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Exposure to PM2.5 is the most significant air pollutant for health risk. The testosterone level in male is vulnerable to environmental toxicants. In the past, researchers focused more attention on the impacts of PM2.5 on respiratory system, cardiovascular system, and nervous system, and few researchers focused attention on the reproductive system. Recent studies have reported that PM2.5 involved in male testosterone biosynthesis disruption, which is closely associated with male reproductive health. However, the underlying mechanisms by which PM2.5 causes testosterone biosynthesis disruption are still not clear. To better understand its potential mechanisms, we based on the existing scientific publications to critically and comprehensively reviewed the role and potential mechanisms of PM2.5 that are participated in testosterone biosynthesis in male. In this review, we summarized the potential mechanisms of PM2.5 triggering the change of testosterone level in male, which involve in oxidative stress, inflammatory response, ferroptosis, pyroptosis, autophagy and mitophagy, microRNAs (miRNAs), endoplasmic reticulum (ER) stress, and N6-methyladenosine (m6A) modification. It will provide new suggestions and ideas for prevention and treatment of testosterone biosynthesis disruption caused by PM2.5 for future research. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells have made remarkable progress in recent years. Many studies have reported that human umbilical cord mesenchymal stem cells (hUC-MSCs) have no toxicity, but thromboembolism appeared in patients treated with hUC-MSCs. Therefore, people are still worried about the safety of clinical application. The study aims to determine the safety, potential toxic mechanism and biodistribution of hUC-MSCs. F344RG rats were given 5 or 50 million cells/kg of hUC-MSCs by single administration in compliance with Good Laboratory Practice standards. Standard toxicity was performed. RNA sequencing was then performed to explore the potential toxic mechanisms. In parallel, the biodistribution of hUC-MSCs was examined. The dose of 5 million cells/kg hUC-MSCs had no obvious toxicity on symptom, weight, food intake, hematology, serum biochemistry, urine biochemistry, cytokines, and histopathology. However, blood-tinged secretions in the urethral orifice and 20% mortality occurred at 50 million cells/kg. Disseminated intravascular coagulopathy (DIC) is the leading cause of death. hUC-MSCs significantly upregulated complement and coagulation cascade pathways gene expression, resulting in DIC. Besides, hUC-MSCs upregulated fibrinolytic system suppressor genes A2m, Serping1 and Serpinf2. hUC-MSCs survived in rats for less than 28 days, no hUC-MSC was detected in tissues outside the lungs. There was no toxicity in F344RG rats at 5 million cells/kg, but some toxicities were detected at 50 million cells/kg. hUC-MSCs significantly upregulated complement and coagulation cascade pathways, upregulated the expression of fibrinolytic system suppressor genes A2m, Serping1 and Serpinf2, to inhibit fibrinolytic system, caused DIC, which provided a new insight into the toxic mechanism of hUC-MSCs. [ABSTRACT FROM AUTHOR]

Epsilon toxin (ETX), a potential agent of biological and toxic warfare, causes the death of many ruminants and threatens human health. It is crucial to understand the toxic mechanism of such a highly lethal and rapid course toxin. In this study, we detected the effects of ETX on the proteome and phosphoproteome of MDCK cells after 10 min and 30 min. A total of 44 differentially expressed proteins (DEPs) and 588 differentially phosphorylated proteins (DPPs) were screened in the 10 min group, while 73 DEPs and 489 DPPs were screened in the 30 min group. ETX-induced proteins and phosphorylated proteins were mainly located in the nucleus, cytoplasm, and mitochondria, and their enrichment pathways were related to transcription and translation, virus infection, and intercellular junction. Meanwhile, the protein–protein interaction network screened out several hub proteins, including SRSF1/2/6/7/11, SF3B1/2, NOP14/56, ANLN, GTPBP4, THOC2, and RRP1B. Almost all of these proteins were present in the spliceosome pathway, indicating that the spliceosome pathway is involved in ETX-induced cell death. Next, we used RNAi lentiviruses and inhibitors of several key proteins to verify whether these proteins play a critical role. The results confirmed that SRSF1, SF3B2, and THOC2 were the key proteins involved in the cytotoxic effect of ETX. In addition, we found that the common upstream kinase of these key proteins was SRPK1, and a reduction in the level of SRPK1 could also reduce ETX-induced cell death. This result was consistent with the phosphorylated proteomics analysis. In summary, our study demonstrated that ETX induces phosphorylation of SRSF1, SF3B2, THOC2, and SRPK1 proteins on the spliceosome pathway, which inhibits normal splicing of mRNA and leads to cell death. [ABSTRACT FROM AUTHOR]

Herb-induced liver injury (HILI) shows a high incidence rate and has great impacts on the clinical medication safety of traditional Chinese medicine and the healthy development of the industry. In recent years, the research on HILI has attracted wide attention and made remarkable progress, and related clinical diagnosis and treatment guidelines have been formulated and updated by the academic organizations in China and globally. This article compares the recent guidelines on HILI formulated by different organizations and elaborates on the main achievements in terms of mechanism of toxicity, clinical diagnosis and disease assessment, risk factors, and clinical prevention and treatment, and it also proposes the unmet needs, the research difficulties that need to be taken seriously, and possible prevention and treatment strategies. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is an important environmental pollutant that poses a threat to human health and represents a critical component of air pollutants, food sources, and cigarette smoke. Cd is a known carcinogen and has toxic effects on the environment and various organs in humans. Heavy metals within an organism are difficult to biodegrade, and those that enter the respiratory tract are difficult to remove. Autophagy is a key mechanism for counteracting extracellular (microorganisms and foreign bodies) or intracellular (damaged organelles and proteins that cannot be degraded by the proteasome) stress and represents a self-protective mechanism for eukaryotes against heavy metal toxicity. Autophagy maintains cellular homeostasis by isolating and gathering information about foreign chemicals associated with other molecular events. However, autophagy may trigger cell death under certain pathological conditions, including cancer. Autophagy dysfunction is one of the main mechanisms underlying Cd-induced cytotoxicity. In this review, the toxic effects of Cd-induced autophagy on different human organ systems were evaluated, with a focus on hepatotoxicity, nephrotoxicity, respiratory toxicity, and neurotoxicity. This review also highlighted the classical molecular pathways of Cd-induced autophagy, including the ROS-dependent signaling pathways, endoplasmic reticulum (ER) stress pathway, Mammalian target of rapamycin (mTOR) pathway, Beclin-1 and Bcl-2 family, and recently identified molecules associated with Cd. Moreover, research directions for Cd toxicity regarding autophagic function were proposed. This review presents the latest theories to comprehensively reveal autophagy behavior in response to Cd toxicity and proposes novel potential autophagy-targeted prevention and treatment strategies for Cd toxicity and Cd-associated diseases in humans. [ABSTRACT FROM AUTHOR]

