Journal of Xenobiotics最新文献

Per- and polyfluoroalkyl substances (PFAS) are a global concern due to their persistence, ubiquity, and accumulation in living organisms. Found in soils, biosolids, water, and the food chain, they pose health risks such as hormone disruption, immune damage, reproductive issues, and cancer. Regulations mainly target older PFAS like PFOA and PFOS, while many newer PFAS, including breakdown products, are poorly understood in terms of distribution, behavior, and toxicity. To address this complex issue, this review offers a detailed overview of human exposure to PFAS and their toxic effects. It highlights biosolids as a key, understudied source of PFAS in the environment. The review also discusses limitations of testing, missing long-term cleanup data, and regulatory issues that neglect total exposure and vulnerable populations. Additionally, it evaluates, in the specific context of biosolids management, the effectiveness, scalability, benefits, and drawbacks of various treatment technologies, such as thermal processes (pyrolysis, incineration, smoldering combustion), advanced oxidation, adsorption, hydrothermal liquefaction, and biological degradation. This work combines environmental science, toxicology, and engineering to outline PFAS management in biosolids and proposes a research and policy plan. Focusing on regulating PFAS as a group, validating real-world results, and employing adaptable treatment strategies underscores the need for a coordinated, science-based effort to reduce PFAS risks worldwide.

Lead poisoning is a significant public health issue, contributing to 0.6% of the global disease burden and disproportionately affecting developing countries. Vulnerable populations, such as children, pregnant women, and low-income communities, remain at high risk, often exposed to lead levels exceeding safe thresholds. While the problem is global, this review focuses specifically on the Americas, regions with diverse regulatory landscapes and persistent environmental lead exposure. Regulatory frameworks vary widely, and the lack of global consensus on acceptable blood lead levels leaves important gaps in protection. This review compiles and updates knowledge on emerging sources of lead exposure in the region, evaluates advancements in regulatory approaches, and analyzes the molecular impacts of lead on human health. Using the Comparative Toxicogenomics Database (CTD), lead was found to interact with 3448 genes, including those linked to inflammation and oxidative stress, and is associated with 4401 diseases and 799 disrupted pathways. These findings emphasize the need for regionally tailored interventions, strengthened policies, and further research on its health impacts.

The global increase in municipal and industrial wastewater generation has intensified the need for ecologically resilient and technologically advanced treatment systems. Although traditional biological treatment technologies are effective for organic load reduction, they often fail to remove recalcitrant xenobiotics such as pharmaceuticals, synthetic dyes, endocrine disruptors (EDCs), and microplastics (MPs). Engineered microbial consortia offer a promising and sustainable alternative owing to their metabolic flexibility, ecological resilience, and capacity for syntrophic degradation of complex pollutants. This review critically examines emerging strategies for enhancing microbial bioremediation in wastewater treatment systems (WWTS), focusing on co-digestion, biofilm engineering, targeted bioaugmentation, and incorporation of conductive materials to stimulate direct interspecies electron transfer (DIET). This review highlights how multi-omics platforms, including metagenomics, transcriptomics, and metabolomics, enable high-resolution community profiling and pathway reconstructions. The integration of artificial intelligence (AI) and machine learning (ML) algorithms into bioprocess diagnostics facilitates real-time system optimization, predictive modeling of antibiotic resistance gene (ARG) dynamics, and intelligent bioreactor control. Persistent challenges, such as microbial instability, ARG dissemination, reactor fouling, and the absence of region-specific microbial reference databases, are critically analyzed. This review concludes with a translational pathway for the development of next-generation WWTS that integrate synthetic microbial consortia, AI-mediated biosensors, and modular bioreactors within the One Health and Circular Economy framework.

Wastewater treatment plant (WWTP) effluents can be important sources of contaminants of emerging concern (CEC) for riverine ecosystems, with some accumulation in sediments. This study investigated the ecotoxicological effects of sediment samples collected near three WWTPs. Sediment elutriates, simulating resuspension conditions, and whole sediment samples were tested. Results showed that sediments were toxic to some organisms and beneficial to others. Elutriates from one site significantly reduced luminescence in the bacterium Aliivibrio fischeri, though this was not consistently linked to sediment contaminant levels. Significant noxious effects of elutriates were recorded for the macrophyte Lemma minor (yield reductions up to 48%) and the microalgae Raphidocelis subcapitata (yield reductions up to 25%). Exposure to elutriates resulted in increased Daphnia magna reproduction and increased biomass yield of Chironomus riparius exposed to sediments directly. Overall, there were no major toxicity variations in samples collected upstream and downstream of the effluent outfall. Suggesting limited hazardous potential of the effluent and a potential masking effect of background contamination (mostly metals and polycyclic aromatic hydrocarbons). The complexity of effluent-sourced contamination, coupled with the realistic testing approach, renders this work a valuable contribution to understanding the role of WWTP effluents in surface freshwaters contamination and their effects, especially concerning CECs.

