Search Results (396)

Aflatoxin B1 (AFB1) is a potent foodborne mycotoxin classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC) and is widely recognized for its causal role in hepatocellular carcinoma (HCC). Beyond its well-established hepatotoxicity, increasing evidence indicates that AFB1 also disrupts intestinal homeostasis by impairing epithelial barrier integrity, reducing mucus production, altering gut microbial composition, and disturbing microbial metabolism. These changes promote increased intestinal permeability, facilitating the translocation of bacteria and microbial products and contributing to chronic inflammation through the gut–liver axis. Recent experimental studies further suggest that alterations in short-chain fatty acid (SCFA) production and microbiota-dependent signaling pathways may actively mediate AFB1-induced intestinal and hepatic injury. Although direct evidence linking AFB1-induced dysbiosis to extrahepatic carcinogenesis remains limited, growing evidence indicates that persistent barrier dysfunction, microbial imbalance, and chronic inflammation may create a microenvironment favorable for tumor initiation and progression in tissues beyond the liver. This review critically summarizes current evidence regarding the effects of AFB1 on intestinal barrier function, gut microbiota dysbiosis, bacterial translocation, microbial metabolites, and the gut–liver axis while evaluating the mechanistic evidence supporting these interactions and highlighting the major knowledge gaps that should be addressed in future research. Full article

To reveal the chemical composition and concentration distribution, spatial distribution characteristics, source composition, and health impacts of volatile organic compounds (VOCs) in the two multi-industry industrial parks in Tianjin, 57 VOC species were determined by using SUMMA canister sampling with preconcentration gas chromatography/mass spectrometry. Based on these measurements, the Positive Matrix Factorization (PMF) model was used for source analysis to achieve quantitative identification and contribution analysis of different source factors. The health risks of VOC concentrations were analyzed based on the assessment framework recommended by the United States Environmental Protection Agency (USEPA). The results showed that the average concentrations of TVOCs in A-1 (Industrial Park and Cluster A, 5 m), A-2 (Industrial Park and Cluster A, 10 m), B-1 (Industrial Park and Cluster B, 5 m), and B-2 (Industrial Park and Cluster B, 10 m) were 59.72 ppbv, 45.35 ppbv, 32.44 ppbv, and 21.65 ppbv, respectively. TVOC concentrations were higher at A-1 and B-1 than at A-2 and B-2, and were generally higher at site A than at site B. The VOC components were mainly alkanes (53.5%–71.4%), followed by aromatic hydrocarbons (15.6%–36.2%), alkenes (4.6%–9.9%), and alkynes (3.1%–7.6%). The proportion of aromatic hydrocarbons in A was higher (22.13% and 36.22%), while alkanes dominated absolutely in B (71.4% and 66.9%). n-Hexane was the key species driving the spatial differences (a typical source of VOCs in solvent usage). The concentration in A-1 was 3.1 times that of A-2, and B-1 was 3.3 times that of B-2. It was mainly controlled by local solvent unorganized emissions. The differences in species between the two points at site A for toluene, xylene, etc., were relatively gentle, while at site B, the concentration of the same aromatic hydrocarbons at B-1 was significantly higher than that at B-2, presenting a clearer spatial characteristic, indicating differences in the spatial distribution of organic solvent-related industrial activities in different sites. The source analysis showed that A-1 was dominated by solvent usage (38.64%) and natural gas/LPG sources (36.96%); A-2 by vehicle exhaust (40.20%) and natural gas/LPG sources (36.15%); B-1 by cleaning-agent usage (38.81%) and fuel combustion (30.33%); and B-2 by plastic and rubber production (36.90%) and fuel combustion (31.84%). The health risk assessment showed that benzene, n-hexane, and xylene dominated the non-carcinogenic risks, but the overall non-carcinogenic (HI < 1) and carcinogenic (CR < 1 × 10⁻⁶) risks were both below the threshold. This study reveals inter-site differences in VOC concentrations, compositions, and source contributions across two mixed industrial parks, providing a basis for site-specific VOC control priorities, source-targeted monitoring strategies, and risk management in mixed industrial areas. Full article