Copyright of China Surfactant Detergent & Cosmetics (2097-2806) is the property of China Surfactant Detergent & Cosmetics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Fusarium is one of the most important plant pathogens in the world, affecting plant growth and development and posing a serious threat to global food security and biodiversity. Almost all Fusarium species produce fungal toxins, which are diverse and highly toxic. On the one hand, they can participate in the pathogenic process of Fusarium as one of the pathogenic factors, and on the other hand, they can contaminate food and feed, leading to related diseases in humans and animals. Previous studies have shown that different types of mycotoxins produced by Fusarium infection not only poison plant cells and cause necrosis of plant tissues, but also accelerate the infection of pathogenic fungi. At the same time, in response to the mycotoxins produced by pathogenic fungi, plants activate defense enzymes and initiate the expression of defense related genes, or convert the pathogenic factors into non-toxic or low toxic substances and transport them out of the cell, or directly inhibit the biosynthesis of pathogenic mycotoxins by secreting secondary metabolites. To comprehensively analyze the role of Fusarium mycotoxin in pathogen infection of plants and improve their resistance to pathogens, this article reviews the types, toxicity mechanisms, and roles of mycotoxins in the interaction between plants and pathogens in Fusarium. It also discusses the defense response strategies of plants to mycotoxins, with an aim to provide references for future research on the pathogenic mechanism and pathogen control strategies of Fusarium mycotoxins.

Microcystin-LR (MC-LR) is a toxin produced by cyanobacteria, which is widely distributed in eutrophic water bodies and has multi-organ toxicity. Previous cytotoxicity studies have mostly elucidated the effects of MC-LR on intracellular-related factors, proteins, and DNA at the molecular level. However, there have been few studies on the adverse effects of MC-LR on cell ultrastructure and function. Therefore, research on the cytotoxicity of MC-LR in recent years was collected and summarized. It was found that MC-LR can induce a series of cytotoxic effects, including decreased cell viability, induced autophagy, apoptosis and necrosis, altered cell cycle, altered cell morphology, abnormal cell migration and invasion as well as leading to genetic damage. The above cytotoxic effects were related to the damage of various ultrastructure and functions such as cell membranes and mitochondria. Furthermore, MC-LR can disrupt cell ultrastructure and function by inducing oxidative stress and inhibiting protein phosphatase activity. In addition, the combined toxic effects of MC-LR and other environmental pollutants were investigated. This review explored the toxic targets of MC-LR at the subcellular level, which will provide new ideas for the prevention and treatment of multi-organ toxicity caused by MC-LR. [ABSTRACT FROM AUTHOR]

Copyright of Guangdong Agricultural Sciences is the property of South China Agricultural University, Guangdong Academy of Agricultural Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Patulin, a toxic secondary metabolite of fungi, exists widely and stably in fruits, vegetables, grains, nuts and Chinese medicinal materials. Patulin enters the body through skin contact or food intake, posing a great threat to the health of humans and animals. Previous studies have shown that patulin can induce genotoxicity, immunotoxicity and reproductive toxicity, damaging the intestine, kidney, liver and other organs in the body. The toxic mechanism of patulin involves inducing damage to biological macromolecular structures, oxidative stress injury and cell autophagy as well as damaging intestinal flora homeostasis. In this article, the recent status of patulin contamination in foods is reviewed, with an emphasis on the latest progress in research on the toxicity and mechanism of action of patulin. It is hoped that this review will provide a theoretical basis for patulin detoxification.

Silver nanoparticles (AgNPs) are widely used in daily life and industry because of their excellent antibacterial properties. AgNPs can exist in wastewater in various forms, such as Ag+, Ag2SO4, Ag2CO3, Ag2S, Ag2O, and AgCl. To assess the potential environmental risk of AgNPs and various forms of Ag, their toxic effects were investigated using the common denitrifier species Pseudomonas stutzeri (P. stutzeri). The inhibitory effect of AgNPs and various forms of Ag on P. stutzeri growth and its denitrification performance occurred in a concentration-dependent manner. The denitrification efficiency of P. stutzeri decreased from 95%∼97% to 89∼95%, 74∼95%, and 56∼85% under low, medium, and high exposure doses, respectively, of AgNPs and various forms of Ag. The changes in cell membrane morphology and increases in lactate dehydrogenase (LDH) release indicated that AgNPs and various forms of Ag damaged the cell membrane of P. stutzeri. Oxidative stress caused by excessive accumulation of reactive oxygen species (ROS) increased superoxide dismutase (SOD) and catalase (CAT) activities and decreased glutathione (GSH) levels. Overall, this study will help elucidate the impact of AgNPs and their transformation products on nitrogen removal efficiency in wastewater biological treatment systems.

Abstract Background Agricultural products are frequently co-contaminated by mycotoxins and pesticides. Most studies have only focused on the single toxicities of these chemicals, while their combined effects are neglected. Therefore, we investigated the combined toxic effects of T-2 toxin (T-2) and propiconazole (PRO) on zebrafish (Danio rerio). Results Our data exhibited that T-2 had higher toxicity to embryonic fish (96-h LC50 value of 0.39 mg a.i. L−1) than PRO (96-h LC50 value of 17.16 mg a.i. L−1). The mixture of T-2 and PRO showed an acute synergistic effect on zebrafish. Meanwhile, indicators associated with oxidative stress (SOD, Mn-sod, and cat) displayed significant variations in most exposures to T-2 and PRO mixtures (MTP) compared with the single exposures. The expressions of apoptosis-related genes cas3 and cas9 were also substantially elevated in the high-dose MTP exposure compared with the corresponding T-2 exposure. Besides, the expressions of endocrine system-related genes (TRβ, tsh, crh, cyp19a, and vtg1) were markedly varied in most MTP exposures compared with the corresponding single exposures. Our present results suggested that the mixture of T-2 and PRO could cause enormous effects on oxidative stress, cellular apoptosis, and the hypothalamic–pituitary–thyroid/hypothalamic–pituitary–gonadal (HPG/HPT) axis of zebrafish. Conclusions Our results provided new insights into the development of combined pollution standards for agricultural products. Taken together, the impact of the combined effects could be considered and regulated as priorities.

