Search Results (604)

Metabolic dysfunction-associated steatohepatitis (MASH; formerly non-alcoholic steatohepatitis, NASH) is characterized by oxidative stress, inflammatory activation, hepatocellular injury, and progressive liver dysfunction. However, the global transcriptomic landscape underlying stress-induced hepatic injury remains incompletely understood. In this study, we employed a methionine–choline-deficient (MCD) diet-induced murine model to characterize the phenotypic and transcriptomic alterations associated with liver injury. Male C57BL/6J mice were fed either a control or MCD diet, and hepatotoxicity was assessed by survival analysis, body and liver weight measurements, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, histopathological examination, RNA sequencing, quantitative real-time PCR (qRT-PCR), and tumor necrosis factor-alpha (TNF-α) enzyme-linked immunosorbent assay (ELISA). MCD feeding markedly reduced survival and body weight while inducing hepatomegaly and significant elevations in serum ALT and AST, indicating severe hepatocellular injury. Histopathological analysis demonstrated hepatic steatosis, hepatocellular ballooning, and lobular inflammation without histological evidence of fibrosis. Transcriptomic profiling revealed extensive gene expression remodeling, characterized by activation of inflammatory pathways, enrichment of MAPK-related signaling, dysregulation of lipid metabolism, suppression of antioxidant defense systems, impairment of cytochrome P450-mediated detoxification, and upregulation of apoptosis-associated genes. qRT-PCR further validated the differential expression of representative genes involved in inflammatory signaling (Tlr4, Nfkb1, Nlrp3, and Casp1), MAPK signaling (Fos), xenobiotic metabolism (Cyp4f18), lipid metabolism (Apoa4 and Lpl), extracellular matrix remodeling (Mmp12), and oxidative stress responses (Sod1 and Gstp1). In addition, elevated serum TNF-α levels provided protein-level evidence supporting activation of the TLR4/NF-κB/TNF-α/NLRP3 inflammatory axis. Although fibrosis-associated transcriptional responses were detected, the absence of histological fibrosis suggests transcriptional priming of fibrogenic pathways rather than established fibrogenesis. Collectively, these findings provide a transcriptomic framework linking oxidative stress, impaired detoxification, inflammatory activation, and stress-responsive signaling to MCD-induced hepatic injury. The MCD model provides a valuable experimental platform for characterizing hepatic stress-response transcriptomes and for generating hypotheses that can subsequently be evaluated in environmentally relevant toxicological models. Nevertheless, caution should be exercised when extrapolating these findings to obesity-associated human MASLD, as the MCD model lacks key metabolic features of the human disease, including obesity and insulin resistance. Therefore, the present findings should be interpreted primarily as transcriptomic signatures of stress-induced hepatic injury rather than as a direct representation of the pathophysiological processes underlying human obesity-associated MASLD. Full article

Triphenyl phosphate (TPhP) is a ubiquitous environmental contaminant and endocrine disruptor potentially associated with an increased risk of thyroid cancer (TC). However, whether TPhP directly contributes to TC remains unclear. This study integrated network toxicology and machine learning to investigate potential molecular associations between TPhP exposure and thyroid oncogenesis. By integrating multi-source databases and transcriptomic data, we constructed a TPhP–TC interaction network and established a TC risk prediction model using 127 machine learning algorithm combinations, identifying ten candidate hub genes. GO and KEGG enrichment analyses indicated that these genes are predominantly enriched in phosphorus metabolism, purine metabolism, and nuclear receptor signaling pathways, implying that TPhP may be linked to tumorigenesis through the disruption of metabolic reprogramming. SHAP analysis highlighted AHR and SLC20A2 as critical contributors to model performance. Molecular docking predicted stable binding between TPhP and all hub proteins in silico, with binding energies ranging from −9.2 to −6.6 kcal/mol. This study offers two computational contributions: (1) a quantifiable framework for predicting pollutant-associated TC risk and (2) systematic computational evidence for potential TPhP thyroid toxicity. These findings address a critical gap in understanding potential links between endocrine-disrupting chemical exposure and thyroid carcinogenesis, generating hypotheses for future experimental validation. Full article