Background/Objectives: Skin cancer is a major health concern worldwide and has led to the quest for safer and more effective topical chemopreventive agents. In this study, the in vivo efficacy of a hydrogel formulation containing kaempferol and ferulic acid-loaded nanoparticles was evaluated for the management of DMBA-croton oil-induced skin cancer in Swiss albino mice. Methods: Drug-loaded nanoparticles prepared via nanoprecipitation were incorporated into hyaluronic acid to obtain single-drug (FAPG, KMPG) and dual-drug-loaded (FKMG) hydrogel formulations. Skin tumors were induced via DMBA as an initiator followed by croton oil as a promoter, with tumor onset observed after a similar latency period of approximately 5–6 weeks in all carcinogen-exposed groups. Treatment was initiated after week 6 and continued until week 16. Results: The gel formulation had a skin-compatible pH and the desired rheological and spreadability properties. The dual drug-loaded hydrogel formulation had a more controlled and prolonged release profile. Compared with the negative and vehicle control groups, the FKMG-treated group presented a marked reduction in tumor incidence and tumor burden, along with improved body weight gain. Biochemical analysis revealed the restoration of antioxidant and enzyme activity in treated animals, particularly in animals treated with FKMG. Histopathological examination revealed near-normal skin architecture in FKMG-treated mice, indicating strong protective effects. Additionally, significant downregulation of TNF-α and IL-6 suggested effective suppression of tumor-promoting inflammatory pathways. Conclusions: Overall, the FKMG formulation exhibited superior chemopreventive efficacy compared with the FAPG and KMPG treatments, highlighting its potential as a promising topical therapeutic strategy against chemically induced skin carcinogenesis. Full article

The LW-9 peptide was previously identified through screening of purified molecules from the venom of the spider Phoneutria nigriventer and has been described as an immunomodulatory compound with potential application in cancer therapy. The molecule was biochemically characterized and subjected to in silico analyses to evaluate its toxicity and efficacy profiles. LW-9 exhibits a molecular mass of 1235.522 Da and the amino acid sequence PyrKKDRFLGLM-CONH₂. Secondary and tertiary structures were modeled using computational approaches. The results indicated low permeability across biological membranes, including the blood–brain barrier. In silico predictions further suggested that LW-9 is neither carcinogenic nor mutagenic; however, it may act as a potent inhibitor of the CYP3A4 enzyme, raising concerns regarding potential drug–drug interactions. Overall, LW-9 shows promise as an immunomodulatory agent for cancer applications, while its pharmacokinetic properties and possible interactions with other drugs continue to be investigated. Full article

Background: Upper tract urothelial carcinoma (UTUC) is a rare malignancy representing approximately 5–10% of all urothelial cancers. Key risk factors include smoking, chemical exposures, selected metabolic conditions, and hereditary cancer syndromes. This narrative review summarises current knowledge on UTUC molecular pathogenesis, major risk determinants, and contemporary therapeutic strategies. Methods: This study was conducted as a narrative review with a structured literature search. PubMed, Web of Science, Embase, and Scopus were searched using predefined combinations of UTUC-related terms covering molecular pathogenesis, carcinogenic risk factors, and treatment strategies. The review was prepared according to SANRA principles to improve transparency and consistency; however, no formal systematic review methodology or meta-analysis was performed. Results: Available genomic studies indicate that UTUC has a molecular profile distinct from urothelial bladder carcinoma (UBC), with recurrent alterations involving FGFR3, HRAS, KMT2D, CDKN2A, KRAS, MYC, and BRIP1. Smoking, aristolochic acid exposure, Lynch syndrome, and possibly early-onset urolithiasis contribute to carcinogenesis through distinct but incompletely understood mechanisms. Surgical treatment remains the standard of care for high-risk localised disease, whereas perioperative chemotherapy, immunotherapy, and targeted agents are expanding treatment options, particularly in advanced disease. A substantial proportion of the therapeutic evidence, however, is derived from broader urothelial carcinoma populations rather than UTUC-specific studies. Conclusions: UTUC is biologically heterogeneous and shaped by both molecular alterations and environmental exposures. Although substantial progress has been made, important gaps remain in understanding UTUC-specific carcinogenic mechanisms and in defining evidence-based personalised treatment strategies. Better integration of molecular, environmental, and clinical data is needed to improve risk stratification and treatment selection. Full article