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Nano-tungsten carbide (nano-WC) is widely used in composite materials due to its special physical and chemical properties. Owing to their small size, nano-WC nanoparticles easily enter organisms through the respiratory tract, which may cause health hazards. However, only a few studies have reported the toxicity of nano-WC. In this study, a 10 mg/kg nano-WC suspension and 0.9% normal saline were quantitatively perfused into the lungs of two groups of healthy male SD rats by tracheal instillation, and the in vivo pulmonary toxic effects were systematically evaluated. Additionally, as multiple organs and tissues are involved, systemic effects were observed throughout the body and mainly manifested as inflammatory damage. The concentrations of tungsten ions in various organs and alveolar lavage fluid were measured by ICP–MS, and the results showed that the lung was the target organ, as it had the highest concentration of ions. In addition, the abnormal increases in the tungsten ion concentrations in the liver and kidney may be closely related to the immune damage we observed. This study provides a theoretical basis and data support for the systematic evaluation of the health hazards of nano-WC and a reference for the safe use of nanomaterials. • The in vivo toxicity of nano-WC was systematically evaluated by rat experiments. • Systemic effects were observed and mainly manifested as inflammatory damage. • The concentrations of tungsten ions were measured by ICP–MS. [ABSTRACT FROM AUTHOR]

The interplay between pesticides plays a critical role in ecotoxicology since these chemicals rarely emerge as single substances but rather in mixtures with other chemicals. In the present work, we purposed to clarify the combined toxic impacts of pyraclostrobine (PYR) and metiram (MET) on the zebrafish by using numerous indicators. Results exhibited that the 4-day LC50 value of MET to fish embryos was 0.0025 mg a.i. L−1, which was lower compared with PYR (0.019 mg a.i. L−1). Combinations of PYR and MET presented a synergetic impact on fish embryos. Contents of POD, CYP450, and VTG were drastically increased in the plurality of the single and joint treatments relative to the baseline value. Three genes, including vtg1, crh, and il-8, related to the endocrine and immune systems, were also surprisingly up-regulated when fish were challenged by the individual and mixture pesticides compared with the baseline value. These results afforded valuable information on the latent toxicity mechanisms of co-exposure for PYR and MET in the early growth stage of fish. Moreover, our data also revealed that frequent application of these two pesticides might exert a potentially ecotoxicological hazard on aquatic ecosystems. Collectively, the present study provided valuable guidance for the risk evaluation of chemical combinations. [ABSTRACT FROM AUTHOR]

Over the years, the safety of traditional Chinese medicine (TCM) has received widespread attention, especially the central nervous system‐related adverse reactions. Indeed, the complexity of TCM has limited the widespread application of TCM. The article summarizes the main components associated with neurotoxicity, including alkaloids, terpenes, flavonoids, saponins, proteins, and heavy metals, by reviewing the literature on the neurotoxicity of TCM. It has been established that the neurotoxicity mechanisms mainly include mitochondrial damage, oxidative damage, inhibition of cell proliferation (including transcriptional and DNA damage), changes in cell membrane permeability, and apoptosis. By reviewing the latest literature, this paper provides the foothold for follow‐up studies and can assist clinicians in preventing neurotoxicity via rational and safe TCM drug use. The neurotoxicity associated with traditional Chinese medicine has attracted widespread attention, and the development and application of TCM have largely been limited by the complexity of its components and their corresponding toxicity. By reviewing the main component types and toxicity mechanisms of traditional Chinese medicine‐induced neurotoxicity, this paper provides the foothold for clinical application and future studies on TCM. [ABSTRACT FROM AUTHOR]

The traditional Mongolian medicine Hunqile-7 (HQL-7), which is mainly used to relieve pain in clinic, has certain toxicity. Therefore, toxicological investigation of HQL-7 is of great significance to its safety assessment. In this study, the toxic mechanism of HQL-7 was explored based on a combination of metabolomics and intestinal flora metabolism. UHPLC-MS was used to analyze the serum, liver and kidney samples of rats after intragastric administration of HQL-7. The decision tree and K Nearest Neighbor (KNN) model were established based on the bootstrap aggregation (bagging) algorithm to classify the omics data. After samples were extracted from rat feces, the high-throughput sequencing platform was used to analyze the 16s rRNA V3-V4 region of bacteria. The experimental results confirm that the bagging algorithm improved the classification accuracy. The toxic dose, toxic intensity, and toxic target organ of HQL-7 were determined in toxicity tests. Seventeen biomarkers were identified and the metabolism dysregulation of these biomarkers may be responsible for the toxicity of HQL-7 in vivo. Several kinds of bacteria was demonstrated to be closely related to the physiological indices of renal and liver function, indicating liver and kidney damage induced by HQL-7 may be related to the disturbance of these intestinal bacteria. Overall, the toxic mechanism of HQL-7 was revealed in vivo, which not only provides a scientific basis for the safe and rational clinical use of HQL-7, but also opens up a new field of research on big data for Mongolian medicine. Graphical Abstract [ABSTRACT FROM AUTHOR]

