Aflatoxins (AFs) are one of the most toxic mycotoxins that can easily contaminate agricultural products and have adverse effects on both humans and animals. To understand the AF contamination in maize in Gansu Province and the risk of dietary exposure, LC-MS was used to determine the AFs in maize in Gansu Province in accordance with national standards. The results showed that the concentration range of AFs detected in maize was ND ∼15.9 μg/kg, and the detection rates of AFB1, AFB2, AFG1 and AFG2 were 13.3%, 5%, 6.7% and 4.2%, respectively. The estimated daily intake and margin of exposure (MOE) for infants, children, adolescents, and adults were 0.00575-0.0197 µg/kg bw/d, and 69.56-20.34, respectively. The consumption of maize may have adverse health effects in all age groups studied as all calculated MOEs were less than 10,000.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, stemming from a complex interplay of genetic, environmental, and lifestyle factors. Aflatoxin B1 (AFB1), a prevalent food contaminant, is a known HCC risk factor, but its molecular mechanisms remain incompletely understood. This study investigated the contribution of BUB1B, a crucial spindle assembly checkpoint regulator, in AFB1-induced hepatocyte malignant transformation, we assessed AFB1's impact on cell proliferation, viability, cell cycle regulation, and BUB1B expression. BUB1B knockdown via siRNA revealed its role in epithelial-mesenchymal transition (EMT), cell motility, and proliferation. AFB1 exposure significantly altered cell proliferation and cell cycle dynamics, correlating with increased BUB1B expression. Furthermore, we identified a significant interaction between BUB1B and the IL12A-JAK2/STAT4 signaling pathway, suggesting a mechanism for immune evasion and tumor progression. These findings highlight BUB1B's critical role in AFB1-induced hepatocarcinogenesis and establish its potential target for HCC. Further research is needed to fully elucidate the underlying molecular mechanisms and explore the therapeutic implications of BUB1B inhibition in HCC treatment.

Rutin, a dietary flavonoid, exhibits anti-inflammatory, antioxidant, and immunomodulatory properties. The underlying mechanism of protection of rutin against Aflatoxin B1 (AFB1)-induced immunotoxicity is not completely elucidated. This study investigated the protective effect of rutin against Aflatoxin B1 (AFB1)-induced immunotoxicity in male Wistar rats, supported by molecular docking and dynamics simulations.

Forty male Wistar rats were grouped into five: control (corn oil), AFB1 (0.75 mg/kg bwt), AFB1 (1.5 mg/kg bwt), rutin (50 mg/kg bwt), and AFB1 (1.5 mg/kg bwt) + Rutin (50 mg/kg bwt) orally for 30 days.

AFB1 exposure increased (p < 0.05) oxidative and inflammatory markers, altered hematological indices, and caused histological damage in the spleen and bone marrow. Elevated indoleamine 2,3-dioxygenase (IDO) activity, reduced CD4+ T cells, and unchanged tryptophan 2,3-dioxygenase (TDO) activity were also observed. Docking revealed strong binding affinities for AFB1 (-9.5 kcal/mol), rutin (-9.7 kcal/mol), and AFB1-rutin (-10.4 kcal/mol) with IDO. Rutin co-treatment restored oxidative, inflammatory, and hematological indices, mitigated histological damage, and normalized CD4+ T cells and IDO activity, as supported by computational studies.

The activities/expression of immunosuppressive indoleamine 2, 3-dioxygenase is mostly regulated by inflammation and oxidative stress. This study provides new insights into the mechanisms underlying the modulation of immunotoxicity of AFB1 by dietary rutin.

In environmental toxicology, aflatoxin B1 (AFB1) is recognized for its detrimental effects on reproductive and intestinal health. This study elucidates how AFB1-induced elevations in stearoyl ethanolamide (SEA) and homocysteine (HCY) impact male fertility and intestinal function in mice. AFB1 was found to markedly reduce sperm concentration and exacerbate sperm damage in mice, primarily by increasing serum SEA and HCY levels. These metabolites compromise testicular structure and function, disrupt the blood-testicular barrier, and downregulate critical testicular proteins including DAZL, SYCP1, SYCP2, StAR, and CYP17A1. Transcriptomic analysis revealed that SEA and HCY broadly alter testicular gene expression, activate NOD-like receptor signaling pathways, induce testicular inflammation, and promote apoptosis. Additionally, SEA and HCY impair intestinal barrier function by reducing the expression of tight junction proteins ZO-1 and Occludin. Functional network analysis indicated that SEA and HCY regulate intestinal immune responses by promoting M1 macrophage polarization and the upregulation of pro-inflammatory cytokines, while simultaneously inhibiting anti-inflammatory factors. This study underscores the multifaceted adverse effects of SEA and HCY on male reproductive health and gut integrity, and highlights the need for further research into mechanisms and potential interventions to mitigate these harmful outcomes.

Mycotoxins are potent triggers of hepatocellular carcinoma (HCC) due to their intricate interplay with cellular macromolecules and signaling pathways. This study integrates machine learning and biomolecular analyses to elucidate the mechanisms underlying mycotoxin-induced hepatocarcinogenesis. Using a data set of 1767 mycotoxins and 1706 non-mycotoxin fungal metabolites, we evaluated 51 machine learning models. The KPGT model achieved optimal performance with an ROC-AUC of 0.979 and balanced accuracy of 0.930. Clustering analysis identified six distinct mycotoxin clusters with unique structural features. Network toxicology analysis revealed distinct protein-protein interaction patterns across different mycotoxin clusters, identifying key regulatory proteins including EGFR, SRC, and ESR1. GO enrichment analysis uncovered cluster-specific effects on protein complexes and macromolecular assemblies, particularly in membrane organization and vesicular transport. KEGG pathway analysis demonstrated systematic perturbation of major signaling cascades, with each mycotoxin cluster distinctly modulating protein kinase networks and receptor tyrosine kinase pathways. Molecular docking analyses validated these interactions, with binding affinities ranging from -9.6 to -4.7 kcal/mol. Notably, cluster 5 showed strong binding to SRC (-9.6 kcal/mol), EGFR (-9.5 kcal/mol), and ESR1 (-7.8 kcal/mol), providing structural insights into toxin-macromolecule recognition. These findings enhance our understanding of mycotoxin-protein interactions in HCC development and suggest potential therapeutic strategies targeting these macromolecular interfaces.

Aflatoxins are potent carcinogens and pose significant risks to food safety and public health worldwide. Aflatoxins include Aflatoxin B1 (AFB1), Aflatoxin B2 (AFB2), Aflatoxin G1 (AFG1), Aflatoxin G2 (AFG2), and Aflatoxin M1 (AFM1). AFB1 is particularly notorious for its carcinogenicity, classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC). Chronic exposure to aflatoxins through contaminated food and feed can lead to liver cancer, immunosuppression, growth impairment, and other systemic health issues. Efforts to mitigate aflatoxin contamination have traditionally relied on chemical treatments, physical separation methods, and biological degradation. However, these approaches often pose challenges related to safety, efficacy, and impact on food quality. Recently, cold plasma treatment has emerged as a promising alternative. Cold plasma generates reactive oxygen species, which effectively degrade aflatoxins on food surfaces without compromising nutritional integrity or safety. This review consolidates current research and advancements in aflatoxin detoxification, highlighting the potential of cold plasma technology to revolutionize food safety practices. By exploring the mechanisms of aflatoxin toxicity, evaluating existing detoxification methods, and discussing the principles and applications of cold plasma treatment.