Bumblebees are dominant pollinators threatened by environmental antibiotic residues. This study investigated sublethal chloramphenicol (12 and 120 μg/L) effects on Bombus terrestris after 15 days’ exposure. The results showed that chloramphenicol exposure had no significant effect on the survival rate and cumulative food intake of bumblebees, confirming the sublethal property of the tested concentrations. However, chloramphenicol significantly dysregulated the expression of genes related to learning–memory (DopR2, Oamb, NMDA), immunity (abaecin, defensin) and detoxification (cyp9Q6) in bumblebees. High-dose chloramphenicol significantly increased carboxylesterase activity and reduced malondialdehyde content, while superoxide dismutase activity remained unchanged. In addition, chloramphenicol exposure significantly reshaped the gut microbiota structure of bumblebees, reduced the abundance of core beneficial symbiotic bacteria, and increased the proportion of drug-resistant bacteria. Our findings indicate that sublethal concentrations of chloramphenicol can impair bumblebee health through multiple pathways, including regulating gene expression, altering antioxidant enzyme activity and disrupting gut microbiota homeostasis. This study provides multi-dimensional toxicological data and a scientific basis for the ecological risk assessment of agricultural antibiotic residues to pollinator insects. Full article

Frailty is a multidimensional geriatric syndrome that lacks a consistent definition, complicating its clinical management. Epigenetic data suggest that frailty involves altered CpG sites, potentially driven by environmental epigenetic factors (the exposome) that influence aging. Systematically reviewing studies from 2009 to 2025, we quantified frailty prevalence, pooled weighted methylation beta values for associated CpG sites, performed enrichment analysis, and conducted structural network analysis to evaluate chemical interactions, following the PRISMA 2020 guidelines and with the study prospectively registered in PROSPERO (ID 1159037). Results showed a pooled frailty prevalence of 17.4% with extreme heterogeneity (I² = 98.88%), and a combined methylated beta effect of −0.1378 (CI: −0.4156, 0.1400) with high heterogeneity (I² = 100%), highlighting sources of variability. Interestingly, we found a CpG site (cg04772644) shared between Chinese and German cohorts, and, upon mapping, four frailty-related genes (CDC42BPB, SLC1A5, RXRB, and SLC22A18AS) were shared across cohorts. Indeed, these genes are significantly enriched in pathways including thrombin signaling, G protein-coupled receptor signaling, and immune cell differentiation signaling. Finally, our system toxicology analysis demonstrated that arsenite, bisphenol A, benzamide, dorsomorphin, and trichostatin A directly interact with the four shared genes, suggesting that the chemical exposome contributes to the observed epigenetic heterogeneity of frailty and the concomitant clinical manifestations. Full article

Redox homeostasis is the balance between oxidative processes and antioxidant defenses and is fundamental to cellular integrity. This review critically synthesizes current evidence on the phytochemical composition, redox-modulating mechanisms, and therapeutic bioactivities of Fagonia cretica L. (F. cretica), with the aim of evaluating its translational potential as a natural antioxidant and anticancer agent. F. cretica has emerged as a phytochemically rich candidate containing highly bioactive secondary metabolite for redox-targeted therapeutic applications. Its diverse secondary metabolite profile, including alkaloids, flavonoids, tannins, saponins, terpenoids, glycosides, and phenolic compounds, confers broad biological activity. Bioactive constituents, particularly kaempferol, catechin, quercetin, and arbutin, directly neutralize reactive oxygen species (ROS) and modulate inflammatory pathways through inhibition of COX-1, COX-2, and nitric oxide production. These compounds influence important major ROS-sensitive redox signaling pathways: activation of the Keap1/Nrf2/ARE axis to upregulate cytoprotective genes such as HO-1, NQO1, and GCL, suppression of the NF-κB pathway to attenuate pro-inflammatory cytokine transcription, including TNF-α, IL-1β, and IL-6, and interference with the MAPK-PI3K/Akt cascade to disrupt aberrant cancer cell survival and proliferation. Bioactive compound-rich extracts of F. cretica exhibit anticancer activity in MCF-7 breast cancer cells by inducing DNA damage, cell cycle arrest, and apoptotic signaling through the FOXO3a/p53 pathways. Similar effects have been reported in colorectal (HCT-116) and prostate (PC-3) cancer cells through DNA (cytosine-5)-methyltransferase 1 (DNMT1) downregulation, oxidative stress induction, and ER-β activation. Moreover, these extracts demonstrate cytotoxic effects in HepG2 and Caco-2 intestinal cancer cells, often associated with topoisomerase inhibition and caspase activation. Despite encouraging preclinical evidence, systematic studies encompassing pharmacokinetic profiling, toxicological characterization, and human clinical trials remain essential to translate these findings into safe, evidence-based therapeutic applications. Full article