Neuroblastoma is an aggressive pediatric malignancy with limited therapeutic options for high-risk disease, underscoring the need for alternative treatment strategies. Drug repurposing offers a promising approach to accelerate the identification of effective anti-cancer agents. In this study, we investigated the anti-carcinogenic effects of hydroquinidine, a class IA antiarrhythmic ion channel blocker, and spiramide, a dopamine D₂/serotonin 5-HT₂ receptor antagonist and endoplasmic reticulum stress inducer, in SH-SY5Y human neuroblastoma cells. Cells were treated with increasing concentrations of each compound and evaluated using cell viability, colony formation, wound healing, proliferation, apoptosis, and quantitative gene expression assays. Both compounds induced a dose-dependent reduction in cell viability, with spiramide exhibiting greater potency than hydroquinidine. Functional assays revealed significant suppression of clonogenic survival, cell migration, and DNA synthesis, accompanied by increased oxidative stress and cell death. Molecular analyses demonstrated coordinated transcriptional regulation of apoptosis- and cell cycle-related genes, characterized by upregulation of BAX, CDKN1A, and CDKN1B, and downregulation of BCL-2 and CCND1. Notably, spiramide consistently produced stronger cytotoxic and wound-closure inhibitory effects, suggesting a greater contribution of oxidative stress- and apoptosis-associated pathways. Collectively, these findings indicate that hydroquinidine and spiramide disrupt neuroblastoma cell growth through complementary stress- and cell cycle-associated pathways and identify them as promising candidates for further preclinical evaluation. Full article

The development of multi-targeted therapeutic agents is increasingly recognized as essential for treating multifactorial diseases. Butyrolactone I and butyrolactone III, γ-butyrolactone derivatives isolated from the marine fungus Aspergillus terreus, represent structurally related natural products with largely unexplored polypharmacological potential. This study employed a comprehensive in silico approach combining ADMET profiling, quantum chemical calculations, molecular docking, and molecular dynamics simulations to evaluate their therapeutic potential across multiple pharmacological targets. Physicochemical analysis revealed favorable drug-like properties for both compounds, with complete compliance with Lipinski’s Rule of Five, high predicted gastrointestinal absorption (>80%), and acceptable toxicity profiles (toxicity class 4, LD₅₀ = 2000 mg/kg). Neither compound showed hepatotoxic, neurotoxic, cardiotoxic, carcinogenic, or mutagenic liabilities. Frontier molecular orbital analysis (DFT/B3LYP/6-31G(d,p)) revealed comparable HOMO energies (−6.054 and −6.059 eV), with butyrolactone III exhibiting enhanced kinetic stability based on a larger HOMO–LUMO gap (4.662 eV vs. 4.443 eV) and higher chemical hardness (η = 2.331 eV vs. 2.222 eV). Molecular docking against four therapeutic targets revealed target-selective binding profiles: butyrolactone III demonstrated binding affinity toward acetylcholinesterase exceeding donepezil (−9.0 vs. −8.3 kcal/mol), while butyrolactone I exhibited MDM2 binding affinity slightly exceeding nutlin-3a (−7.8 kcal/mol). Both compounds showed moderate interactions with COX-2 and topoisomerase IV. Molecular dynamics simulations validated the stability of AChE complexes (RMSD < 2.0 Å) and the MDM2–butyrolactone I complex (RMSD: 0.69 ± 0.09 Å), while the MDM2–butyrolactone III complex exhibited significant instability (RMSD up to 3.55 Å), highlighting the critical role of the prenyl group in MDM2 recognition. These findings, consistent with, though not a direct experimental validation of, previously published in vitro data, support the evaluation of butyrolactone III as a scaffold for neuroprotective agents and butyrolactone I as a p53 pathway modulator for cancer therapy, illustrating the potential value of fungal metabolites in multi-target drug discovery and the role of integrated computational approaches in prioritizing candidates for subsequent experimental testing. Full article

The presence of aflatoxin B1 (AFB1) is ubiquitous in the environment, and it is considered one of the most powerful natural carcinogenic substances. In this study, a highly sensitive electrochemical aptasensor was designed to detect aflatoxin B1 (AFB1) in peanuts. Iron–cobalt-doped magnetic carbon (Fe-Co/NPC) was used to enhance the conductivity of the electrode and catalytic performance, providing an increased specific surface area. Gold nanoparticles (AuNPs) were used to immobilize an aptamer. And cDNA-polyacrylic acid (cDNA-PAA) nanogels served as a high-density carrier for cDNA and an active signal amplification unit, significantly increasing the charge transfer resistance (Rct) through steric hindrance and electrostatic repulsion. Unlike traditional aptasensors that relied on passive blocking agents, we designed a competitive displacement mechanism. AFB1 competed with cDNA-PAA during detection in order to bind to the aptamer, which resulted in the removal of the non-conductive complex and a substantial increase in the electrochemical signal. Under the optimal conditions, the aptasensor had a linear response range of 1–1000 ng/L and a limit of detection (LOD) of 0.3 ng/L. It displayed high specificity, reproducibility, and stability. In spiked peanut samples, the recoveries ranged from 98.04% to 100.86%. Due to its sensitivity and reliability, this aptasensor has a great determination of AFB1 in food safety applications. Full article