Aflatoxin B1 (AFB1) is common in the diets of humans and animals and often leads to adverse health effects. Propolis, with its strong antioxidant activity, can reduce oxidative stress and modulate gut microbiota composition. However, the underlying mechanism by which propolis alleviates AFB1-induced intestinal barrier damage remains unclear. This study was designed to investigate the protective effects of oral propolis supplementation in AFB1-exposed rats. Thirty-two male Sprague-Dawley rats were divided into four groups: control, AFB1, propolis, and AFB1+propolis. After 4 weeks, serum oxidative stress markers were examined, and gut microbiota was analyzed by 16S rRNA sequencing. Intestinal sections were processed by Hematoxylin & Eosin staining, and the expression level of tight junction proteins was assessed by immunostaining. Propolis supplementation in AFB1-exposed rats tended to decrease oxidative stress, and it also restructured the gut microbiota by preventing a decrease in the relative abundances of Lactobacillus, Roseburia, and Phascolarctobacterium. Propolis restored intestinal permeability impaired by AFB1 by ameliorating intestinal morphological damage and increasing the expression levels of tight junction proteins. Propolis supplementation may contribute to the modulation of gut microbiota by alleviating oxidative stress and improving intestinal barrier damage in AFB1-exposed rats.

Aflatoxins, particularly aflatoxin B1 (AFB1), are potent mycotoxins adversely affecting poultry performance, health, and product quality. Mitigation strategies are critical for poultry productivity. This study assessed the efficacy of Prosopis farcta biochar and Lactobacillus fermentum in mitigating AFB1-induced toxicity in quails, with a focus on performance, antioxidant status, and product quality. Two experiments were conducted with quails during growing (7-35 days) and laying (70-98 days) periods under five dietary treatments: Negative Control (basal diet), Positive Control (AFB1-contaminated diet), and AFB1 diets supplemented with Mycofix Plus, biochar, or biochar combined with L. fermentum. Growth performance, antioxidant status, meat and egg quality, and liver enzyme activity were evaluated. AFB1 significantly impaired performance, reduced meat and egg quality, and elevated oxidative stress and liver enzymes (P < 0.01). Supplementation with biochar, particularly in combination with L. fermentum, significantly alleviated these effects, improving body weight, glutathione peroxidase activity, and reducing malondialdehyde and liver enzyme levels (P < 0.01). Biochar and its combination with L. fermentum effectively mitigated aflatoxicosis in quails, enhancing health and productivity metrics. Integrating biochar and L. fermentum in poultry diets is a promising approach to managing mycotoxin challenges, improving economic and product quality outcomes in poultry systems.

Exposure to aflatoxin (AF) triggers the production of inflammatory molecules and free radicals, leading to chronic inflammation, cancer, and neurodegenerative diseases. This systematic review evaluated the effects of AFB1 on the nervous system, particularly focusing on Alzheimer's disease (AD). A comprehensive search was conducted in Scopus, Cochrane Library, PubMed, and Web of Science databases up to 1 June 2024, without restrictions. From 993 records retrieved, 16 articles were included in the systematic review. AFB1 participates in various biochemical processes and pathological conditions. The study highlights that AFB1 contributes to AD by inducing DNA damage, oxidative stress, and endoplasmic reticulum (ER) stress, impairing DNA repair mechanisms. This results in neuronal damage, cognitive decline, and neurodegeneration. AFB1 also affects key signaling pathways, reduces sodium-potassium pump activity, and disrupts cell cycle regulation involving p53, leading to neurotoxicity, inflammation, and the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles. Additionally, network analysis revealed 309 genes associated with AD, inflammation, angiopathy, and aflatoxin B1 (AFB1). Among these, ESR1 exhibited the highest number of direct connections to other nodes within the network. The gene TP53 played a pivotal role in mediating communication among genes, while the EP300 gene significantly influenced the overall network structure. Additionally, KEGG enrichment analysis demonstrated that these 309 genes are substantially involved in pathways related to cancer, the FoxO signaling pathway, apoptosis, and AD. In summary, the study highlights that AFB1 causes DNA damage and stress, leading to cognitive decline and neurodegeneration. It disrupts signaling pathways, damages neurons, and affects DNA repair, contributing to neurotoxicity and inflammation. PROSPERO registration number: CRD420250651007.

Aflatoxin B1 (AFB1) exhibits significant toxicity and pose a serious threat to food safety, environmental hygiene, and public health even in trace amounts. Hence, the development of a rapid, accurate, and sensitive detection technology has become a pivotal aspect of ensuring control standards. In this study, we introduce the UIO66 and two defective dichloroacetic acid@UIO66 (DCA@UIO66, DU) metal-organic framework nanoparticles, named DU1 and DU2, characterized by different defect levels. It is noteworthy that DU1 exhibits superior DNA sensing capability compared to UIO66 and DU2. With a fluorescence quenching efficiency of 92.66 % and a recovery efficiency of 1256.75 %, DU1 demonstrates the substantial potential in the detection field. Furthermore, we employ cascade isothermal amplification to assist DU1-mediated fluorescence sensors in detecting AFB1. AFB1 is efficiently identified through an aptamer competition process facilitated by magnetic nanoparticles, which initiates the exponential amplification triggered rolling circle amplification reaction, and converts trace amounts of toxin signal into a large number of long single-stranded DNA molecules. Upon recognition of the amplification product by the fluorescent probe on DU1, a more stable double-stranded DNA is formed and leaves the surface of DU1, leading to a significant change in fluorescence intensity. This method exhibits acceptable sensitivity, with a detection limit of 0.09 pg mL-1 and a wide detection range spanning from 0.2 pg mL-1 to 20 pg mL-1. Additionally, this assay exhibits satisfactory specificity and high accuracy in practical sample applications. Our proposed method offers a solid theoretical framework and technical backing, thereby facilitating the establishment of a new generation of mycotoxin detection standards.

The photodegradation of aflatoxins G1 and G2 (AFG1 and AFG2) is crucial for mitigating the health risks associated with these potent mycotoxins, as it enhances food safety and protects human health by reducing their persistence and bioavailability in contaminated environments. This study investigates the efficient photodegradation of AFG1 and AFG2 using a novel Bimetallic MIL-53 (Al, Ni)/ZnO nanoparticle composite as a photocatalyst. The catalyst was synthesized in two stages: Chemical synthesis of zinc oxide nanoparticles (ZnO NPs) and hydrothermal synthesis to form the composite. Optimization of a ZnO-based photocatalyst, synthesized by varying proportions of NiCl₂·6H₂O and Al(NO₃)₃·9H₂O, revealed that a 0.547 g:0.864 g ratio maximized photocatalytic degradation of AFG1 and AFG2. Through experimental design, the degradation process was optimized, identifying pH 4.1, 109 mg of photocatalyst, 35 mg L-1 of AF concentration, and 3 mM of H2O2 concentration as optimal conditions. The predicted removal efficiencies for AFG1 and AFG2 were 97.43% and 98.69%, respectively. Kinetic studies utilizing the pseudo-first-order rate equation revealed rate constants of 0.058 ± 0.002 and 0.060 ± 0.003 min-1 for AFG1 and AFG2, respectively. Additionally, the half-life times for AFG1 and AFG2 photodegradation were found to be 11.95 and 11.55 min, respectively. Catalyst reuse investigations demonstrated that the composite could be reused at least 5 times without significant loss of efficacy. These findings highlight the effectiveness of the Bimetallic MIL-53 (Al, Ni)/ZnO NPs composite as a stable and efficient photocatalyst for the removal of AFG1 and AFG2 under mild conditions, showcasing its potential for practical applications in environmental remediation processes.