• A novel carbon nanotube/ionic liquid/gold nanoparticle-nanocomposite was developed. • A cell-based biosensor was used to sensitively detect the cytotoxicity of six OPFRs. • The alkyl-substituted TBEP and TnBP exhibited higher toxicity. • The cytotoxic mechanism of six OPFRs on human cells was elucidated. • The data showed a significant enrichment of genes in both the p53 and PPAR pathways. In recent years, organophosphorus flame retardants (OPFRs) have been widely used as substitutes for brominated flame retardants with excellent properties, and their initial toxicological effects on the water ecosystem and human health have gradually emerged. However, to date, research on the cytotoxicity and health risks of OPFRs is still limited. Therefore, this study aims to systematically explore the cytotoxic effects and toxic mechanisms of OPFRs on cells. Human liver cancer (HepG2) cells were adopted as an ideal model for toxicity evaluation due to their rapid growth and metabolism. This study proposes a sensitive electrochemical cell–based sensor constructed on a graphitized multi-walled carbon nanotube/ionic liquid/gold nanoparticle-modified electrode. The sensor was used to detect the cytotoxicity of tri(2-butylxyethyl) phosphate (TBEP), tributyl phosphate (TnBP), triphenyl phosphate (TPhP), tri(1,3-dichloro-2-propyl) phosphate (TDCIPP), tri(2-chloropropyl) phosphate (TCPP) and tri(2-chloroethyl) phosphate (TCEP) in the liquid medium, providing insight into their toxicity in water environments. The half-maximal inhibitory concentration (IC 50) of TBEP, TnBP, TPhP, TDCIPP, TCPP and TCEP on HepG2 cells were 179.4, 194.9, 219.8, 339.4, 511.8 and 859.0 μM, respectively. Additionally, the cytotoxic mechanism of six OPFRs was discussed from the perspective of oxidative stress and apoptosis, and four indexes were correlated with toxicity. Furthermore, transcriptome sequencing was conducted, followed by a thorough analysis of the obtained sequencing results. This analysis demonstrated a significant enrichment of the p53 and PPAR pathways, both of which are closely associated with oxidative stress and apoptosis. This study presents a simplified and efficient technique for conducting in vitro toxicity studies on organophosphorus flame retardants in a water environment. Moreover, it establishes a scientific foundation for further investigation into the mechanisms of cytotoxicity associated with these compounds. [Display omitted] [ABSTRACT FROM AUTHOR]

Microplastics (MPs) have been widely detected in the world's water, which may pose a significant threat to the ecosystem as a whole and have been a subject of much attention because their presence impacts seas, lakes, rivers, and even the Polar Regions. There have been numerous studies that report direct adverse effects on marine organisms, but only a few have explored their ecological effects on freshwater organisms. In this field, there is still a lack of a systematic overview of the toxic effects and mechanisms of MPs on aquatic organisms, as well as a consistent understanding of the potential ecological consequences. This review describes the fate and impact on marine and freshwater aquatic organisms. Further, we examine the toxicology of MPs in order to uncover the relationship between aquatic organism responses to MPs and ecological disorders. In addition, an overview of the factors that may affect the toxicity effects of MPs on aquatic organisms was presented along with a brief examination of their identification and characterization. MPs were discussed in terms of their physicochemical properties in relation to their toxicological concerns regarding their bioavailability and environmental impact. This paper focuses on the progress of the toxicological studies of MPs on aquatic organisms (bacteria, algae, Daphnia, and fish, etc.) of different trophic levels, and explores its toxic mechanism, such as behavioral alternations, metabolism disorders, immune response, and poses a threat to the composition and stability of the ecosystem. We also review the main factors affecting the toxicity of MPs to aquatic organisms, including direct factors (polymer types, sizes, shapes, surface chemistry, etc.) and indirect factors (persistent organic pollutants, heavy metal ions, additives, and monomer, etc.), and the future research trends of MPs ecotoxicology are also pointed out. The findings of this study will be helpful in guiding future marine and freshwater rubbish studies and management strategies.

Background: Agricultural products are frequently co-contaminated by mycotoxins and pesticides. Most studies have only focused on the single toxicities of these chemicals, while their combined effects are neglected. Therefore, we investigated the combined toxic effects of T-2 toxin (T-2) and propiconazole (PRO) on zebrafish (Danio rerio). Results: Our data exhibited that T-2 had higher toxicity to embryonic fish (96-h LC50 value of 0.39 mg a.i. L−1) than PRO (96-h LC50 value of 17.16 mg a.i. L−1). The mixture of T-2 and PRO showed an acute synergistic effect on zebrafish. Meanwhile, indicators associated with oxidative stress (SOD, Mn-sod, and cat) displayed significant variations in most exposures to T-2 and PRO mixtures (MTP) compared with the single exposures. The expressions of apoptosis-related genes cas3 and cas9 were also substantially elevated in the high-dose MTP exposure compared with the corresponding T-2 exposure. Besides, the expressions of endocrine system-related genes (TRβ, tsh, crh, cyp19a, and vtg1) were markedly varied in most MTP exposures compared with the corresponding single exposures. Our present results suggested that the mixture of T-2 and PRO could cause enormous effects on oxidative stress, cellular apoptosis, and the hypothalamic–pituitary–thyroid/hypothalamic–pituitary–gonadal (HPG/HPT) axis of zebrafish. Conclusions: Our results provided new insights into the development of combined pollution standards for agricultural products. Taken together, the impact of the combined effects could be considered and regulated as priorities. [ABSTRACT FROM AUTHOR]

The environmental safety and health impacts of nanosilver have attracted much attention due to their continuous detection in water. Although the effects of nanosilver on aquatic organisms have been reported, the ecotoxicity and underlying mechanism of nanosilver in aquatic organisms are not fully understood. Fish gills are the primary target organs of pollutant exposure in aquatic environments, and is important to clarify the impact of nanosilver on aquatic organisms by systematically and comprehensively revealing the effect of nanosilver on fish gills. Here, we review the ecotoxicity and potential mechanisms of nanosilver on fish gills. Studies have shown the most commonly used and toxic nanosilver for studying the effects of nanosilver on fish gills is 5-30 nm. Nanosilver mainly affects various physiological functions of fish gills, such as respiration, ion, and osmotic pressure regulation, by disrupting the structure and components of tissues or cells (e.g., cell membranes and mitochondria), as well as interfering with tissue lipid, amino acid, and carbohydrate metabolism. The main mechanisms of toxicity induced by nanosilver in fish gills are gill membrane damage, oxidative stress, and silver ion release. This review provides a scientific basis for the detrimental effects of nanosilver on aquatic ecological environment health and the protection of fish resources., Competing Interests: Declaration of Competing Interest ☒ The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