Particulate matter (PM), a complex mixture of solid particles and liquid droplets, originates from both natural sources, such as sand, pollen, and marine salts, and anthropogenic activities, including vehicle emissions and industrial processes. While PM itself is not inherently toxic in all its forms, it often acts as a carrier of xenobiotic toxicants, such as heavy metals and organic pollutants, which adhere to its surface. This combination can result in synergistic toxic effects, significantly enhancing the potential harm to biological systems. Due to its small size and composition, PM can penetrate deep into the respiratory tract, acting as a physical "shuttle" that facilitates the distribution and bioavailability of toxic substances to distant organs. The omnipresence of PM in the environment leads to unavoidable and constant exposure, contributing to increased morbidity and mortality rates, particularly among vulnerable populations like the elderly, children, and individuals with pre-existing health conditions. This exposure also imposes a substantial financial burden on healthcare systems, as treating PM-related illnesses requires significant medical resources and leads to higher healthcare costs. Addressing these challenges necessitates effective mitigation strategies, including reducing PM exposure, improving air quality, and exploring novel approaches such as AI-based exposure prediction and nutritional interventions to protect public health and minimize the adverse effects of PM pollution.

This study aimed to evaluate the cardioprotective effects of two different doses of saroglitazar (SAR) in an animal model of cardiotoxicity induced by 5-fluorouracil (5-FU). Thirty-five rats were randomly allocated into five groups: the negative control, which received distilled water; the 5-FU (150 mg/kg as I.P.) group; the N-acetylcysteine (100 mg/kg) group; and the SAR (0.5 and 5 mg/kg) groups. The last three groups received 5-FU on day 10 along with their treatment. An open field test was performed at zero-time and at the end of the study. On day eleven the animals were euthanized and blood samples were used for measuring troponin I, CK-MB, natriuretic peptide, lipid profile, LDH, ALT, AST, CRP, ESR, TNF-α, IL1β, MDA, and total antioxidant capacity (TAOC). Cardiac tissues were sent for histopathological examination. The study revealed that 5-FU elevated the levels of cardiac-specific and injury-related biomarkers, inflammatory and oxidative stress markers, and that the use of SAR, particularly the high dose, decreased all the cardiac- and other injury-related biomarkers as well as attenuating inflammatory and oxidative stress biomarkers. SAR-treated groups exhibited a significant increase in locomotor activity and a decrease in anxiety-like behavior, indicated by a reduction in time spent in one square and an increase in total movement time. Additionally, the histopathological findings greatly supported the biochemical results evidenced by stopping the detrimental effects caused by 5-FU through structural and functional alterations of cardiac tissues manifested as ameliorating congestion, inflammation, degeneration, arterial wall thinning, and endothelial loss. The dual-acting PPAR agonist SAR demonstrated cardiac protection activity, particularly the high dose, by attenuating cardiac-specific and nonspecific injury biomarkers along with anti-inflammatory and antioxidant activities and attenuated anxiety induced by 5-FU. These findings render SAR a promising candidate to be tested in clinical trials. Further studies are warranted with other cardiotoxicants to confirm these findings.

Antibiotics have played an evolving role in poultry production, generally transitioning from widespread use to more precise and controlled applications. Despite this shift, the long-term consequences of earlier practices continue to affect current and future generations. This review aims to explore the multifaceted consequences of antibiotic use in poultry production, with particular emphasis on the growing challenge of antimicrobial resistance (AMR). Evidence demonstrates that antibiotic use affects the gut microbiome, often resulting in long-lasting decreased diversity and restructuring of the bacterial communities. Moreover, consequences extend to the surrounding environment, including the airborne microbiome, water systems, and poultry litter, where alterations in microbial communities tend to be more subtle, whereas changes in genetic elements related to resistance are often more pronounced (drift). The emergence and persistence of resistance in these environments facilitate the spread of resistance genes across ecological boundaries, contributing to the broader dissemination of AMR. These findings highlight the complex, interconnected nature of AMR, underscoring the urgent need for responses grounded in the One Health framework. Such approaches are essential for safeguarding both public and environmental health while maintaining sustainable poultry production practices.