CdS and Cd-deficient CdS (D-CdS) were prepared using a simple hydrothermal method. Pristine CdS exhibited slow electron transfer and limited active sites in periodate (PI) activation, while Cd vacancy defect engineering proposed in this work effectively overcame these drawbacks. The optimal Cd-deficient D-CdS8 could effectively activate PI and exhibit excellent degradation performance toward tetracycline (TC). Within 90 min, the D-CdS8/PI system could achieve 92.3% removal of 10 mg L⁻¹ TC. This study systematically explores the influences of different factors and coexisting substances on TC degradation. Radical quenching experiments revealed that IO₃· and ·OH were the dominant reactive species for TC degradation in D-CdS8/PI system. Electrochemical characterization indicated that the introduction of Cd vacancies made D-CdS8 possess higher electron transfer efficiency. The D-CdS8/PI system achieved enhanced PI activation and improved TC degradation, with reaction rates 2.15 times superior to the CdS/PI system. Furthermore, degradation pathways and toxicological analysis of intermediates for TC degradation were also conducted. This study provided a simple and feasible strategy for developing efficient defective catalysts for the remediation of antibiotic-contaminated water. Full article

Tire wear particles (TWPs) are a significant source of microplastics and chemical additives in the environment; however, differences in the toxicity of particles from different vehicle types remain unclear. This hydroponic study compared the phytotoxicity of leachates from aircraft- and automobile-derived TWPs on mung bean. Both leachates inhibited seed germination and seedling growth, with aircraft TWP leachates showing stronger effects, including greater germination delays and more pronounced reductions in shoot height, root length, and root surface area. Physiological analyses revealed that TWP leachates induced oxidative stress, characterized by significant suppression of superoxide dismutase (SOD) activity, compensatory increases in catalase (CAT) and peroxidase (POD) activities, and marked accumulation of malondialdehyde (MDA), indicating severe membrane lipid peroxidation. Chlorophyll content decreased in all groups, with greater reductions under aircraft leachates. Toxicological Priority Index (ToxPi) modeling identified zinc as the shared primary risk factor, while aircraft tire-specific additives (e.g., dicyclohexylamine, 1,2-dihydro-2,2,4-trimethylquinoline) constituted a distinct risk component linked to differentiated formulations. Aircraft TWP leachates thus exhibit stronger phytotoxicity through multiple pathways. These findings support refined environmental risk assessment and targeted control measures for aircraft TWPs. Full article

Drug repurposing represents a rational and resource-efficient strategy to expand the oncological armamentarium by leveraging the established pharmacology, clinical experience, and safety-monitoring frameworks of approved non-oncological agents. Clozapine (CZP), an atypical antipsychotic characterized by broad receptor pharmacology, complex biotransformation, and clinically relevant toxicological liabilities, has emerged as a candidate of interest following preclinical evidence of context-dependent anticancer activity across multiple tumor types. As such, CZP provides an informative case study at the interface between therapeutic drug action and xenobiotic behavior. This review provides a critical and integrated synthesis of the current evidence supporting the repurposing of CZP in oncology, with particular emphasis on the relationship between its molecular mechanisms, dose–exposure requirements, pharmacological complexity, and potential toxicity. Analysis of in vitro and in vivo studies across glioblastoma, non-small cell lung cancer, breast cancer, and melanoma brain metastasis models indicates that CZP can impair tumor cell proliferation and survival through a form of mechanistic plasticity. Rather than acting through a single conserved pathway, CZP appears to disrupt shared upstream processes related to pro-survival signaling, cellular stress tolerance, and metabolic homeostasis, while engaging tumor-specific downstream responses, including autophagic cell death, mitochondria-dependent apoptosis, oxidative stress, and coordinated modulation of survival and angiogenic pathways. Despite this mechanistic rationale, translation remains substantially constrained, most notably by the order of magnitude gap between anticancer-effective concentrations in vitro and clinically achievable plasma exposures, requiring careful distinction between potentially useful anticancer pharmacology and nonspecific xenobiotic-induced cellular stress and clinically unacceptable toxicity. Key limitations include the discrepancy between anticancer-effective concentrations observed in vitro and exposures achievable during standard psychiatric dosing, the limited understanding of how CZP metabolism and metabolite formation may influence efficacy and toxicity, the absence of integrated pharmacokinetic–pharmacodynamic and toxicokinetic modeling, and the lack of dedicated clinical trial evidence. To address these challenges, this review examines complementary translational strategies, including patient-derived organoids, co-culture systems, microphysiological platforms, pharmacokinetic and toxicological modeling, and computational digital twin frameworks. Together, these approaches may support a biologically informed and risk-aware evaluation of CZP, helping to identify responsive tumor contexts, anticipate exposure-related liabilities, and prioritize rational combination strategies. By integrating therapeutic potential with xenobiotic pharmacology and toxicology, this review positions CZP within the evolving landscape of precision oncology and evidence-driven drug repurposing. Full article