Chlorpyrifos (CLP) and deltamethrin (DTM) are among the most widely utilized organophosphate and pyrethroid insecticides globally. Their simultaneous presence in aquatic environments poses significant threats to fish health and challenges the sustainability of aquaculture practices. Despite their prevalence, the combined toxic effects of CLP and DTM on hook snout carp (Opsariichthys bidens Günther) remain insufficiently understood. In this study, O. bidens were exposed to waterborne treatments of CLP, DTM, or their combination for 30 days, and the biochemical and molecular responses of the liver tissue were systematically assessed. Acute toxicity tests revealed that the combined exposure to CLP and DTM resulted in synergistic toxicity. Significant alterations in the activities of key enzymes, including superoxide dismutase (SOD), catalase (CAT), caspase-3 (CASP-3), and caspase-9 (CASP-9), relative to the control group, demonstrated that co-exposure induced oxidative stress in O. bidens. Additionally, the elevated transcriptional levels of immune-related genes such as cxcl-c1c, il-8, and il-1 suggested a pronounced inflammatory response triggered by the pesticide mixture. Conversely, the significantly reduced expression of p53 and esr indicated that combined exposure disrupted apoptotic regulation and endocrine system function in the fish. In summary, these findings demonstrated that co-exposure to CLP and DTM induced liver damage in O. bidens by impairing antioxidant enzyme activity, disrupting apoptosis regulation, and altering the transcriptional profiles of genes involved in immune and endocrine pathways. These results provided new insights into the physiological and molecular mechanisms of pesticide-induced hepatotoxicity in fish and offered valuable information for evaluating the ecological risks associated with pesticide mixtures in aquatic environments., Competing Interests: Declaration of Competing Interest ☒ The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

Dinotefuran is a chiral insecticide widely used to control Nilaparvata lugens in agriculture. However, little is known about the toxic effects of dinotefuran enantiomers on aquatic organisms. In this study, zebrafish were exposed to 1.00 and 10.00 mg/L dinotefuran enantiomers for 96 h, after which multivariate pattern recognition, metabolite identification, and pathway analysis were performed. Principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) were then conducted to reveal the metabolic perturbations caused by dinotefuran enantiomers. Metabolic pathway analysis revealed the perturbation of five main pathways, including phenylalanine, tyrosine and tryptophan biosynthesis; phenylalanine metabolism; retinol metabolism; arginine and proline metabolism; and glycerophospholipid metabolism. These disturbed metabolic pathways were strongly correlated with energy, amino acid metabolism, and lipid metabolism. Pathway analysis also indicated that the metabolic pathway changes induced by the same level of R and S-dinotefuran were enantioselective. Our research may provide better insight into the risk of chiral dinotefuran in aquatic organisms in the environment. [ABSTRACT FROM AUTHOR]

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Pydiflumetofen (PYD) is primarily used to control fungal disease. The potential risks posed by PYD enantiomers to the aquatic ecosystem are currently unclear. In this study, the enantioselective toxicity and fate of PYD in Danio rerio were investigated, and the enantioselective toxic mechanism and metabolic pathway were explored. The acute toxicity of R-PYD was 10.7–14.7-fold than that of S-PYD against Danio rerio embryos, larvae, and adults. Meanwhile, R-PYD presented a stronger effect on embryo hatching and abnormalities, adult tissue damage and oxidative stress. R-PYD inhibited the succinate dehydrogenase (SDH) activity more than S-PYD because of its better interaction with SDH with a lower binding free energy (-59.35 kcal/mol), explaining the mechanism of enantioselective toxicity. Remarkable enantioselectivity was observed in uptake, distribution, and elimination. R-PYD showed preferential uptake with the higher uptake rate constants and slow metabolism with a longer half-life, resulting in the bioaccumulation of R-PYD with higher BCFk (7.37 at 0.05 mg/L and 14.69 at 0.2 mg/L). Besides, muscle is an important tissue for PYD accumulation, existing potential food risk. Eleven PYD metabolites were qualitatively identified, and the metabolic pathway was proposed, including hydroxylation, N-demethylation, demethoxylation, hydrolysation (phase Ⅰ), and acetylation and glucuronidation (phase Ⅱ). The predicted toxicity of the metabolite indicated that several highly toxic metabolites need to be considered in the future. This study provides a new perspective for evaluating the ecological and human health risks of chiral pesticides.

The extensive utilization of pesticides results in their frequent detection in aquatic environments, often as complex mixtures, posing risks to aquatic organisms. The hook snout carp (Opsariichthys bidens) serves as a valuable bioindicator for evaluating the impacts of environmental pollutants in aquatic ecosystems. However, few studies examined the toxic effects of pesticides on O.bidens , let alone the characterization of the combined effects resulting from their mixtures. This study aims to elucidate the toxic effects of beta-cypermethrin and pyraclostrobin on O.bidens , individually and in combination, focusing on biochemical, transcriptional, and molecular responses. By organizing and analyzing the toxicogenomic databases, both pesticides were identified as a contributor to processes such as apoptosis, oxidative stress, and inflammatory responses. The acute toxicity test revealed comparable acute toxicity of beta-cypermethrin and pyraclostrobin on O.bidens , with LC 50 being 0.019 and 0.027 mg/L, respectively, whereas the LC 50 decreased to 0.0057 and 0.0079 mg/L under the combined exposure, indicating potential synergistic effects. The activities of enzymes involved in oxidative stress and detoxification were significantly altered after exposure, with superoxide dismutase (SOD) and catalase (CAT) increasing, while malondialdehyde (MDA) levels decreased. The activity of CYP450s was significantly changed. Likewise, the expression levels of genes (mn-sod , p53 , esr , il-8) associated with oxidative stress, apoptosis, endocrine and immune systems were significantly increased. Combined exposure to the pesticides significantly exacerbated the aforementioned biological processes in O.bidens. Furthermore, both pesticides can modify protein activity by binding to the surface of SOD molecules and altering protein conformation, contributing to the elevated enzyme activity. Through the investigation of the synergistic toxic effects of pesticides and molecular mechanisms in O.bidens , our findings highlight the importance of assessing the combined effects of pesticide mixtures in aquatic environments. [Display omitted] • Beta-Cypermethrin + pyraclostrobin enhanced the acute toxicity in Opsariichthys bidens. • Activities of SOD, CAT, MDA and CYP450s were obviously altered by pesticide exposure. • Genes related to oxidative stress, apoptosis, endocrine and immune system were induced. • Combined exposure of pesticides exacerbated these biological processes in O.bidens. • Both pesticides altered SOD activity by binding to the surface of the enzyme. [ABSTRACT FROM AUTHOR]