Cadmium is a toxic heavy metal classified by the International Agency for Research on Cancer as a human carcinogen and recognized as an endocrine-disrupting chemical. The present study aimed to evaluate tissue-specific susceptibility to cadmium-induced oxidative damage to membrane lipids (lipid peroxidation, LPO) and to assess the antioxidative effects of melatonin in porcine tissue homogenates representing endocrine (the thyroid and the ovary) and non-endocrine (the liver, the kidney, and the brain) organs. Homogenates were incubated with cadmium chloride (CdCl₂; 2.5–1000 µM) without/with melatonin (0.1–5.0 mM). Lipid peroxidation was assessed spectrophotometrically by measuring malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) levels. Cadmium significantly increased LPO in the liver (2.5–1000 μM) and in the kidney (25–1000 μM), whereas no prooxidative effect was observed in endocrine tissues or in the brain. Liver damage was mitigated by melatonin doses as low as 0.1 μM across the 250–1000 μM cadmium range, while protection in the kidney was limited to higher melatonin concentrations (2.5–5.0 mM) against damage induced by 100–1000 μM cadmium concentrations. The findings demonstrate pronounced tissue-specific differences in susceptibility to cadmium-induced oxidative stress and support the potential of melatonin as a preventive agent against heavy metal-induced oxidative stress, particularly in non-endocrine organs. Full article

The current study describes the synthesis and preliminary anticancer assessment of a novel series of C3/C28-bis-1,2,4-triazolyl-sulfanylacetate-betulin (AP1–5) derivatives to identify potent agents for clinical development. The cytotoxicity of AP1–5 was evaluated using the Alamar blue assay against MCF-7, A375, PANC-1 (cancer cells) and HaCat (human keratinocytes) cells. Moreover, the molecular mechanisms responsible for cytotoxicity were investigated through in vitro (DCFDA/H₂DCDFA assay, caspase-3/7 assay, and morphological analysis) and in silico assays (network pharmacology, molecular docking, molecular dynamics simulation, and ADMET predictions). The result highlighted AP5, containing unsubstituted 1,2,4-triazoles, as the lead derivative of the series with increased potency against MCF-7, with an IC₅₀ value of 7.41 μM compared to its phenyl-substituted analogs (AP1–4). The derivatives induced apoptosis, marked by fragmented nuclei, round cells, disorganized cytoskeletons, and activation of caspases-3/-7 through a ROS-decreasing mechanism. The network pharmacology assessment predicted AP5 may interact with key proteins in the PI3K/Akt pathway, such as MAP2K1, MDM2, IGF1, JAK2, IL2 and FGFR1, as well as ESR1, PGR and MMP2. Molecular docking suggested MMP-2 is the most favorable target for AP5 among the validated proteins, while molecular dynamics simulations supported the predicted AP5–MMP-2 interaction. Moreover, the ADMET profiling of AP5 showed acceptable intestinal absorption, non-glycoprotein-P substrate status, and reduced hepatic metabolism compared to betulin. However, the ADMET analysis also highlighted some potential toxicity risks such as DILI, genotoxicity, carcinogenicity and skin sensitization that need to be further investigated. Altogether, these promising findings support the further exploration of AP5 as a promising drug candidate for breast cancer in vivo to assess its potency and toxicity. Full article

Uridine diphosphate glucuronosyltransferase 2B (UGT2B) enzymes constitute a critical subgroup of phase II metabolizing enzymes that modulate the clearance of steroid hormones, carcinogens, and numerous anticancer agents, thereby influencing cancer susceptibility, progression, and therapeutic outcomes. This review provides a comprehensive synthesis of the genetic, regulatory, and functional roles of UGT2B family members, particularly UGT2B4, UGT2B7, UGT2B10, UGT2B15, UGT2B17, and UGT2B28, in oncogenesis and cancer treatment. We summarize evidence from molecular, epidemiological, pharmacogenetic, and clinical studies demonstrating how UGT2B expression patterns, polymorphisms, copy number variations, epigenetic regulation, and microRNA-mediated control shape intratumoral hormone homeostasis, carcinogen detoxification, and drug resistance across multiple malignancies, including prostate, breast, lung, colorectal, hematological, and hormone-dependent cancers. UGT2B enzymes metabolize several widely used anticancer drugs and active metabolites, thereby affecting pharmacokinetics, efficacy, and toxicity. Understanding the context-specific roles of UGT2B family members offers a compelling opportunity for therapeutic exploitation. In particular, rational combination strategies incorporating UGT2B inhibitors or modulators alongside standard anticancer agents may enhance drug effectiveness without increasing dosage, while simultaneously enabling the dose reduction of the partner agent to mitigate dose-dependent toxicities. Such approaches are especially relevant for therapies with narrow therapeutic indices. Overall, this review highlights UGT2B enzymes as multifunctional determinants of cancer risk and treatment response and underscores their promise as biomarkers and actionable targets for precision oncology and optimized combination regimens. Full article