Nanoplastics (NPs) and heavy metal cadmium (Cd) are common co-existing pollutants in freshwater environments, but their combined toxic effects on the liver of herbivorous economic fish remain unclear. In this study, grass carp (Ctenopharyngodon idella) were exposed to polystyrene nanoplastics (PS-NPs, 100 nm) and/or Cd to investigate their individual and combined effects on hepatic toxicity. The results revealed that co-exposure interactively suppressed interleukin-10 (IL-10) expression and heme oxygenase-1 (HO-1) antioxidant response, and induced more severe hepatic necrosis, melanization, and fibrinoid necrosis, with the highest integrated biomarker response index and extensive disruption of lipid and steroid metabolism pathways. This study clarified the toxicological interaction of NPs and Cd on the liver of grass carp, and provided a theoretical basis for understanding the combined toxicity of NPs and heavy metal pollution in extreme contamination scenarios or accidental pollution events. Full article

Despite their high effectiveness in reducing material flammability, modern brominated flame retardants (BFRs) remain poorly understood with respect to the toxic substances they generate during combustion. BFRs such as 1,2-bis(pentabromodiphenyl)ethane (DBDPE) and tetrabromophthalate diol (PHT4-DIOL) have been introduced following the limitations on legacy brominated additives. However, their thermal decomposition pathways and toxic product emission profiles under real fire conditions remain poorly characterized. Exposure to elevated temperatures may promote the formation of halogenated toxicants and environmentally persistent compounds, raising concerns that extend beyond conventional fire-safety performance. The combustion behavior of DBDPE-, PHT4-DIOL-, and BFR-containing epoxy resins was investigated using a steady-state tube furnace designed to reproduce realistic fire scenarios. Controlled temperature and ventilation conditions were applied to simulate representative stages of fire. Combustion emissions were comprehensively characterized using Fourier transform infrared spectroscopy (FT-IR) to analyze asphyxiant and irritant gases and solid-phase microextraction gas chromatography–mass spectrometry (SPME-GC-MS) for volatile and semi-volatile organic compounds. The results presented that the incorporation of BFRs substantially altered combustion emission profiles, promoting the formation of brominated and mixed-halogenated species alongside toxic gaseous products. Significant differences in the composition and distribution of combustion byproducts were observed between non-modified and BFR-containing materials, indicating that the environmental and toxicological consequences of these additives cannot be adequately assessed solely through flammability-reduction metrics. These conclusions provide new knowledge of the environmental impacts of brominated flame retardants and highlight the importance of integrated fire-safety assessment strategies that simultaneously consider flame-inhibition efficiency, combustion toxicity, and environmental persistence. Full article