Heavy metals and pesticides are significant pollutants in aquatic environments, often leading to combined pollution and exerting toxic effects on aquatic organisms. With the rapid growth of modern industry and agriculture, heavy metal cadmium (Cd) and pesticide triazophos (TRI) are frequently detected together in various water bodies, particularly in agricultural watersheds. However, the combined toxic mechanisms of these pollutants on fish remain poorly understood. This experiment involved a 21-day co-exposure of Cd and TRI to the hook snout carp Opsariichthys bidens to investigate the toxic effects on liver tissues at both enzymatic and transcriptional levels. Biochemical analysis revealed that both individual and combined exposures significantly increased the content or activity of caspase-3 (CASP-3) and malondialdehyde (MDA). Moreover, the impact on these parameters was greater in the combined exposure groups compared to the corresponding individual exposure groups. These findings suggested that both individual and combined exposures could induce mitochondrial dysfunction and lipid peroxidation damage, with combined exposure exacerbating the toxicological effects of each individual pollutant. Furthermore, at the molecular level, both individual and combined exposures upregulated the expression levels of cu-sod , cat , and erβ , while downregulating the expression of il-1. Similar to the patterns observed in the biochemical parameters, the combined exposure group exhibited a greater impact on the expression of these genes compared to the individual exposure groups. These results indicated that exposure to Cd, TRI, and their combination induced oxidative stress, endocrine disruption, and immunosuppression in fish livers, with more severe effects observed in the combined exposure group. Overall, the interaction between Cd and TRI appeared to be synergistic, shedding light on the toxic mechanisms by which fish livers responded to these pollutants. These findings contributed to the understanding of mixture risk assessment of pollutants and were valuable for the conservation of aquatic resources. [Display omitted] • Triazophos exhibited higher acute toxicity to the hook snout carps than cadmium. • Combination of cadmium and triazophos showed synergistic acute toxicity. • Cadmium and triazophos exposures induced changes in caspase-9 and MDA levels. • Expressions of ap , klf2α , il-1 , and erα were obviously altered by the co-exposure. [ABSTRACT FROM AUTHOR]

Metal‐based nanoparticles (NPs) are particularly important tools in tissue engineering‐, drug carrier‐, interventional therapy‐, and biobased technologies. However, their complex and varied migration and transformation pathways, as well as their continuous accumulation in closed biological systems, cause various unpredictable toxic effects that threaten human and ecosystem health. Considerable experimental and theoretical efforts have been made toward understanding these cytotoxic effects, though more research on metal‐based NPs integrated with clinical medicine is required. This review summarizes the mechanisms and evaluation methods of cytotoxicity and provides an in‐depth analysis of the typical effects generated in the nervous, immune, reproductive, and genetic systems. In addition, the challenges and opportunities are discussed to enhance future investigations on safer metal‐based NPs for practical commercial adoption. [ABSTRACT FROM AUTHOR]

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Organic modified layered double hydroxides (O-LDHs), known as attractive adsorbents for organic pollutants, may pose severe toxicity to the aquatic organisms during their large-scale application. However, little information is available on the toxicity of O-LDHs and the joint toxicity with the coexisted organic pollutants. Herein, we employed organic three-dimensional layered double hydroxide (O3D-LDH) and methyl orange (MO) as representative to investigate the toxicity mechanisms of single substance and its binary mixture on green algae Chlorella vulgaris. Results showed that O3D-LDH and MO presented concentration-dependent toxicity, the binary mixture showed additive effect after exposed to low O3D-LDH concentration (≤ 50 mg/L), but antagonism was observed for the other. It revealed that the agglomeration of O3D-LDH and microalgae influenced chlorophyll content, eventually inhibiting the growth of algae. Overall, this toxicity investigation was critical for understanding the environmental risk of organic LDHs to provide theorical guidance for their practical application in the water purification. [ABSTRACT FROM AUTHOR]

An increasing number of inorganic ultraviolet filters (UVFs), such as nanosized zinc oxide (nZnO) and titanium dioxide (nTiO2), are formulated in sunscreens because of their broad UV spectrum sunlight protection and because they limit skin damage. However, sunscreen-derived inorganic UVFs are considered to be emerging contaminants; in particular, nZnO and nTiO2 UVFs have been shown to undergo absorption and bioaccumulation, release metal ions, and generate reactive oxygen species, which cause negative effects on aquatic organisms. We comprehensively reviewed the current study status of the environmental sources, occurrences, behaviors, and impacts of sunscreen-derived inorganic UVFs in aquatic environments. We find that the associated primary nanoparticle characteristics and coating materials significantly affect the environmental behavior and fate of inorganic UVFs. The consequential ecotoxicological risks and underlying mechanisms are discussed at the individual and trophic transfer levels. Due to their persistence and bioaccumulation, more attention and efforts should be redirected to investigating the sources, fate, and trophic transfer of inorganic UVFs in ecosystems. [ABSTRACT FROM AUTHOR]

T-2 toxin is a secondary metabolite produced by Fusarium spp., and belongs to the type A mycotoxins in the cephalosporins family. T-2 toxin is highly toxic, and it pollutes not only crops in the field,but also granary which leads the post-harvest lost of grain, furthermore, it causes huge damage to human and animal health. Therefore, it becomes world widely the target to be prevented and controlled in the food industry and livestock industry in recent years. At present, the research on the biological toxicity of T-2 toxin is more indepth, but it still lacks adequate study on detoxification of T-2 toxin, especially the biological detoxification. The harm, mechanism and physical, chemical and biological methods of detoxification of T-2 toxins were reviewed. Focusing on the acquisition of efficient detoxification enzymes and the development of detoxification processes are conducive to the healthy development of multiple industries in China, such as grain industry, livestock industry, and by-product deep processing.