Aflatoxin B1 (AFB1), a mycotoxin commonly present in feed, has several toxic effects. AFB1 seems to have a neurotoxic effect that leads to neurobehavioral impairment. On the other hand, Lutein and Zeaxanthin (LUT/ZEA) have antioxidant and anti-inflammatory effects. Here, we aimed to compare the effects of AFB1 and the co-treatment with LUT/ZEA on neurobehavioural and biochemical changes viz-a-viz oxido-inflammatory response in male rats' hippocampal and pre-frontal cortexes. Experimental rats of the Wistar strain (n = 40) were randomly grouped into treatment cohorts: Control (corn oil 2 mL/kg), AFB1 (75 μg/kg), LUT/ZEA only (100 mg/kg), AFB1 + LUT/ZEA (75 μg/kg + 100 mg/kg), and AFB1 + LUT/ZEA (75 μg/kg + 200 mg/kg). All groups were administered their respective treatment orally for 28 days, while behavioural tests were conducted using open field tests (OFT), Y-maze, novel object tests (NORT), and forced swim tests (FST) 1 h after treatment on day 26-28. The animals were euthanized on day 29. In the hippocampal and pre-frontal cortex, antioxidant indicators (SOD, CAT, GSH, GST, GPx, TSH), inflammatory mediators (XO, NO, MPO), and acetylcholinesterase activity were measured. Our finding presents the anti-oxidant effect of lutein/Zeaxanthin in the brains of AFB1-intoxicated rats, indicating better cognitive and spatial memory capacity in Y-maze and NORT, an improvement in locomotive and explorative behaviour in OFT and reduction in anxio-depressive-like behaviour in LUT/ZEA co-treated rats. Acetylcholinesterase activity was enhanced in LUT/ZEA co-treated rats. LUT/ZEA co-treatment dampened oxido-inflammatory mediators by decreasing XO, NO, and MPO levels and increasing antioxidant activities (SOD, CAT, GSH, GST, GPx, TSH) in the prefrontal and hippocampal cortices. We surmise that mechanistically, co-treatment with LUT/ZEA effectively lessened AFB1 neurotoxicity through anti-inflammatory and antioxidant pathways and essentially improved the experimental rats' neurobehavioural outcomes.

Processed jujube products are susceptible to contamination by fungi such as Aspergillus spp., which produces mycotoxins that could lead to health problems in consumers. In this study, 58 samples of processed jujube products (including 5 types such as dried jujubes) were collected from different markets in Shihezi (Xinjiang, China). The fungal diversity and the fungi isolated from processed jujube products were systematically analyzed through high-throughput sequencing and molecular biological identification (based on the ITS and/or BenA and CaM regions). In total, the 105 strains of fungi were isolated and identified as belonging to the dominant genera were Aspergillus, Cladosporium, Alternaria, and Penicillium. High-throughput sequencing indicated that Alternaria, Didymella, Cladosporium, and Aspergillus were the dominant fungi in processed jujube products. ELISA showed that A. flavus produced about 19.3862-21.7583 μg/L, 6.5309-11.0411 μg/L, 0-15.4407 μg/L, 0-5.6354 μg/L, and 0-6.0545 μg/L of AFT, AFB1, AFB2, AFM1, and AFM2, respectively. In addition, concentrations of OTA produced by A. niger, A. tubingensis, and A. ochraceus were found to range from 5.2019 to 18.5207 μg/L. Therefore, the separation of Aspergillus with good mycotoxin-producing abilities from processed jujube products poses a latent threat to consumer health.

Accurate and rapid aflatoxin B1 (AFB1) detection is essential for ensuring the safety of food supplies. In this paper, we introduce a distance-readout paper-based microfluidic chip (DPMC) that offers a sensitive and reliable method for the detection of AFB1. The DPMC comprises a DNA hydrogel sensitive valve and a paper-based capillary channel. Upon exposure to AFB1, the hydrogel valve regulates the flow speed of the tested liquid into the capillary channel. Quantitative detection of AFB1 can be achieved without the need for complex instrumentation for external equipment by visually observing the distance traveled by the tested liquid through the capillary channel over a specified period. Under optimal conditions, the DPMC allows for quantitative detection of AFB1 solution concentrations ranging from 100 to 1000 pM by the naked eye, with a detection limit of 17.64 pM. This method has been successfully employed for quantitative detection of AFB1 in lotus seed samples, yielding a recovery rate between 85.2% and 118.4%. This approach provides a rapid, portable, sensitive, and highly selective visualization platform for on-site AFB1 detection.

The distribution of major causes of liver cancer (LC) in the United States (US) has changed significantly over time. This study analyzes recent temporal trends in the causes of LC in the US from 1990 to 2021 and predicts future trends.

We obtained detailed data on LC in the US from the Global Burden of Disease (GBD) 2021 study. Estimated annual percentage change (EAPC) values for LC in the US were then calculated using linear regression models. An exponential smoothing (ES) projection model and Bayesian Age-Period-Cohort (BAPC) projection model were then used to predict the future disease burden of LC. Risk factors for LC were also assessed.

In 2021, the disease burden of LC in the US was significantly higher than in 1990. Hepatitis C virus (HCV)-associated LC resulted in the greatest burden of disease. The fastest growing burden of disease was attributed to metabolic dysfunction-associated steatotic liver disease (MASLD)-associated LC. Higher burdens of disease were seen in older and male populations.

In the US, the disease burden of LC from different etiologies continues to rise. As such, targeted prevention and control strategies should be developed to address these unique disease characteristics.

Environmental pollutants significantly impact liver disease development, progression, and outcomes. This review examines the complex relationship between environmental exposures and liver pathology, from malignant conditions like hepatocellular carcinoma to steatotic and cholestatic liver diseases. Key environmental factors include air pollutants, volatile organic compounds, persistent organic pollutants, heavy metals, and per- and polyfluoroalkyl substances. These compounds can act through multiple mechanisms, including endocrine disruption, metabolic perturbation, oxidative stress, and direct hepatotoxicity. The impact of these exposures is often modified by factors such as sex, diet, and genetic predisposition. Recent research has revealed that even low-level exposures to certain chemicals can significantly affect liver health, particularly when combined with other risk factors. The emergence of exposomics as a research tool promises to enhance our understanding of how environmental factors influence liver disease. Importantly, exposure effects can vary by demographic and socioeconomic factors, highlighting environmental justice concerns. Implementation of this knowledge in clinical practice requires new diagnostic approaches, healthcare system adaptations, and increased awareness among medical professionals. In conclusion, this review provides a comprehensive examination of current evidence linking environmental exposures to liver disease and discusses implications for clinical practice and public health policy.