In this study, a new series of (E)-4-((2-(2-(4-amino-3-methyl-5-oxo-4,5-dihydro-1H-1,2,4-triazol-1-yl)acetyl)hydrazono)methyl)phenyl 4-halogenobenzenesulfonates (3a–3d), where 3a = F, 3b = Cl, 3c = Br, and 3d = I, were successfully synthesized via a straightforward synthetic route. The structures of the obtained compounds were fully characterized and confirmed by spectroscopic techniques, including FT-IR, ¹H NMR, and ¹³C NMR, as well as LC-MS/MS analysis. 1,2,4-triazole-based hydrazone derivatives (3a–3d) were investigated using IR and NMR spectroscopy and DFT calculations. Intermolecular interactions, HOMO-LUMO, dipole moment, polarization, first-order hyperpolarizability, and molecular electrostatic potential studies on the molecules were examined. The HOMO and LUMO energy gap study supports the charge transfer probability in the molecules. These were conducted to investigate the reactivity and stability of heterocyclic molecules in bioactivity analysis. Electron density mapping within the molecular electrostatic potential plot and electrostatic potential representation within the iso-surface plot evaluated the concept of charge distribution in the molecule as nucleophilic reactions and electrophilic regions. The predicted nonlinear optical (NLO) properties of the molecules are much greater than those of urea. The results obtained from these investigations collectively provide evidence that the molecules possess nonlinear optical applications. Novel triazole–hydrazone-functionalized aryl sulfonate derivatives (3a–3d) were evaluated for their anticancer potential against a panel of brain and non-brain cancer cell lines. Compound 3b exhibited the most favorable overall biological profile, displaying potent activity against SH-SY5Y neuroblastoma (GI = 7.59 μM) and U87MG glioblastoma cells (GI = 13.85 μM), together with the lowest toxicity toward normal FL fibroblasts (GI = 62.02 μM). Compounds 3c and 3d demonstrated remarkable potency against IDHmut-U87 glioma cells (GI = 3.87 and 3.27 μM, respectively), although their selectivity toward cancer cells was limited. DNA degradation studies revealed substantial fragmentation, particularly in C6 and SH-SY5Y cells, while migration assays indicated reduced cellular motility. Molecular docking studies identified compound 3b as the strongest PI3Kα binder, supporting a possible. In addition, the antimicrobial activities of compounds 3a–3d were evaluated against selected Gram-positive and Gram-negative bacteria as well as Candida species using the broth microdilution method. The compounds exhibited measurable antimicrobial effects with MIC values ranging from 156 to 625 µg/mL, showing moderate growth inhibition against the tested microorganisms. Although the observed activity was lower than that of the reference antimicrobial agents, the results indicate that these triazole–hydrazone derivatives possess a detectable level of antimicrobial activity and provide a basis for further structural optimization. Collectively, the results suggest that compound 3b represents the most promising lead structure due to its balanced combination of potency, selectivity, and predicted target engagement. Molecular docking was performed to evaluate the binding potential of newly synthesized triazole derivatives (3a–3d) against PI3Kα. The docking protocol was validated by re-docking alpelisib, yielding an RMSD of 0.64 Å. Among the tested compounds, 3b showed the most favorable binding energy (−9.94 kcal/mol) and estimated Ki value (52.13 nM), consistent with its superior in vitro activity. Its interactions with key PI3Kα residues, including Val851, Ser854, Met922, and Asp933, support a stable binding mode within the ATP-binding pocket. In silico ADME and toxicity analyses suggested acceptable drug-likeness characteristics, absence of major hepatotoxic, mutagenic, and carcinogenic liabilities, and moderate predicted acute toxicity profiles. These findings suggest that 3b is the most promising derivative for further validation. Full article