Heavy metals contamination is a serious problem in the aquatic environment. Some of them are very important, having biological roles for aquatic organisms, and called essential heavy metals. In contrast, other heavy metals are considered harmful even at low concentrations. The toxic levels of heavy metals may be of agricultural, industrial and mining activities. This will cause water pollution and changes in the physicochemical characteristics of the aquatic environment. This pollution has deleterious toxic effects on fish and raises concerns over its potential impact on human health. The most common heavy metals are arsenic, chromium, lead and mercury, which affect human health and are considered systemic toxicants. These metals induce organ damage even at low levels of exposure and according to the US Environmental protection agency and international agency for research on cancer, they classified as carcinogens. For all the above reasons, this review was written to contribute to heavy metals' role in the environment, toxic mechanism and toxic effects on fish.

Methyl tert-butyl ether (MTBE), a widely used gasoline additive and a ubiquitous environmental pollutant in many countries and regions, can cause various kinds of toxic effects on human health. However, the molecular mechanism underlying its toxic effects remains elusive. The present study aimed to explore the cytotoxicity, DNA damage and oxidative damage effects of MTBE on human bronchial epithelial cells (16HBE) and the possible role of DNA polymerase β (pol-β) in this process. RNA interference (RNAi) was used to obtain pol-β gene knocked-down cells (pol-β−). CCK-8 assay was adopted to analyze the cell viability. Alkaline single-cell gel electrophoresis (SCGE) was performed to detect the DNA damage effects of MTBE. The enzyme activity of GSH-Px, SOD, CAT and the level of MDA were assessed. The data indicated that when treated with MTBE at the concentration exceeding 50 μmol/L and for the time exceeding 24 h, the pol-β− exhibited significantly decreased cell viability and increased DNA damage effects, as compared to the control (P < 0.05). Furthermore, there was significant difference in the levels of GSH-pX, SOD, CAT and MDA between the pol-β− and the control (P < 0.05). Our investigation suggests that MTBE can cause obvious cytotoxicity, DNA damage and oxidative damage effects on 16HBE cells. DNA polymerase β may be involved in protecting 16HBE cells from the toxic effects induced by MTBE exposure. These findings provide a novel insight into the molecular mechanism underlying the toxic effects of MTBE on human cells. [ABSTRACT FROM AUTHOR]

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The natural co-occurrence of multiple mycotoxins has been reported in cereals and cereal products worldwide. Even though the dietary exposure to mycotoxins constitutes a serious human health, most reports are limited to the toxic effect of individual mycotoxins. The purpose of the present study was to assess the combined toxic effects of zearalenone (ZEN) and fumonisin B1 (FB1) and the potential interaction of their mixture on zebrafish (Danio rerio) embryos. Our results showed that ZEN possessed the higher toxicity to embryonic zebrafish (7-day LC50 value of 0.78 mg a.i. L−1) compared with FB1 (7-day LC50 value of 227.7 mg a.i. L−1). The combination of ZEN and FB1 exerted an additive effect on zebrafish embryos. Meanwhile, the activities of antioxidant CAT, caspase-3, and detoxification enzyme CYP450, as well as the expressions of six genes (Mn-sod, cas9, bax, cc-chem, ERα, and crh) associated with oxidative stress, cellular apoptosis, immune system, and endocrine system were prominently altered in the mixture exposure compared with the corresponding single treatment group of ZEN or FB1. Taken together, the regulatory standards of mycotoxins in food and feed should be updated based on the mixture effects of mycotoxins, and there is an increased need on effective detoxification methods for controlling and reducing the toxicity of multiple mycotoxins in animal feed and throughout the food supply chain.

Context Chloranthus serratus (Thunb.) Roem. et Schult. (Chloranthaceae) is an herb widely used as a folk medicine treating inflammatory diseases, although it is toxic. Objective To investigate hepatotoxicity and related mechanisms induced by ethanol extracts of different parts of C. serratus in rats. Materials and methods Sprague Dawley rats were divided into control (Con), ethanol extract of roots (ER), stems (ES), and leaves (EL) groups, and acute oral toxicity studies were conducted. The rats received doses of 4.14, 3.20, and 1.16 g/kg/d extracts for 14 days, respectively. Liver index, liver function and oxidative stress biomarkers, liver pathology, ultrastructure, TNF-α, ICAM-1, and Nrf2/HO-1 proteins expression levels were determined. Results The LD50 of ER, ES, and EL were higher than 10.35, 8.05, and 2.90 g/kg/p.o., respectively. The liver indexes in the extract groups increased significantly. EL dramatically increased TP, GLB, AST, ALT, ALP, TBA, MDA, ICAM-1, and TNF-α levels (p

Background: Although humans and animals are often simultaneously exposed to a variety of mycotoxins via feed and food consumption, in which aflatoxin B1 (AFB1) and deoxynivalenol (DON) is one of the most prevalent combination of mycotoxins. Many toxicological studies have merely focused on the impacts of single mycotoxins. In the present study, the combined toxicity and the related mechanism of AFB1 and DON to zebrafish (Danio rerio) were investigated. Results: Results exhibited that DON had lower toxicity to embryonic zebrafish with a 7-day LC50 of 218.3 mg a.i. L−1 in comparison to AFB1 (0.031 mg a.i. L−1). The mixture of AFB1 and DON elicited an additive combined effect on zebrafish embryos. The levels of CAT, caspase-3, and T4 markedly varied in most single and mixture groups. The expressions of four genes (cas3, apaf-1, cc-chem, and cyp19a) associated with oxidative stress, cellular apoptosis, immune system, and endocrine system were markedly varied upon the mixture exposure in comparison to the corresponding single exposure of AFB1 or DON. Conclusions: Our results revealed that the impacts of a mixture could not be estimated solely based on toxicities of the single mycotoxins. Taken together, our comprehensive investigation on the mycotoxin mixtures and their potential mechanisms could better reflect the reality of mycotoxin contamination in food and feed. [ABSTRACT FROM AUTHOR]