Aflatoxin B1 (AFB1) exposure often causes serious food safety problems and illnesses in humans and animals, even at extremely low content. Therefore, effective degradation of AFB1 is vitally significant. Biodegradation by enzymes is an effective method to eliminate hazardous toxins, but the degradation efficiency and cost of the enzyme limit its wide application. In this work, we found that CotA derived from Bacillus subtilis can rapidly degrade AFB1 into small molecules with low toxicity. Molecular docking analysis was used to evaluate the feasibility of rapid degradation of AFB1 by CotA, and the UPLC-Q-TOF-MS was used to deduce the degradation products and pathways. Two biotransformation pathways were proposed based on the structures of these degradation products. Inspired by commercial Ni-NTA purification media, Ni-grafted magnetic nanoparticles (PNMP) were designed to capture CotA from cell-lysis buffer onto the PNMP surface, enabling direct immobilization of CotA to form PNMP@CotA. The PNMP@CotA exhibits higher activity, good tolerance to temperature and pH than free CotA. Furthermore, in vitro and in vivo experiments revealed a significant reduction in the toxicity of AFB1 degradation products.

Aflatoxins, known for their carcinoginc properties and produced by Aspergillus fungi, pose a substantial threat to public health, particularly in regions with hot and humid climates, where individuals are exposed to these toxins through contaminated food. The primary objective of this study was to assess the extent of aflatoxin exposure in the Emirate of Sharjah employing Aflatoxin M1 (AFM1) as a biomarker in urine samples from adult participants. Furthermore, this study aimed to explore the relationship between dietary habits and AFM1 levels in order to establish a potential link.

In a cross-sectional study design, a total of 144 adults (73 females and 71 males) were recruited for participation. The urine samples obtained from participants were subjected to analysis for AFM1 concentrations utilizing the enzyme-linked immunosorbent assay (ELISA) method. Additionally, structured questionnaires were administered to collect information on the dietary and lifestyle habits of the participants. To explore the relationship between dietary factors and AFM1 levels, various statistical analyses, including linear regression and the Mann-Whitney U test, were performed.

AFM1 was detected in 69 % of the samples under invstigation, wherein males exhibited a higher mean level (0.912 ng/mg creatinine) in comparison to females (0.676 ng/mg creatinine). The overall mean concentration of AFM1 was determined to be 0.792 ng/mg creatinine. It is worth noting that there was a significant correlation between rice consumption and heightened AFM1 exposure among males, while no such correlation was observed among females.

This study conducted in the UAE provides novel perspectives on aflatoxin exposure, shedding light on the gender-specific correlation between rice consumption and aflatoxin levels among males. These findings hold significant implications for guiding public health interventions and underscore the pivotal role of ongoing surveillance and stringent food safety regulations in mitigating the hazards associated with aflatoxin contamination.

Aflatoxin B1 (AFB1) is a prevalent contaminant in food and feed matrices, known for its hepatotoxic effects. Its metabolic breakdown generates reactive oxygen species (ROS), leading to oxidative stress and subsequent liver damage. Mitigating oxidative stress is, therefore, essential for ameliorating the hepatocellular damage and systemic toxicity caused by AFB1. Here, we synthesized arginine carbon dots (Arg-CDs) with robust antioxidant properties through a simple hydrothermal method using arginine and citric acid. Our investigation demonstrated that Arg-CDs effectively mitigate oxidative stress in nematodes. Furthermore, in murine models of AFB1-induced hepatic injury, Arg-CDs effectively restored liver function, as evidenced by the improvement in histopathological features and biochemical markers. Notably, Arg-CDs administration upregulated the transcriptional activity of nuclear factor erythroid 2-related factor 2 (Nrf2), along with its downstream antioxidant effectors and phase II detoxifying enzymes under AFB1 exposure. Moreover, Arg-CDs alleviated hepatic inflammatory injury by modulating the NLRP3/Caspase-1/GSDMD-mediated pyroptosis pathway. Arg-CDs also demonstrated therapeutic potential in enhancing intestinal barrier function in AFB1-exposed mice. Collectively, these findings highlight the potential of Arg-CDs as a novel and biocompatible therapeutic modality for alleviating AFB1-induced hepatic and intestinal damage.

Aflatoxin B1 (AFB1) exhibits hepatotoxic properties in both humans and animals. Contradictory findings regarding corticosterone suggest that it may either aggravate AFB1 toxicity or reduce its Lethal Dose 50 % (LD50), potentially through the role of the glucocorticoid receptor (GR). Additionally, microRNAs (miRNAs) are known to modulate the toxic effects of AFB1. Nevertheless, whether the modulation of GR-targeting miRNAs can alleviate AFB1-induced hepatotoxicity has not been thoroughly investigated. This study examined the expression of GR and its associated microRNAs in AFB1-induced hepatotoxicity in mice, using GR-targeting antagomirs to mitigate AFB1 toxicity. AFB1 exposure elicited liver inflammation and oxidative stress in mice, while also reducing detoxification capacity. Notably, a decrease in GR protein expression was observed in liver tissue and hepatocytes. Additionally, miR141-3p, miR200a-3p, miR384-5p, miR183-5p, miR181a-5p, and miR181b-5p were upregulated and identified as regulators of GR expression. AFB1 induced cytotoxicity in AML12 cells, as evidenced by decreased GR protein levels and increased expression of miR141-3p, miR200a-3p, and miR495-3p. Inhibition of miR141/200a/495-3p reduced AFB1-induced cytotoxicity in AML12 cells. Furthermore, GR-targeting antagomirs (antagomir141/200a/495-3p) alleviated AFB1-induced hepatotoxicity in mice. This study highlights potential therapeutic targets for AFB1-induced liver diseases and offers new insights into strategies to mitigate the harmful effects of aflatoxin exposure.

Aflatoxin B1 (AFB1) is a prevalent environmental and forage contaminant that poses significant health risks to both humans and livestock due to its toxic effects on various organs and systems. Among its toxicological effects, nephrotoxicity is a hallmark of AFB1 exposure. However, the precise mechanisms underlying AFB1-induced kidney damage in donkeys remain poorly understood. To investigate this, we established a donkey model exposed to AFB1 by administering a diet supplemented with 1 mg AFB1/kg for 30 days. Kidney apoptosis was assessed using TUNEL staining, while gene expression and protein levels of Endonuclease G (EndoG), as well as genes related to endoplasmic reticulum (ER) stress and apoptosis, were quantified by RT-qPCR and Western blotting. Our findings indicate that AFB1 exposure resulted in significant kidney injury, apoptosis, and oxidative stress. Notably, AFB1 exposure upregulated the expression of EndoG and promoted its translocation to the ER, which subsequently induced ER stress and activated the mitochondrial apoptotic pathway. These results suggest that AFB1-induced kidney damage in donkeys is mediated through the oxidative stress and mitochondrial apoptosis pathways, primarily involving the EndoG-IRE1/ATF6-CHOP signaling axis.

Exploring the toxicity and metabolic mechanisms of aflatoxin B1 (AFB1) in ruminants can help to develop strategies to prevent or reduce the transfer of the toxin and its metabolites to milk and meat. This study aimed to explore the effects of 3 concentrations of dietary AFB1 (0, 50, and 500 μg/kg) on hepatic injury and metabolism in Saanen goats via histological examination, western blot analysis, as well as integrated multiomics techniques. Eighteen Saanen goats were assigned to 1 of 3 treatments and the AFB1 challenge lasted for 14 d. Results showed that the liver tissue was enlarged and the relative organ index of the liver was linearly increased with elevated AFB1 levels. The hepatocyte apoptosis rate was significantly increased after AFB1 exposure, and the western blotting results revealed that both the external apoptotic pathway and mitochondrial-mediated intrinsic apoptotic pathway might be involved in AFB1-induced hepatocyte apoptosis. We identified 251, 269, and 154 significant differentially expressed genes (DEG) and 340, 596, and 127 significant differential metabolites in comparisons between the control (CON; 0 μg/kg) and low-dose (LO; 50 μg/kg) groups, the CON and high-dose (HI; 500 μg/kg) groups, and the LO and HI groups, respectively. The DEG annotated were mainly involved in the cell part, cell, single-organism process, cellular process, binding, and other functional categories. The identified metabolites primarily belonged to glycerophospholipids, prenol lipids, carboxylic acids, and derivatives. Integrative analysis of transcriptomics and metabolomics revealed that glycerophospholipids metabolism and choline metabolism in cancer were the most affected pathways related to AFB1 exposure. The identified differential metabolites, DEG, and pathways might have played a crucial role in the hepatic injury induced by AFB1 in goats.