Background: In May 2011 the IARC (International Agency for Research on Cancer) classified radiofrequency electromagnetic fields as a possible human carcinogen mainly based on epidemiological studies about the association between mobile phone (MP) use and brain tumors. Considering that brain tumors have long latencies of around 30 years, it is unlikely that this association is due to an ‘initiating’ activity of MPs since virtually all studied brain tumor cases must have had already a covertly growing tumor when they started MP use. But there could be other adverse effects exerted by a MP when acting on later stages of malignant development. We propose that MP use acts adversely by increasing tumor growth rate and model it by an impact on the latency distribution shifting the age-incidence function to younger age. Methods: We calculate (1) relative risks (RRs) for MP use in comparison to the meta-analytic RR estimate for glioma in adults; (2) RRs for neuroepithelial childhood brain tumors in comparison to the findings of the MOBIkids study; and (3) hazard ratios in comparison to the results of the Million Women Study (MWS). Results: The meta-analytical odds ratio for glioma and long-term MP use in adults of 1.22 (95% confidence-interval: 1.02–1.46) could be explained by a shift in the age-incidence function by 32% of MP usage duration. Applying a 20% shift for childhood neuroepithelial brain tumors reproduced the ORs that were predominantly less than 1 in the MOBIkids study. For glioma risk in perimenopausal women in relation to long-term MP use in the MWS we found hazard-ratios close to 1 applying a 32% shift in the age-incidence function. Conclusions: The standard interpretation of relative risk estimates must be revised if exposure to the agent commenced after the malignant development has already started. All reported RR estimates of MP use can be reproduced by positing MP use increased tumor growth rate. However, since these results are obtained applying a modeling approach, further tests using epidemiological methods, which will be difficult or hardly feasible, or utilizing more promising laboratory methods are needed. Full article

The release of persistent azo dyes into aquatic systems remains a critical environmental and toxicological concern due to their high chemical stability, resistance to biodegradation, and potential to generate carcinogenic aromatic amines. This study evaluates the adsorption of Amberlite XAD-4 (X4), a hydrophobic polystyrene–divinylbenzene resin, for the removal of the toxic azo dye Direct Red 23 (DR 23) from aqueous solutions. Batch experiments were performed to assess the influence of contact time and initial dye concentration, supported by kinetic and equilibrium modeling. Adsorption proceeded through a multistage mechanism involving thin-layer diffusion, intraparticle diffusion, and final equilibrium, which was reached after 48 h. The pseudo-second-order kinetic model (PSO) with R² = 0.9648 best described the adsorption behavior. Equilibrium data was fitted by the Langmuir isotherm (R² = 0.9990), yielding a maximum adsorption capacity of 56.8 mg g⁻¹, consistent with the experimentally observed saturation plateau. FTIR spectra revealed characteristic shifts in aromatic, –N=N– (≈1500 cm⁻¹), and –SO₃²⁻ (1180–1040 cm⁻¹) bands, which, corroborating the data provided by SEM/EDX analysis, completes the adsorption of DR 23 on the X4 matrix. TG/DSC analysis showed modifications in thermal behavior after adsorption without compromising resin stability, supporting strong dye–resin interactions. Overall, the integrated kinetic, isotherm, spectroscopic, and thermal analyses demonstrate that X4 is stable and an adsorbent with desorption capability using chemical agents, highlighting its potential for mitigating the environmental and toxicological risks associated with azo dye contamination in wastewater. Full article

Increasing volumes of dye-containing wastewater generated by the textile industry have become a serious environmental issue, particularly in Indonesia, where textile production contributes substantially to industrial activity. Among synthetic dyes, methylene blue (MB) is widely used because of its low cost and high solubility in water; however, its persistence, toxicity, and potential carcinogenicity make its removal from wastewater highly important. Conventional treatment methods are often limited by incomplete degradation and secondary waste generation. In this study, iron oxide nanoparticles (IONPs) were synthesized through a green route using Psidium guajava leaf extract as both a reducing and stabilizing agent. Characterization by PSA, UV-Vis, SEM-EDX, and XRD confirmed the formation of magnetite-like iron oxide particles with sizes ranging from 209.2 to 291.4 nm. Photocatalytic experiments showed high MB degradation efficiency (94.7–99.0%) under UV irradiation, highlighting the potential of guava leaf-mediated IONPs as low-cost, sustainable photocatalysts for wastewater treatment. Full article