for antibiotic-independent antibacterial materials. Here we report monodisperse PtPdCuFe high-entropy alloy (HEA) nanozymes with multi-enzyme activities, 2.14 ± 0.18 nm in diameter, prepared by oleylamine-assisted pyrolysis. We propose that synergistic metal interactions and abundant defects may endow the nanozymes with pH-gated peroxidase-like (POD-like), catalase-like (CAT-like), and superoxide dismutase-like (SOD-like) activities. At pH 5.5, the nanozymes exert POD-like activity to decompose H₂O₂ into hydroxyl radicals (•OH), triggering an ROS burst that destroys the bacterial wall, causes intracellular content leakage, and ultimately kills bacteria. At pH 7.4, they exert SOD- and CAT-like activities: ~84% of H₂O₂ was removed within 25 min and O₂ rose to ~50% within 60 s, indicating potential to alleviate wound hypoxia, yet to be validated in future animal experiments. At the lowest effective concentration tested (16 µg·mL⁻¹), bactericidal efficiencies against Escherichia coli and Staphylococcus aureus were ~56% and ~57%, respectively. At 64 µg·mL⁻¹, killing reached ~90%, with >90% of bacteria showing severe membrane disruption and protein leakage. At this concentration, ~90% of mammalian cells remained viable and the hemolysis rate stayed below 5%. Full article

Viral, fungal, and bacterial pathogens substantially reduce crop productivity, postharvest quality, and agricultural sustainability. Although synthetic pesticides remain widely used, concerns over environmental persistence, residues, and pathogen resistance have increased interest in safer alternatives. Plant secondary metabolites (PSMs) are promising candidates, but their application is often limited by poor water solubility, volatility, rapid degradation, and inconsistent field performance. This review evaluates the antiviral, antifungal, and antibacterial activities of major PSM classes, including phenolics, terpenoids, nitrogen-containing compounds, and sulfur-containing metabolites, and discusses their biotechnological applications in plant disease management. Recent studies were assessed with emphasis on metabolite sources, target pathogens, mode of action, formulation strategy, and biological efficacy. Evidence indicates that PSMs act through multiple mechanisms, including membrane disruption, inhibition of viral replication, suppression of fungal growth, interference with bacterial metabolism, and activation of plant defense responses. Nanoformulations, encapsulation systems, controlled-release carriers, and green-synthesized nanoparticles can improve stability, delivery, and bioefficacy. Despite this potential, broader agricultural implementation requires further field validation, formulation standardization, long-term stability assessment, and regulatory harmonization. Full article

Background & Aim: The emergence of multidrug-resistant pathogens, particularly methicillin-resistant Staphylococcus aureus (MRSA), necessitates the development of novel antimicrobial strategies. Green synthesis approaches and composite nanomaterials have attracted considerable attention as promising alternatives to conventional antimicrobial agents. Therefore, this study aimed to synthesize a carbon nanosphere/zeolitic imidazolate framework-8 (CNS@ZIF-8) nanocomposite using Rheum cordatum Losinsk. root-derived carbon nanospheres and to evaluate its antioxidant, antibacterial, antibiofilm, and anti-virulence properties against MRSA and methicillin-sensitive S. aureus (MSSA). Methods: Carbon nanospheres (CNS) were green-synthesized from the roots of Rheum cordatum Losinsk. and subsequently integrated with ZIF-8 to fabricate the CNS@ZIF-8 nanocomposite. The synthesized materials were characterized using UV–Vis spectroscopy, Fourier-transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDX), and X-ray diffraction (XRD). Antioxidant activity was assessed using DPPH and ABTS radical scavenging assays. Antibacterial activity was evaluated by determining the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). Antibiofilm activity, SEM-based bacterial morphology analysis, and quantitative real-time PCR of virulence- and resistance-associated genes (icaA, dltA, dltB, mepA, and norA) were also performed. Results: Characterization analyses confirmed the successful synthesis of the CNS@ZIF-8 nanocomposite. CNS@ZIF-8 exhibited antibacterial activity against both MRSA and MSSA, with MIC and MBC values of 128 and 256 µg/mL, respectively. SEM analysis revealed severe membrane disruption and morphological damage in treated bacterial cells. Gene expression analysis demonstrated significant downregulation of biofilm formation-, cell wall modification-, and efflux pump-associated genes. CNS@ZIF-8 also showed enhanced antioxidant activity compared with pristine ZIF-8, with IC₅₀ values of 45.1 ± 0.55 µg/mL (DPPH) and 9.1 ± 0.44 µg/mL (ABTS), whereas ZIF-8 exhibited IC₅₀ values of 149.2 ± 0.32 and 22.3 ± 0.31 µg/mL, respectively. However, CNS alone displayed the strongest radical scavenging activity. The antioxidant standard butylated hydroxytoluene (BHT) exhibited IC₅₀ values of 23.4 ± 0.42 µg/mL (DPPH) and 26.3 ± 0.63 µg/mL (ABTS). Conclusion: The CNS@ZIF-8 nanocomposite demonstrated promising antioxidant, antibacterial, antibiofilm, and anti-virulence activities against S. aureus, particularly MRSA. These findings suggest that CNS@ZIF-8 represents a multifunctional nanomaterial with potential for the development of alternative therapeutic strategies against multidrug-resistant bacterial infections. Full article