Aflatoxin (AF) is a toxic metabolite produced by the fungus Aspergillus. The various subtypes of AFs include B1, B2, G1, G2, M1, and M2, with Aflatoxin B1 (AFB1) being the most toxic. These AFs are widespread in the environment, particularly in soil and food crops. The World Health Organization (WHO) has classified AFB1 as a highly potent natural Class 1A carcinogen. Excessive exposure to AFB1 can lead to poisoning in both humans and animals, posing substantial risks to food safety and livestock breeding industries. This review provides an overview of the metabolic processes, detection methods, and the detrimental impacts of AFB1 on animal reproduction, immunity, nerves, intestines, and metabolism. Furthermore, it explores the preventive and control capacities of natural active substances, trace elements, and microorganisms against AFB1. Ultimately, this paper serves as a reference for further research on the pathogenic mechanism of AFB1, the development of preventive drugs, and the selection of effective detoxification measures for AFB1 in animal feed.

In this review, we explore the application of next-generation sequencing in liver cancer research, highlighting its potential in modern oncology. Liver cancer, particularly hepatocellular carcinoma, is driven by a complex interplay of genetic, epigenetic, and environmental factors. Key genetic alterations, such as mutations in TERT, TP53, and CTNNB1, alongside epigenetic modifications such as DNA methylation and histone remodeling, disrupt regulatory pathways and promote tumorigenesis. Environmental factors, including viral infections, alcohol consumption, and metabolic disorders such as nonalcoholic fatty liver disease, enhance hepatocarcinogenesis. The tumor microenvironment plays a pivotal role in liver cancer progression and therapy resistance, with immune cell infiltration, fibrosis, and angiogenesis supporting cancer cell survival. Advances in immune checkpoint inhibitors and chimeric antigen receptor T-cell therapies have shown potential, but the unique immunosuppressive milieu in liver cancer presents challenges. Dysregulation in pathways such as Wnt/β-catenin underscores the need for targeted therapeutic strategies. Next-generation sequencing is accelerating the identification of genetic and epigenetic alterations, enabling more precise diagnosis and personalized treatment plans. A deeper understanding of these molecular mechanisms is essential for advancing early detection and developing effective therapies against liver cancer.

It has been known since the early days of the discovery of aflatoxin B1 (AFB1) that there were large species differences in susceptibility to AFB1. It was also evident early on that AFB1 itself was not toxic but required bioactivation to a reactive form. Over the past 60 years there have been thousands of studies to delineate the role of ~10 specific biotransformation pathways of AFB1, both phase I (oxidation, reduction) and phase II (hydrolysis, conjugation, secondary oxidations, and reductions of phase I metabolites). This review provides a historical context and substantive analysis of each of these pathways as contributors to species differences in AFB1 hepatoxicity and carcinogenicity. Since the discovery of AFB1 as the toxic contaminant in groundnut meal that led to Turkey X diseases in 1960, there have been over 15,000 publications related to aflatoxins, of which nearly 8000 have addressed the significance of biotransformation (metabolism, in the older literature) of AFB1. While it is impossible to give justice to all of these studies, this review provides a historical perspective on the major discoveries related to species differences in the biotransformation of AFB1 and sets the stage for discussion of other papers in this Special Issue of the important role that AFB1 metabolites have played as biomarkers of exposure and effect in thousands of human studies on the toxic effects of aflatoxins. Dr. John Groopman has played a leading role in every step of the way-from initial laboratory studies on specific AFB1 metabolites to the application of molecular biomarkers in epidemiological studies associating dietary AFB1 exposure with liver cancer, and the design and conduct of chemoprevention clinical trials to reduce cancer risk from unavoidable aflatoxin exposures by alteration of specific AFB1 biotransformation pathways. This article is written in honor of Dr. Groopman's many contributions in this area.

This study focuses on the integration of a custom-built and optimally trained YOLO v5 model into a smartphone app developed with Java language. A dual-modal immunochromatographic rapid detection system based on a deep learning strategy for smartphones was developed for grade determination and predicting the concentration of aflatoxin B1 (AFB1). Innovative distance-type quantum dot microsphere fluorescent immunochromatographic chips enable semi-quantitative analysis by naked eye, and conventional colloidal gold nanoparticle colorimetric strips were also prepared. The compact and versatile hardware device making it easily integrable into smartphones of varying dimensions. Moreover, the wireless charging functionality of smartphones was to tackle power supply challenges. After optimized training, the accuracy, mAP@0.5, precision, and recall metrics of the YOLO v5 model all soared to 98 %. For the dual-modal immunochromatographic chips, the R2 values for the standard curve fits were as high as 0.993, with a broad linear range of 0.05-40 ng/mL and a standard deviation lower than 0.03 at each concentration. Finally, this system determined the grade of the AFB1 concentration with an accuracy of up to 98 % and it exhibited an ultra-sensitive quantitative detection capability with a limit of detection as low as 2.2 pg/mL, showcasing the reliability of the deep learning strategy for practical applications in smartphones. This robust technological foundation paves the way for potentially community-based, family-oriented, and personalized applications.

Groundnuts are considered as one of the most important cultivated food crops globally. Groundnuts are used for vegetable oil production, which generate a variety of by-products, such as peanut press cake (PPC). Groundnuts are sensitive to infection by aflatoxigenic fungi. Aflatoxins are highly toxic to both humans and livestock, and contaminated crops containing high aflatoxin concentrations are deemed unsafe for consumption and trade. Innovative aflatoxin management strategies are needed and the insect production sector could be such a solution. Larvae of the black soldier fly (BSFL) were exposed to a PPC diet naturally contaminated with aflatoxins. After an exposure lasting eleven days, data on larval survival and biomass were collected. The PPC, BSFL and the residual material were analysed by LC-MS/MS to determine the concentration of eight different aflatoxins. A bio-accumulation factor and a molar mass balance were calculated. BSFL survival and biomass were not affected by exposure to the aflatoxin-contaminated PPC diet. The aflatoxins did not accumulate in the insect body, providing a promising outlook for the safety of rearing insects on aflatoxin contaminated PPC with the purpose of using them as food- and/or feed. Aflatoxin B1 (AFB1) was the dominant compound found in PPC. Formation of aflatoxicol, aflatoxin P1, and aflatoxin M1 occurred and taking these metabolites into account, a complete molar mass balance, thus full recovery, for AFB1 was obtained. This differs from previous studies using artificially spiked substrates in which 17-38% was recovered. This calls for additional studies comparing naturally contaminated with artificially spiked feedstuff.