Although benzene is a confirmed environmental carcinogen, the mechanism of its carcinogenicity remains largely unclear. The suggested oncogene, miR-221, is elevated and plays important roles in various tumors, but its role in benzene-induced carcinogenesis remains unknown. In the present study, we constructed hydroquinone (HQ, a representative metabolite of benzene with biological activity)-transformed malignant cell line (16HBE-t) and analyzed the level of miR-221 in it with qRT-PCR. Exosomes from 16HBE-t cells incubated with or without an miR-221 inhibitor were isolated by ultracentrifugation, characterized by transmission electron microscopy and laser scanning confocal microscope, and then transfected into 16HBE cells. The effects of exosomal miR-221 on apoptosis induced by HQ in recipient cells were determined using flow cytometry. The amount of miR-221 in 16HBE-t was significantly increased compared with controls. When recipient cells ingested exosomes derived from 16HBE-t, miR-221 was increased, and apoptosis induced by HQ was inhibited. Blocking miR-221 in 16HBE-t using an inhibitor did not significantly alter miR-221 or apoptosis in recipient cells. Exosomal miR-221 secreted by 16HBE-t inhibits apoptosis induced by HQ in normal recipient cells. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Biological invasion refers to the process that organisms invade into another new environment through natural or man-made way from the original habitat, causing economic losses or ecological disasters to biodiversity, agriculture, forestry, animal husbandry and fishery production and human health. Human activities and the development of global integration accelerate the occurrence of biological invasion, which poses a serious threat to the global biodiversity and economy. Since entering the 21st century, biological invasion has continued. Pomacea canaliculata Lam, native to the Amazon River Basin of South America, was introduced into southern China as an aquatic economic animal in the 1980s because of its rich protein content and high nutrient content. Later, it was abandoned in the fields due to excessive blind breeding, too strong fishy smell and poor taste, and spread to the aquatic environment such as rice fields through canals and rivers. Because of its strong fecundity, adaptability and stress resistance, miscellaneous food habits and lack of natural enemies, the snail has become a disaster in many areas of southern China, which poses a major threat to the biodiversity, ecosystem, crops and aquatic plants in the invaded areas. In addition, Pomacea canaliculata is the intermediate host of Angiostrongylus cantonensis, which causes eosinophilic meningitis, and has indirect potential harm to human health. In 2000, the IUCN Expert Committee on alien invasive species listed Pomacea canaliculata as one of the world's 100 malignant alien invasive species. In March 2003, the State Environmental Protection Administration listed the first batch of 16 alien species to invade China. The control methods of Pomacea canaliculata can be divided into four aspects. First of all, physical methods are used to collect snails and eggs manually. During the peak breeding period, human resources are concentrated to collect snails in fields, canals and other areas. During the spawning period, bamboo chips and wooden sticks are inserted in the rice fields to attract the snails to lay eggs and destroy the collected eggs. However, this method has the characteristics of high frequency spawning, strong sustainability of prevention and control, rapid spread with the current, and it is difficult to control. In addition, the artificial fishing cost is high and the timeliness cannot be met for the large area where the Pomacea snail occurs. The second is chemical control. Though the molluscicides, such as spiromethane, tetraacetaldehyde and copper sulfate, are put in the rice fields, rice fields and channels at the same time. Although the effect is obvious, it is easy to cause serious environmental pollution if it is not used properly, and the snail is easy to produce drug resistance. The secondary biological method is to make use of the thin shell and meat of Fushou snail, which is high in protein, low in fat and has more in the areas where snails occur, ducks, fish and crabs are cultivated. However, in the process of biological control, it is necessary to strictly control the number of biological population to avoid animal feces polluting the water environment and damaging people's water sanitation. Finally, in order to prevent and control Pomacea canaliculata with camellia seed cake, saponins and other plant sources, it has become a hot spot in the field of snail control due to its long-term, economic and ecological safety to non target cells. However, there are few studies on the extraction and preparation of botanical toxicants and their toxic effects on Pomacea canaliculata. The results showed that castor seed was highly toxic, and the main toxic components were ricinine and ricin. Among them, ricin was one of the most toxic plant toxin proteins, which has a strong insecticidal and bactericidal effect. When it entered the animal body, it would be decomposed by the object itself, and it would not accumulate in the biological chain and produce drug resistance. Ricinine is a kind of alkaloid with low toxicity, which can cause vomiting and various toxic reactions. It can lead to liver and kidney damage, convulsion, hypotension and death. At present, there is no report on the toxicity of castor oil extract to Pomacea canaliculata. The biological soaking method was used to prepare the botanical toxicant from the extract of Ricinus communis L. seed. The toxic effects of different extract concentrations (0, 0.5, 1.5, 3.0, 4.5, 6.0 g/L) on the snails were studied. The liver tissue physiological and biochemical indexes of the snails treated with sublethal concentrations of 1.58 (LC25), 3.82 (LC50) and 6.05 (LC75) g/L and their correlation were further studied analysis of the mechanism of its toxic action. The results showed that after 48h treatment, the mortality of Pomacea canaliculata increased with the increase of time and concentration, and the mortality of Pomacea canaliculata was significantly different under different concentrations (P<0.05). The protein content (TP), malondialdehyde (MDA) content and catalase (CAT) activity in hepatopancreatic tissue were significantly different from those in the control group after 48h of sublethal concentration treatment. There was a significant negative correlation between catalase (CAT) activity and malondialdehyde (MDA) content (P<0.05). The extract of Ricinus communis L. seed can cause damage of liver tissue and disorder of metabolism by affecting the content of protein (TP), malondialdehyde (MDA) and the activity of catalase (CAT) in the liver tissue, so as to achieve the toxic effect. The results of molluscicidal test and physiological and biochemical indexes showed that castor seed had potential molluscicidal effect on Pomacea canaliculata. [ABSTRACT FROM AUTHOR]

Aflatoxin B 1 (AFB 1 ), the most toxic and harmful mycotoxin, has a high likelihood of occurring in animal feed and human food, which seriously affects agriculture and food safety and endangers animal and human health. Recently, natural plant products have attracted widespread attention due to their low toxicity, high biocompatibility, and simple composition, indicating significant potential for resisting AFB 1 . The mechanisms by which these phytochemicals resist toxins mainly involve antioxidative, anti-inflammatory, and antiapoptotic pathways. Moreover, these substances also inhibit the genotoxicity of AFB 1 by directly influencing its metabolism in vivo , which contributes to its elimination. Here, we review various phytochemicals that resist AFB 1 and their anti-AFB 1 mechanisms in different animals, as well as the common characteristics of phytochemicals with anti-AFB 1 function. Additionally, the shortcomings of current research and future research directions will be discussed. Overall, this comprehensive summary contributes to the better application of phytochemicals in agriculture and food safety.

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)