Acrolein (ACR) and glyoxal (GO) are highly reactive carbonyls originating from endogenous metabolism, environmental pollution, and thermal food processing. This study compares the toxic mechanisms and redox effects of a 24 h exposure to ACR (30, 60, 90 µM) and GO (2, 5, 10 mM) in PBMCs. We assessed cell viability, lipid membrane fluidity, reactive oxygen/nitrogen species (ROS/RNS), free protein functional groups, reduced glutathione (GSH), non-enzymatic antioxidant capacity (NEAC), antioxidant enzyme activity (CAT, GPx), and protein expression levels (CAT, SOD1). Both aldehydes reduced viability in a concentration-dependent manner (ACR was over 30-fold more toxic than GO based on viability curves). These toxins increased membrane fluidity near the surface, while GO also altered the hydrophobic core. Both triggered a profound accumulation of ROS/RNS. At specific dose thresholds (ACR ≥ 60 µM; GO ≥ 5 mM), both toxins depleted GSH and NEAC, decreased protein thiol/amino groups, and suppressed CAT/GPx catalytic activity and CAT/SOD1 protein expression. In conclusion, ACR emerged as a markedly more potent inducer of oxidative stress and antioxidant failure than GO in PBMCs, disrupting both non-enzymatic (GSH, NEAC) and enzymatic (CAT, GPx, SOD1) defenses. These results support prioritizing ACR in exposure risk assessments and developing biomarkers of carbonyl-induced immune dysfunction. Full article

Antimicrobial resistance (AMR) has intensified the need for antibacterial agents with alternative chemical scaffolds and mechanisms of action. Plant-derived antibacterial compounds represent a chemically diverse source of bioactive molecules, but their therapeutic potential depends not only on in vitro potency but also on mechanistic validation, pharmacokinetic exposure, pharmacodynamic relationships, and biological safety. This review critically examines evidence published from 2014 to 2026 on major classes of plant-derived antibacterial compounds, emphasizing bacterial susceptibility, mechanisms of action, pharmacokinetics, and safety. Reported antibacterial effects include alterations in the cell envelope and membrane, disruption of energy metabolism, inhibition of protein synthesis and nucleic acid-associated targets, efflux and resistance modulation, and interference with quorum sensing, biofilm formation, and virulence. However, mechanistic evidence varies substantially among studies. Pharmacokinetic data reveal marked heterogeneity in absorption, bioavailability, tissue distribution, metabolism, protein binding, and elimination, while quantitative integration of antibacterial potency with active exposure and PK/PD remains limited. Cytotoxicity and in vivo toxicity studies further indicate that selectivity and tolerability are compound-, formulation-, dose-, and model-dependent. Overall, therapeutic translation requires integration of chemically defined antibacterial activity, validated mechanisms, infection-site exposure, PK/PD, host–cell selectivity, systemic safety, and efficacy in relevant infection models. Full article