Date (Phoenix dactylifera L.) seeds (PDL) have recently evoked significant attention for their therapeutic potential against numerous diseases. Aflatoxin B1 (AFB1) is an inevitable environmental hazard that pollutes foods and may harm the heart. This study investigated the beneficial effect of PDL against cardiac toxicity induced by AFB1 in male offspring. Female albino rats received PDL (200 mg/kg) orally for 14 days before mating till weaning and AFB1 (50 μg/kg) intramuscularly throughout gestation and lactation. At postnatal day 60, male offspring hearts were collected. Compared to AFB1 intoxicated group, PDL-treated offspring displayed improved cardiac biomarkers, an increase in their antioxidant defense, and a decrease in the cardiac proinflammatory cytokines. Additionally, a reduction in the expression levels of Bcl2 and Nrf2 was observed, with genes linked to increased cardiac caspase-3, Bax, ACE1, P53, and cytochrome C levels. In conclusion, PDL acts as a potential adjuvant agent for ameliorating cardiac toxicity and apoptosis resulting from exposure to AFB1. This is attributed to its antioxidative and anti-inflammatory effects, as well as its capacity to sequester free radicals within cardiac tissue.

Aflatoxins (AFTs) are a form of mycotoxins mainly produced by Aspergillus flavus and Aspergillus parasiticus, which are common contaminants in various agricultural sources such as feed, milk, food, and grain crops. Aflatoxin B1 (AFB1) is the most toxic one among all AFTs. AFB1 undergoes bioactivation into AFB1-8,9-epoxide, then leads to diverse harmful effects such as neurotoxicity, carcinogenicity, hepatotoxicity, reproductive toxicity, nephrotoxicity, and immunotoxicity, with specific molecular mechanisms varying in different pathologies. The detoxification of AFB1 is of great importance for safeguarding the health of animals and humans and has increasingly attracted global attention. Recent research has shown that melatonin supplementation can effectively mitigate AFB1-induced multiple toxic effects. The protection mechanisms of melatonin involve the inhibition of oxidative stress, the upregulation of antioxidant enzyme activity, the reduction of mitochondrial dysfunction, the inactivation of the mitochondrial apoptotic pathway, the blockade of inflammatory responses, and the attenuation of cytochrome P450 enzymes' expression and activities. In summary, this review sheds new light on the potential role of melatonin as a potential detoxifying agent against AFB1. Further exploration of the precise molecular mechanisms and clinical efficacy of this promising treatment is urgently needed.

In this study, we developed a colloidal gold immunochromatographic strip (CGIS) method that used the matrix-matched calibration curves of contamination ratio models to quantitatively determine the total aflatoxin in five herbal medicines. This approach addresses issues related to false results and poor accuracy associated with conventional methods. The CGIS was analyzed using a Vertu touch reader, and the matrix-matched calibration was established based on the absorbance ratios of the T and C lines, as well as the logarithmic values of the total aflatoxin concentrations. The total aflatoxins could be accurately and digitally detected from 2.5 to 40 μg/kg, and the LOD of total aflatoxins was 1 μg/kg in the five herbal medicines. The recovery rates from the spiked samples ranged from 65.1% to 98.6%, and the RSD was less than 16.9%. A total of 229 samples were analyzed by both CGIS and HPLC-FLD, with agreement ranging from 78.4% to 132.6% (Arecae semen), 82.6% to 133.0% (Nelumbinis semen), 79.9% to 117.9% (Coicis semen), 78.1% to 119.0% (Platycladi semen), and 76.1% to 123.0% (Ziziphi spinosae semen). This process for the discrimination of the CGIS results was established to assess if samples met the requirement of aflatoxin limits, which could save approximately 75% in time and reduce the workload of retesting by a designated confirmatory reference method to less than 10%. This study demonstrated that the application of matrix-matched calibration curves based on contamination ratio models to CGIS can effectively enhance the rapid quantitative determination capability of total aflatoxins in herbal medicine matrices.

Aflatoxin B1 (AFB1) a mycotoxin found in chicken feed that possess a global hazard to poultry health. However different potent compounds like bovine lactoferrin (bLF) may prove to be protective effects against AFB1. This study aims to explore the protective effect of bLF against AFB1-induced injury in the liver and kidney in broiler. For this purpose, 600 broilers chicks were randomly alienated into 5 groups (n = 120 each): negative control; positive control (3 mg/kg AFB1), and bLF high, medium, and low dosage groups (600 mg/kg, 300 mg/kg, and 150 mg/kg, respectively). The results highlight that AFB1 toxicity in birds exhibited low feed intake, reduction in weight gain, and a decrease in FCR while, bLF regulated these adverse effects. Meanwhile, AFB1 group showed higher levels of alanine transaminase (ALT) and aspartate aminotransferase (AST) and lower levels of superoxide dismutase (SOD) and glutathione (GSHpx) in liver, while urea and creatinine were decline in kidney. Supplementation with bLF effectively controlled these biomarkers and control the negative effects of toxicity. Furthermore, hematoxylin and eosin (H&E) staining exhibited normal morphological structures within liver and kidney in the bLF treated groups, while degenerative changes were observed in AFB1 group. Similarly, bLF, decreased oxidative stress and thus prevented apoptosis in the liver and kidney cells of the birds. Whereas, mRNA level of mitochondrial apoptosis related gene including Bcl-2 (Bak and Bax), caspase-3 and caspase-9 was upregulated, while bcl2 gene were downregulated in AFB1 group. Dietary supplementation of bLF effectively normalizes the expression of these genes. AFB1 exposed birds shown to decrease gene expression level of the crucial component of Nrf2 pathway, responsible to regulate antioxidant defense. Interestingly, bLF reverse these detrimental effects of and restore the normal expression levels of Nrf2 pathway. Conclusively, our findings demonstrate that bLF mitigates the detrimental effects of AFB1, besides regulation of the apoptosis-related genes via mitochondrial pathways. These findings validate that the bLF (600 mg/kg) could be used as protective agent against AFB1-induced liver and kidney damage.

The incidence of multiple-organ cancers has recently increased due to simultaneous exposure to various environmental carcinogens. Houttuynia cordata Thunb. (H. cordata) is recognized for its many health benefits, including its anti-cancer properties. The fermentation of its leaves has been shown to significantly enhance the bioflavonoid content and its bioactivities. This study aimed to evaluate the effectiveness of fermented H.cordata leaf (FHCL) extracts against combined carcinogens and investigate the underlying mechanisms. The crude ethanolic extract of FHCL was partitioned to obtain hexane- (HEX), dichloromethane- (DCM), ethyl acetate- (ETAC), butanol- (nBA), and residue fractions. The crude ethanolic extract (200-250 μg/mL) and the DCM fraction (50 μg/mL) significantly reduced NO production in RAW264.7 macrophages. In addition, the crude extract and the DCM and ETAC fractions showed anti-genotoxicity against aflatoxin B1 and 2-amino-3,4-dimethylimidazo [4,5-f]quinoline (MeIQ) in Salmonella typhimurium assays (S9+). Despite demonstrating genotoxicity in the Salmonella mutation assay (with and without S9 activation), oral administration of the crude extract at 500 mg/kg of body weight (bw) for 40 days in rats did not induce micronucleated hepatocytes, indicating that the extract is non-genotoxic in vivo. Moreover, the crude extract significantly decreased Phase I but increased Phase II xenobiotic-metabolizing enzyme activities in the rats. Next, the anti-cancer effects of FHCL were evaluated in a dual-organ carcinogenesis model of the colon and liver in rats induced by 1,2-dimethylhydrazine (DMH) and diethylnitrosamine (DEN), respectively. The crude extract significantly reduced not only the number and size of glutathione S-transferase placental form positive foci in the liver (at doses of 100 and 500 mg/kg bw) but also the number of aberrant crypt foci in rat colons (at 500 mg/kg bw). Furthermore, FHCL significantly reduced the expression of proliferating cell nuclear antigen (PCNA) in the colon (at 100 and 500 mg/kg bw) and liver (at 500 mg/kg bw) of the treated rats. In conclusion, FHCL exhibits significant preventive properties against colon and liver cancers in this dual-organ carcinogenesis model. Its mechanisms of action may involve anti-inflammatory effects, the prevention of genotoxicity, the modulation of xenobiotic-metabolizing enzymes, and the inhibition of cancer cell proliferation. These findings support the use of FHCL as a natural supplement for preventing cancer.