Bisphenol A (BPA) is a common industrial chemical primarily used in the manufacture of plastics, and it has been found in more than 90% of people worldwide. As an endocrine disruptor, BPA can impair reproduction, development, immunity, metabolism, and cognition; it also disturbs immune balance and thus fosters chronic inflammation. A number of population-based studies have indicated a link between environmental BPA exposure and atopic dermatitis (AD). Nevertheless, the detailed molecular pathways connecting BPA to AD remain poorly understood. AD is the leading chronic recurrent inflammatory skin disorder, characterized by severe itching and repeated eczema-like lesions. Its prevalence is roughly 13% among children and 5% among adults, and its global incidence continues to rise, imposing heavy health and economic burdens on societies. To clarify whether and how BPA may promote or worsen AD, we carried out a comprehensive computational study that integrated network toxicology, transcriptomic data, machine learning, molecular docking, and molecular dynamics simulations. From the CTD, ChEMBL, and SwissTargetPrediction databases, we collected 5701 potential BPA targets; from GeneCards and OMIM, we obtained 3270 genes linked to AD. The overlap between these two gene sets gave a group of common candidate genes. Enrichment analyses using GO and KEGG showed that these common genes were significantly overrepresented in the PI3K-Akt signaling pathway, Th17 cell differentiation, and the JAK-STAT signaling pathway—all central to immune and inflammatory regulation. We then built a protein–protein interaction (PPI) network by submitting the common genes to the STRING database and employed Cytoscape to extract hub genes from that network. By integrating human AD transcriptomic profiles with the hub genes and applying two machine learning techniques (LASSO and SVM), we identified six core toxic targets of BPA in AD: TIGIT, JAK3, IL22, S100A8, CCL2, and FCER1G. These six targets fall into two main functional categories: immune dysregulation and inflammatory cell infiltration. Subsequent molecular docking and molecular dynamics simulation experiments confirmed that BPA binds well to all six targets and can form stable complexes with them. Collectively, our findings offer a preliminary experimental foundation for future investigations into the pathogenesis of BPA-induced AD and provide important molecular evidence for understanding how environment–gene interactions contribute to complex inflammatory skin diseases such as AD. Full article

Ochratoxin A (OTA) is a prevalent foodborne mycotoxin that has been increasingly recognized as a potential environmental contributor to neurodegenerative diseases. Despite extensive research, a systematic integration of how OTA replicates the specific pathological hallmarks of Alzheimer’s Disease (AD) is currently lacking. This study provides a comprehensive systematic review of the mechanistic evidence linking OTA exposure to AD-related pathways, utilizing the Adverse Outcome Pathway (AOP) framework to categorize complex toxicological data into biological key events (KEs). A systematic literature search was conducted across PubMed, Scopus, and Web of Science. A total of 24 peer-reviewed articles were selected for synthesis, comprising 14 in vitro studies and 10 in vivo investigations. The integrated evidence demonstrates that OTA exposure triggers a robust toxicological cascade that replicates several key mechanistic pathways associated with AD in experimental models. Early molecular triggers involve significant redox imbalance and mitochondrial bioenergetic failure, which serve as catalysts for sustained neuroinflammation and microglial activation. In vivo data, from multiple animal models, consistently show that these cellular dysfunctions culminate in structural damage. This systematic integration provides a clearer roadmap for future risk assessment and emphasizes the urgent need for refined regulatory guidelines to protect neurological health from chronic mycotoxin exposure. Full article

Polycyclic aromatic hydrocarbons (PAHs) represent a major class of ubiquitous environmental pollutants, posing significant risks to ecosystems and human health due to their persistence, toxicity, and potential for bioaccumulation. This review provides a comprehensive synthesis of current scientific knowledge on PAHs, integrating insights from chemical kinetics, environmental fate, and toxicological mechanisms. The fundamental structural chemistry of PAHs and its direct influence on their physicochemical properties and environmental properties are discussed. The major anthropogenic and natural sources of PAHs are detailed, alongside the chemical kinetics behind their formation during incomplete combustion and their transformation in environmental media. Unlike previous reviews that address PAH sources, remediation, or health effects as separate topics, this review uniquely traces the mechanistic continuum from molecular formation kinetics through physicochemical partitioning and environmental transport to toxicological endpoints, providing a causally linked framework for understanding how structural properties ultimately determine biological outcomes. A central focus is placed on the environmental fate and transport of PAHs across atmospheric, aquatic, and terrestrial compartments, highlighting processes such as gas–particle partitioning, sediment accumulation, and long-range transport. The review further elucidates the complex toxicological pathways of PAHs, including metabolic activation to reactive intermediates, DNA adduct formation, oxidative stress, and their roles in carcinogenesis and other systemic health effects. The analysis reveals strong scientific consensus on the carcinogenic mechanism of parent PAHs via CYP450-mediated metabolic activation to diol-epoxide intermediates while identifying critical areas of uncertainty: the current regulatory framework based on 16 priority PAHs underestimates total carcinogenic risk by a factor of 2–5, mixture toxicology remains poorly characterized, and dose–response relationships for non-cancer endpoints (cardiovascular, neurodevelopmental, immunotoxic) lack the quantitative data needed for robust risk assessment. Finally, human exposure pathways and health risk characterization approaches are discussed, highlighting the need for cumulative, mixture-based assessment frameworks. Full article