Background: Acute lung injury (ALI) features oxidative stress, macrophage dysfunction, and barrier disruption, with limited safe therapies. Plant-derived exosome-like nanovesicles (PENs) delivered noninvasively to the lung are promising but understudied. Methods: In vitro, HELNs were evaluated for their ability to scavenge ROS, restore mitochondrial membrane potential (MMP) modulate M1/M2 polarization, and suppress pro-inflammatory cytokines. RNA-seq was also used to evaluate the TNF/NOD-like pathway and mitochondrial-related gene expression. In vivo, the evaluated parameters included biodistribution, therapeutic outcomes (lung wet/dry weight ratio, BALF protein concentration, MPO and MDA levels, histology), immune cell profiles, and cytokines. Biosafety was assessed via hematology, serum biochemistry, and histology. Results: In vitro, HELNs acted dose-dependently by scavenging ROS, recovering MMP, promoting M2 and suppressing M1 polarization, and reducing TNF-α, IL-6 release. Additionally, RNA-seq confirmed downregulation of TNF/NOD-like signals and regulated mitochondrial gene expression. In vivo, nebulized HELNs preferentially accumulated in inflamed lungs, with significantly higher pulmonary retention than intravenous delivery. HELNs reduced lung wet/dry weight ratio, BALF protein, MPO and MDA levels, and histological injury scores; decreased neutrophils and CD4⁺/CD8⁺ T cells; increased alveolar macrophages and Tregs; and lowered TNF-α, IL-1β, IL-6. No significant systemic toxicity was observed. Conclusions: Nebulized HELNs offer a safe, effective, noninvasive ALI therapy by disrupting the oxidative stress-inflammation vicious cycles, reprogramming pulmonary immunity, and restoring barrier integrity, with strong translational potential. Full article

Azoles are the most widely used antifungal agents in clinical practice, with important applications in human medicine, agriculture, and veterinary science. This review systematically summarizes the structural features, classification, six-decade development history, mechanisms of action, antifungal spectra, and resistance mechanisms of azole antifungals. Based on the number of nitrogen atoms in the azole ring, these compounds are divided into imidazoles (two nitrogens) and triazoles (three nitrogens), which differ markedly in target enzyme selectivity, pharmacokinetic properties, and safety. Tetrazoles, as a new generation of drugs, exhibit lower basicity and reduced inhibition of human CYP450 enzymes, and have demonstrated improved selectivity and better safety profiles in preclinical studies; however, their clinical advantages still require further validation. Since the introduction of the first clinically used imidazole clotrimazole in 1969, azoles have evolved from topical formulations to orally or intravenously administrable triazoles across four generations, each iteration broadening the antifungal spectrum and improving safety and pharmacokinetics. Azoles act by inhibiting fungal sterol 14α-demethylase (CYP51), thereby blocking ergosterol biosynthesis and disrupting fungal cell membrane integrity. Their spectrum covers most clinically relevant fungi, but significant inter-generational differences exist. However, the widespread emergence of resistance mechanisms—including efflux pump overexpression, target enzyme alterations, biofilm formation, and other mechanisms—combined with cross-resistance risks between agricultural azole fungicides and clinical azoles, severely compromises their clinical utility. This review also discusses future directions, including novel tetrazoles, dual/multi-target inhibitors, AI-assisted drug design, and cross-sectoral resistance control within the One Health framework. Full article

Background: The hominoid loss of urate oxidase (uricase) represents a classic evolutionary trade-off, shifting uric acid (UA) from a metabolic waste product to a potent physiological modulator. In modern metabolic environments, however, this adaptation drives hyperuricemia and gout, transforming UA into a primary pathological substrate. Objective: This review aims to dissect the molecular architecture and biophysical networks of the renal and intestinal urate transportosome, delineate the dual intracellular/extracellular “urate paradox,” and synthesize genotype-based pharmacogenetic strategies to achieve personalized clinical management. Mechanistic Insights: During the Miocene epoch, inactivating pseudogenization of the UOX gene fixed a novel metabolic phenotype characterized by fructose-driven lipid deposition and enhanced antioxidant protection. Structurally, systemic urate homeostasis is strictly governed by a macromolecular interactome assembled by the four-domain scaffold protein PDZK1 on the epithelial apical membrane. Pathogenic gain-of-function variants in reabsorption facilitators (SLC22A12/URAT1, SLC2A9/GLUT9) or loss-of-function mutations in the efflux pump (ABCG2/BCRP) disrupt this delicate vector kinetics. Within the extracellular space, soluble urate acts as a critical hydrophilic radical scavenger. Paradoxically, upon URAT1/GLUT9-mediated internalization or intracellular supersaturation, intracellular urate triggers a pro-oxidant cascade mediated by NADPH oxidase (NOX4) activation and mitochondrial electron transport chain decoupling. This chronic cellular stress activates downstream p38 MAPK and NF-κB signaling pathways, driving localized endothelial injury and macrovascular inflammation, while crystalline monosodium urate (MSU) orchestrates NLRP3 inflammasome assembly in macrophages. Pharmacogenetic Implications: Striking ethno-geographic heterogeneity dictates immediate clinical stratification. The HLA-B*58:01 allele, an absolute molecular contraindication for allopurinol due to life-threatening severe cutaneous adverse reactions (SCARs), exhibits a critical genetic gradient in northern and eastern Eurasian populations, surging from under 1% in ethnic Caucasians to over 10% in indigenous populations of East/North Asian ancestry. Furthermore, structural defects in ABCG2 (such as the p.Q141K variant) alter the ATP-binding cassette domain, inducing standard allopurinol resistance and elevated statin exposure, which mandates a therapeutic pivot toward selective xanthine oxidase inhibitors (febuxostat) or precision uricosurics (benzbromarone, dotinurad) matched to the patient’s interactive network profile. Conclusions: Transitioning from generalized epidemiological guidelines to a comprehensive “transportosome genetic passport” is a fundamental prerequisite for predicting single-nucleotide polymorphism (SNP)-driven therapeutic responses and mitigating visceral complications. Full article