The substances that cause abnormal DNA structures are known as DNA damage-inducing factors, and their resulting DNA damage has been extensively studied and proven to be closely related to cancer, neurodegenerative diseases, and aging. Prolonged exposure to DNA damage-inducing factors can lead to a variety of difficult-to-treat diseases, yet these factors have not been well summarized. It is crucial to use a combination of environmental science and life science to gain a deep understanding of the environmental sources and biological consequences of DNA damage-inducing factors for mechanistic research and prevention of diseases such as cancer. This article selected 14 representative carcinogenic exogenous DNA damage-inducing factors and summarized them through a literature search, including both exogenous and endogenous DNA damage factors, and explored the types of DNA damage caused by the relevant damage factors.

Mycotoxins are toxic secondary metabolites produced by various types of fungi that are known to contaminate various food products; their presence in the food chain poses significant risks to human and animal health and leads to enormous economic losses in the food and feed industry worldwide. Ensuring food safety and quality by detoxifying mycotoxin is therefore of paramount importance. Several procedures to control fungal toxins have been extensively investigated, such as preventive measures, physical and chemical methods, and biological strategies. In recent years, microbial degradation of mycotoxins has attracted much attention due to its reliability, efficiency, and cost-effectiveness. Notably, bacterial species from the Bacillus genus have emerged as promising candidates for mycotoxin decontamination owing to their diverse metabolic capabilities and resilience in harsh environmental conditions. This review manuscript aims to provide a summary of recent studies on the biodegradation of fungal toxins by Bacillus bacteria, thereby illustrating their potential applications in the development of mycotoxin-degrading products.

Mycotoxins have strong immunotoxicity and can induce oxidative stress and mitochondrial dynamics imbalance. Mitochondrial antiviral signaling protein (MAVS) in the RIG-I like receptor (RLR) pathway of innate immunity is located on mitochondria, and whether it is affected by mycotoxins has not been reported yet. This experiment used porcine alveolar macrophages (PAM) to evaluate the antagonism of three isomers of chlorogenic acid (chlorogenic acid, isochlorogenic acid A, and neochlorogenic acid) against combined mycotoxins (Aflatoxin B1, Deoxynivalenol, and Ochratoxin A) induced mitochondrial damage and their effects on the RLR pathway, providing assistance for further elucidating the mechanism of mycotoxin immunotoxicity. Western blotting, enzyme linked immunosorbent assay (ELISA), and flow cytometry were used to detect relevant indicators. All three types of chlorogenic acid treatment can antagonize the cytotoxicity induced by combined mycotoxins, especially isochlorogenic acid A, which can protect cells from mycotoxins damage by maintaining mitochondrial dynamic homeostasis and improving innate immune function related to the RLR pathway.

Endoplasmic reticulum stress (ERS) is a prominent etiological factor in the pathogenesis of diabetes. Nevertheless, the mechanisms through which ERS contributes to the development of diabetes remain elusive.

Transcriptional expression profiles from the Gene Expression Omnibus (GEO) datasets were analyzed and compared to obtain the differentially expressed genes (DEGs) in T2DM. Following the intersection with ERS associated genes, the ERS related T2DM DEGs were identified. Receiver operating characteristic (ROC) and Least Absolute Shrinkage and Selection Operator (LASSO) analysis were performed to screen out the ERS related biomarker genes and validate their diagnostic values. Gene expression level was detected by qPCR and Elisa assays in diabetic mice and patient serum samples.

By analyzing the transcriptional expression profiles of the GEO datasets, 49 T2DM-related DEGs were screened out in diabetic islets. RTN1, CLGN, PCSK1, IAPP, ILF2, IMPA1, CCDC47, and PTGES3 were identified as ERS-related DEGs in T2DM, which were revealed to be involved in protein folding, membrane composition, and metabolism regulation. ROC and LASSO analysis further screened out CLGN, ILF2, and IMPA1 as biomarker genes with high value and reliability for diagnostic purposes. These three genes were then demonstrated to be targeted by the transcription factors and miRNAs, including CEBPA, CEBPB, miR-197-5p, miR-6133, and others. Among these miRNAs, the expression of miR-197-5p, miR-320c, miR-1296-3P and miR-6133 was down-regulated, while that of miR-4462, miR-4476-5P and miR-7851-3P was up-regulated in diabetic samples. Small molecular drugs, including D002994, D001564, and others, were predicted to target these genes potentially. qPCR and Elisa analysis both validated the same expression alteration trend of the ERS-related biomarker genes in diabetic mice and T2DM patients.

These findings will offer innovative perspectives for clinical diagnosis and treatment strategies for T2DM.

A column-free immunoaffinity purification (CFIP) technique for sample preparation of aflatoxin B1 (AFB1) was developed using an AFB1-specific nanobody (named G8) and an elastin-like polypeptide (ELP). The reversible phase transition between liquid and solid in response to temperature changes was exhibited by the ELP which was derived from human elastin. The G8 was tagged with ELPs of various lengths (20, 40, 60, and 80 repeat units) at the C-terminus using recursive directional ligation (RDL). Coding sequences were then subcloned into pET30a at the multiple cloning sites. Bioactive recombinant proteins were produced by expressing them as inclusion bodies in Escherichia coli BL21 (DE3), then dissolved and refolded. Analysis by indirect competitive enzyme-linked immunosorbent assay (icELISA) and transition temperature (Tt) measurement confirmed that the refolded G8-ELPs preserved the ability to recognize AFB1 as well as phase transition when the temperature rose above Tt. To establish the optimal conditions for cleaning AFB1, the effects of various parameters on recovery were investigated. The recovery in ELISA tests was 95 ± 3.67% under the optimized CFIP workflow. Furthermore, the CFIP-prepared samples were applied for high-performance liquid chromatography (HPLC) detection. The recovery in the CFIP-HPLC test ranged from 54 ± 1.86% to 98 ± 3.58% for maize, rice, soy sauce, and vegetable oil samples. To the best of our knowledge, this is the first report combining the function of both nanobody and ELP to develop a cleanup technique for small molecules in a complex matrix. The CFIP for the sample pretreatment was easy to use and inexpensive. In contrast to conventional immunosensitivity materials, the reagent utilized in the CFIP was entirely biosynthesized without any chemical coupling reactions. This suggests that the nanobody-ELP may serve as a useful dual-functional reagent for the development of sample cleaning or purification methods.