Urolithin (Uro)-B, a gut microbiota metabolite of ellagic acid, has recently gained considerable attention due to its beneficial bioactivities. This study investigated the potential hepatoprotective effect of Uro-B against alpha-naphthyl isothiocyanate (ANIT)-induced cholestatic liver injury (CLI) in mice and explored the possible involved mechanisms. Mice were treated with Uro-B (50 and 100 mg/kg) for four days and received ANIT (75 mg/kg) once on the second day. Our data revealed that Uro-B reduced elevated serum transaminases, alkaline phosphatase, lactate dehydrogenase, and total bilirubin levels associated with ANIT injection. Histopathologically, Uro-B effectively ameliorated ANIT-induced disruption of the hepatic architecture as represented by repressed necro-inflammation and bile duct proliferation. Uro-B also maintained oxidant/antioxidant status that was dysregulated by ANIT. Mechanistically, Uro-B markedly activated Kelch-like ECH-associated protein 1 (Keap-1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling with subsequent upregulation of hepatic heme oxygenase-1 expression. On the other hand, Uro-B suppressed the ANIT-induced expression of nuclear factor kappa-B (NF-κB), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Interestingly, Uro-B repressed peroxisome proliferator-activated receptor alpha (PPARα) expression in the liver. These findings indicate a promising hepatoprotective effect of Uro-B against ANIT-induced CLI in mice. Uro-B modulated the interplay between Keap1/Nrf2, NF-κB/TNF-α, and PPARα signaling pathways, resulting in powerful antioxidant and anti-inflammatory effects.

Dibutyl phthalate (DBP) is used as a plasticizer to enhance flexibility in several household products, cosmetics, and food-contact materials. Due to its harmful effects, DBP is restricted or banned in children's products and food items, particularly in Europe. Due to its endocrine disruptor properties and considering its ability to cross the placental barrier, it is imperative to study DBP's vascular effects in pregnancy, given the vulnerability of this period. Thus, this study investigated the potential effects of DBP on the cardiovascular system using umbilical arteries from healthy pregnant women. Specifically, the impact of DBP on the vascular reactivity after both rapid and 24 h DBP exposure was analyzed, as well as the contractility and the cell viability of vascular smooth muscle cells (VSMC). DBP did not exhibit overt cytotoxic effects on VSMCs, possibly due to its adsorption onto polystyrene surfaces, potentially limiting bioavailability. Interestingly, DBP induced vasorelaxation in a concentration-dependent manner. Although mechanistic insights remain to be fully elucidated, the results suggest the involvement of pathways associated with nitric oxide signaling and calcium handling. Overall, DBP exposure appears to modulate arterial tone regulation, which may have implications for vascular function during pregnancy.

Virgin coconut oil (VCO) has emerged as a functional food oil with considerable health benefits and wide applications in the food, pharmaceutical, and cosmetic industries due to its resident bioactive compounds, including lauric acid (LA). LA is the most abundant saturated medium-chain fatty acid in VCO and has been associated with several pharmacological activities. The literatures show the pharmacological effects of VCO and LA on chronic pathologies, infectious diseases, and metabolic disorders. A robust body of evidence shows that LA and other phenolic compounds are responsible for the VCO protection against toxicities and pharmacological efficacies. This review elucidates the anticancer mechanisms of VCO/LA and their modulation of the chemotherapy-induced side effect toxicity. VCO, LA, and their nanomaterial/encapsulated derivatives promote ROS generation, antiproliferation, apoptosis, cell cycle arrest, the inhibition of metastasis, and the modulation of cancer-related signaling pathways for cancer cell death in vivo and in vitro. VCO mitigates oxidative inflammation and apoptosis to block the underlying mechanisms of the side effect toxicity of chemotherapy. However, the possible beneficial effect of LA on the toxicity of chemotherapy is currently unknown. The available evidence emphasizes the anticancer effect and mechanism of VCO and LA, and the VCO potential to combat adverse side effects of chemotherapy. Thus, VCO and LA are potential adjuvant therapeutic agents in the management of various cancers. Nevertheless, future studies should be targeted at elucidating cancer-related molecular mechanisms to bridge the gap in knowledge.