Landfill tire fires are complex environmental disasters generating toxic pollutants with severe health risks. This study quantified emission dynamics and toxicological consequences of a large-scale tire fire in an urban ecosystem. A comprehensive source-to-receptor approach was applied, integrating Hybrid Single-Particle Lagrangian Integrated Trajectory (HYSPLIT) atmospheric dispersion modeling with comparison against air quality monitoring data. Soil samples collected from the fireground and surrounding urban allotment gardens were analyzed for tire-specific tracers (Zn) and 16 priority polycyclic aromatic hydrocarbons (PAHs). Human health risks were assessed using Incremental Lifetime Cancer Risk (ILCR), Toxic Equivalency Quotient (TEQ), and Mutagenic Equivalency Quotient (MEQ) metrics. Fire emissions were dominated by particulate matter (PM₁₀: 1.34 t) and PAHs (17.7 kg). Soil at the fire site showed severe contamination (Σ PAHs: 148.9 mg/kg), with benzo[a]pyrene as the primary carcinogen. The cumulative ILCR for children reached 9.7 × 10⁻⁴, exceeding the commonly used upper regulatory benchmark of 10⁻⁴. Dermal contact was identified as the dominant exposure pathway for pyrogenic PAHs. Elevated risk levels persisted at distal residential sites (ILCR: 10⁻⁵–10⁻⁴), indicating long-term environmental contamination Ecological risk quotients (RQ) exceeded unity for PAHs across all fire-impacted locations and for Zn and Cu in the immediate vicinity of the fire scene. These findings demonstrate that acute tire fire events can evolve into persistent terrestrial health hazards, highlighting the critical role of dermal exposure in PAH uptake and the need for long-term environmental monitoring and adaptive land-use management strategies to mitigate chronic health risks in urban populations. Full article

Salmonella remains one of the most critical zoonotic pathogens in the poultry sector, linked to animal disease, foodborne illness, and the global crisis of antimicrobial resistance (AMR). Poultry acts as a major reservoir, enabling Salmonella transmission from hatchery to retail products through horizontal, vertical, and environmental routes. Despite the use of biosecurity, vaccination, antibiotics, and chemical decontamination, effective and sustainable control across the poultry value chain remains difficult, particularly in the face of rising multidrug-resistant strains and growing consumer concerns over chemical residues. Bacteriophages (phages), viruses that selectively infect and lyse bacteria, have emerged as a promising biological alternative for Salmonella control. Although many studies have reported the effectiveness of phages against bacterial species, including Salmonella, in the poultry industry, reports on their full potential to combat antimicrobial-resistant Salmonella across the entire poultry value chain remain limited. Therefore, this review synthesizes current evidence on the application of phages throughout the poultry value chain, including on-farm interventions, processing plant decontamination, and food packaging and storage. Findings from the reviewed articles indicate over a 90% reduction in Salmonella spp. in poultry farms and post-harvest meat, along with lower mortality in phage-treated groups compared to untreated groups; however, these outcomes depend on several factors (e.g., phage strains, concentrations, application methods, and environmental conditions). Laboratory, pilot, and field studies consistently demonstrate that phage preparations, especially when formulated as cocktails or combined with complementary interventions, can achieve substantial reductions in Salmonella, including antibiotic-resistant serovars, in live birds, eggs, poultry environments, and meat products. Unlike antibiotics and chemical sanitizers, phages act with high specificity, preserving beneficial microbiota and maintaining the sensory and nutritional quality of poultry products. Their safety has been supported by toxicological and genomic assessments, and several phage-based products have obtained regulatory approval, including Generally Recognized as Safe (GRAS) status for food applications in the United States. By integrating efficacy, safety, regulatory, and practical deployment data, this review highlights bacteriophages as a scientifically validated and One Health–aligned tool capable of reducing Salmonella transmission from farm to fork across the poultry value chain, thereby laying the foundation for their future adoption in the poultry industry. Phage-based interventions offer a sustainable pathway to enhance food safety, limit antimicrobial resistance (AMR) dissemination, and strengthen consumer confidence in poultry products. However, the major limitation is the emergence of phage-resistant bacterial strains, as well as the potential involvement of some phages in the transfer of resistance and virulence genes, which could raise public concern. Nevertheless, the use of phage cocktails and whole-genome sequencing, involving tools such as ResFinder and virulence finder, can facilitate the selection of safe phages for application. Full article