Titanium dioxide nanoparticles (TiO₂-NPs) are widely used nanomaterials, but their potential systemic toxicity following chronic exposure remains a significant concern. This study investigated whether mitochondrial dysfunction represents a key mechanistic link between oxidative stress, apoptosis, and organ injury induced by TiO₂-NPs. Male Wistar rats were orally exposed for 90 days to TiO₂-NPs (15–31 nm) at doses of 215 or 500 mg/kg body weight. Mitochondrial analyses revealed significantly impaired respiratory activity, increased membrane permeability, and mitochondrial swelling, indicating disruption of mitochondrial function and electron transport chain integrity. These alterations were accompanied by increased reactive oxygen species production; depletion of antioxidant defenses, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced glutathione (GSH), and glutathione S-transferase (GST); and enhanced lipid peroxidation. Increased caspase-3 activation further suggested the involvement of mitochondria-dependent apoptotic pathways. Histopathological examination confirmed significant hepatorenal damage, including hepatocellular degeneration, inflammatory infiltration, vascular alterations, and glomerular and tubular lesions. Overall, integrating mitochondrial, oxidative, apoptotic, and histopathological findings supports a mechanistic model in which mitochondrial bioenergetic dysfunction acts as a central event linking oxidative imbalance to apoptosis and tissue injury. These findings contribute to a better understanding of TiO₂-NP-associated health risks and provide mechanistic insights relevant to the safer development and application of nanomaterials. Full article

Crystal (Cry) toxins produced by Bacillus thuringiensis are highly specific insecticidal proteins that are widely used as biological insecticides and function through proteolytic activation in insect midguts, which generates a three-domain toxic core responsible for membrane disruption as well as cleaved N- and C-terminal domains. While the structure and function of this core have been extensively characterized, the fate of the cleaved C-terminal region remains poorly understood. Amyloids are protein fibrils with a characteristic cross-β structure that participate in a wide range of functions in bacteria. Here, using bioinformatic approaches, we demonstrated that the C-terminal domains of Cry are rich in potentially amyloidogenic regions. We investigated the aggregation behavior of C-terminal domains from Cry1Ea11 and Cry1Ab12 proteins using a combination of biochemical and structural approaches. We found that the C-terminal domains of Cry1Ea11 and Cry1Ab12 undergo self-assembly in vitro, forming aggregates with fibrillar morphology. These assemblies bind amyloid-associated dyes, exhibit partial resistance to ionic detergents and proteolytic digestion, and display X-ray diffraction patterns confirming their amyloid properties. Functional assessment in insect cells showed that although these amyloids do not induce detectable cytotoxicity, amyloids of the C-terminal domains of Cry1Ea11 alter the readouts of the MTT assay in a manner consistent with previously described amyloid-associated effects on cellular formazan handling. Together, our findings demonstrate that the C-terminal domains of Cry toxins, which are released in the insect midgut as a result of proteolytic cleavage, are able to form bona fide amyloids that affect the metabolism of insect cells. Full article