Versicolorin A (VERA) is a mycotoxin produced by Aspergillus section Flavi species that is frequently detected in foodstuffs, particularly in corn. VERA is a precursor of aflatoxin B1 (AFB1), which is currently considered to be the most hazardous mycotoxin. While AFB1 has been shown to impair oxidative phosphorylation (OXPHOS), the impact of VERA on mitochondrial function has not been extensively documented until now. The aim of the present study was to investigate the effect of VERA on mitochondrial function in intestinal Caco-2 cells. To this end, OXPHOS was assessed by measuring the oxygen consumption rate using the Seahorse™ real-time analyzer. In contrast to AFB1, a low concentration of VERA (5 µM) was a strong uncoupler of OXPHOS and inhibited respiratory complexes I and III within a few minutes of exposure. After 24 h of exposure, VERA reduced the transcription of all mitochondrial genes encoding proteins involved in the electron transfer chain as well as decreasing the rate of OXPHOS. This effect was associated with the simultaneous down expression of two genes encoding proteins involved in the initiation phase of mitochondrial DNA transcription: POLRMT and TFB2M. Moreover, VERA induced down expression of genes coding for upstream key glycolytic enzymes, hexokinase and phosphofructokinase. These effects led to a reduced rate of ATP production associated with a cytotoxic effect. Given the significant implications of mitochondrial dysfunction for human health, it is crucial to consider the potential involvement of VERA in mitochondrial diseases.

Laccase mediators possess advantage of oxidizing substrates with high redox potentials, such as aflatoxin B1 (AFB1). High costs of chemically synthesized mediators limit laccase industrial application. In this study, thin stillage extract (TSE), a byproduct of corn-based ethanol fermentation was investigated as the potential natural mediator of laccases. Ferulic acid, p-coumaric acid, and vanillic acid were identified as the predominant phenolic compounds of TSE. With the assistance of 0.05 mM TSE, AFB1 degradation activity of novel laccase Glac1 increased by 17 times. The promoting efficiency of TSE was similar to ferulic acid, but superior to vanillic acid and p-coumaric acid, with 1.2- and 1.3-fold increases, respectively. After Glac1-TSE treatment, two oxidation products were identified. Ames test showed AFB1 degradation products lost mutagenicity. Meanwhile, TSE also showed 1.3-3.0 times promoting effect on laccase degradation activity in cereal flours. Collectively, a safe and highly efficient natural mediator was obtained for aflatoxin detoxification.

Aflatoxin B1 (AFB1) is a mycotoxin which is responsible for severe damage to the immune system of humans and livestock. Licochalcone A (Lico A), a polyphenol derived from turmeric, has attracted great attention due to its wonderful antioxidant properties. Ferroptosis, an iron-dependent cell death related to oxidative stress, which plays a crucial role in the resistance of phytochemical to immune-associated injury. Nevertheless, effects of Lico A on the bursa of broilers exposed to AFB1 remain unclear. In this work, broilers were fed diets supplemented with 2 mg/kg of AFB1 and 50 mg/kg of Lico A. Meanwhile, various concentrations of Lico A and AFB1 (15 μM) were used to stimulate macrophages. These results revealed that AFB1 resulted in more severe bursa atrophy and relative weight reduction; the expression of pro-ferroptosis protein ACSL4 and the content of malondialdehyde (MDA) were significantly elevated, while the expression of anti-ferroptosis proteins GPX4, xCT, FSP1 and the content of Glutathione (GSH) was obviously reduced. However, Lico A treatment effectively reversed these effects in the bursa of broilers. Meanwhile, in bursa and macrophages, Lico A mitigated the expression of AFB1-induced apoptosis-associated protein (Caspase-3, Bax, Bcl-2) as well as antioxidant protein (Nrf2, GCLM, HO-1). Importantly, ferroptosis was also observed in macrophages induced by AFB1. Lico A efficaciously alleviated AFB1-induced mitochondrial membrane potential decrease and reactive oxygen species (ROS) production in macrophages; in contrast, Lico A evidently inhibited AFB1-triggered ROS generation and cytotoxicity, which was disabled by the addition of Erastin. Moreover, Liproxstatin-1 significantly inhibited ROS generation induced by AFB1. In summary, the present study elucidates that the main mechanism by which Lico A attenuates AFB1-induced immunotoxicity is through the suppression of ferroptosis, apoptosis, mitochondrial damage and oxidative stress, which is promising for the improvement of immunotoxic effects of AFB1.

Liver cancer, particularly hepatocellular carcinoma (HCC), poses a significant global health challenge due to its high mortality rate. Hepatocellular carcinoma and intrahepatic cholangiocarcinoma (ICC) are the two main types of primary liver cancer (PLC), each with its own set of complexities. Secondary or metastatic liver cancer is more common than PLC. It is frequently observed in malignancies such as colorectal, pancreatic, melanoma, lung, and breast cancer. Liver cancer is often diagnosed at an advanced stage, making it difficult to treat. This highlights the need for focused research on early detection and effective treatment strategies. This review explores the epidemiology, risk factors, and diagnostic techniques for HCC. The development of HCC involves various risk factors, including chronic liver diseases, hepatitis B and C infections, alcohol consumption, obesity, smoking, and genetic predispositions. Various invasive and non-invasive diagnostic techniques, such as biopsy, liquid biopsy, and imaging modalities like ultrasonography, computed tomography scans (CT scans), magnetic resonance imaging (MRI), and positron emission tomography (PET) scans, are utilized for HCC detection and monitoring. Advances in imaging technology and biomarker research have led to more accurate and sensitive methods for early HCC detection. We also reviewed advanced research on emerging techniques, including next-generation sequencing, metabolomics, epigenetic biomarkers, and microbiome analysis, which show great potential for advancing early diagnosis and personalized treatment strategies. This literature review provides insights into the current state of liver cancer diagnosis and promising future advancements. Ongoing research and innovation in these areas are essential for improving early diagnosis and reducing the global burden of liver cancer.

Aflatoxin B1 (AFB1) is recognized as the most toxic mycotoxin, widely present in nature and known to specifically target the liver, leading to severe consequences to animal and human health. The mechanisms underlying AFB1-induced hepatotoxicity involve oxidative stress and apoptosis. Radix Bupleuri (RB) and its extracts (RBE), traditional Chinese herbs with a rich history spanning over 2000 years, have been reported to possess hepatoprotective properties. Nevertheless, the impact of RBE on AFB1-induced liver injury remains to be fully elucidated. The current study utilized Pekin ducks as experimental models to explore the effects of RBE on AFB1-induced liver injury both in vitro and in vivo. In vitro findings indicated that RBE mitigated AFB1-induced cytotoxicity, improved primary duck hepatocytes (PDHs) morphology, and reduced intracellular reactive oxygen species (ROS) levels. In vivo experiments demonstrated that: I) RBE alleviated the growth inhibitory caused by AFB1, as evidenced by improved final body weight and weight gain. II) AFB1 led to significant alterations in serum biochemical parameters (AST, ALT, TP, and ALB) and liver lesions attenuated by RBE supplementation at 2.5 g/kg. III) RBE significantly mitigated oxidative stress induced by AFB1. IV) AFB1-induced changes in mRNA and protein levels associated with oxidative stress and apoptosis were counteracted by RBE. In conclusion, our results suggest that RBE offers protection against AFB1-induced liver injury in ducks, primarily through its antioxidative and anti-apoptotic properties. These findings indicate the potential of RBE in preventing and treating AFB1 poisoning.