Plastid membrane integrity is essential for plant growth, development, and metabolism, yet the functions of vesicle-inducing protein in plastids 1 (VIPP1) throughout the crop life cycle remain unclear. Here, we characterized OsVIPP1 in rice using CRISPR/Cas9 knockout, overexpression, and RNA-interference lines, together with ultrastructural, transcriptomic, metabolomic, and targeted biochemical analyses. osvipp1 knockout seedlings exhibited an albino-lethal phenotype, disorganized thylakoid membranes, disrupted intermembrane connections, and altered expression of chloroplast-encoded genes, supporting an essential role for OsVIPP1 in plastid membrane development. Both overexpression and RNA interference delayed seed germination, reduced plant height, and impaired yield-related traits. Integrated transcriptomic and untargeted metabolomic analyses associated altered OsVIPP1 expression with lipid, carbon, and phytohormone-related pathways. In overexpression seeds, abscisic acid content increased to 1.95 times the wild-type level, accompanied by the accumulation of several fatty acids and soluble sugars, whereas abscisic acid and most fatty acids decreased in RNA-interference seeds. These findings indicate that OsVIPP1 supports thylakoid spatial organization in leaves, whereas altered OsVIPP1 expression is associated with metabolic changes in mature seeds and yield-related phenotypes. Full article

Background and Objectives: Diabetic macular edema (DME) is a heterogeneous complication of diabetic retinopathy, and optical coherence tomography (OCT) biomarkers may provide information beyond central retinal thickness. Evidence on the OCT biomarker profile of Mexican patients with DME remains limited. This study aimed to characterize OCT biomarkers in patients with DME from a tertiary referral center in western Mexico and evaluate their associations with clinical characteristics and best-corrected visual acuity (BCVA). Materials and Methods: We conducted a retrospective cross-sectional study of adults with diabetic retinopathy and DME. Clinical records and OCT scans were reviewed. Biomarkers included central macular thickness, intraretinal cysts, subretinal fluid, hyperreflective foci, ellipsoid zone disruption, external limiting membrane disruption, and disorganization of the retinal inner layers (DRIL). Associations with glycated hemoglobin, retinopathy severity, diabetes treatment, and BCVA were analyzed. Results: Fifty-seven patients and 88 eyes were included. The mean age was 59.6 ± 10.3 years, the mean diabetes duration was 15.9 ± 7.1 years, and the mean HbA1c was 8.5 ± 0.9%. The mean BCVA was 1.24 ± 0.59 logMAR, and the mean central macular thickness was 427.6 ± 190.8 µm. Intraretinal cysts were the most frequent biomarker (78.4%), followed by ellipsoid zone disruption (40.9%), hyperreflective foci (34.1%), DRIL (30.7%), subretinal fluid (21.6%), and external limiting membrane disruption (21.6%). Intraretinal cysts were significantly associated with greater diabetic retinopathy severity (p = 0.025). Conclusions: This study provides a descriptive real-world profile of structural OCT biomarkers in patients with DME attending a tertiary referral center in western Mexico. Intraretinal cysts were the most frequent finding, followed by ellipsoid zone disruption, hyperreflective foci, DRIL, subretinal fluid, and external limiting membrane disruption. These findings provide regional data on the structural characteristics of DME and may serve as comparative evidence for future studies in other populations and clinical settings. Full article

Ultraviolet (UV) radiation is a major environmental stressor that disrupts cellular integrity by inducing oxidative stress, impairing mitochondrial function, and altering immune cell activity, ultimately compromising cellular homeostasis. In this context, carotenoids are widely recognized for their antioxidant and immunomodulatory properties, with C₅₀ carotenoids emerging as a promising subgroup with enhanced biological activity compared with classical C₄₀ carotenoids. Among them, bacterioruberin (BR), a red-pigmented C₅₀ carotenoid mainly produced by haloarchaea, has attracted increasing interest due to its strong antioxidant and cytoprotective potential. Accordingly, this study investigated the mechanisms underlying the protective effects of a bacterioruberin-rich carotenoid extract (BRCE) against UV-induced damage in human peripheral blood mononuclear cells (PBMCs). PBMCs were pre-incubated with BRCE prior to UV exposure and intracellular reactive oxygen species (ROS), mitochondrial membrane potential (Δψm), caspase-3 activation, and the expression of B cell lymphoma 2 (Bcl-2) and granzyme A were evaluated using fluorescence-based assays via confocal microscopy and flow cytometry. BRCE attenuated oxidative stress, preserved mitochondrial membrane potential, reduced caspase-3 activation, and modulated Bcl-2 and granzyme A expression, with more pronounced effects observed at low concentrations. Overall, BRCE exerted a coordinated cytoprotective effect through modulation of oxidative stress, mitochondrial integrity, and apoptosis-related signaling pathways. These findings provide novel insight into the cellular effects associated with the bioactivity of bacterioruberin and support the growing interest in C₅₀ carotenoids as promising photoprotective and immunomodulatory compounds. Full article