Trietazine is an s-triazine-based herbicide commonly applied in agricultural systems, but its stability in aquatic environments has prompted growing concern about unintended effects on non-target organisms. To assess its developmental toxicity and clarify associated mechanisms, we used both wild-type zebrafish embryos and multiple organ-specific transgenic lines as in vivo models of early vertebrate development. The embryos were continuously exposed to trietazine from 8 to 96 h post-fertilization, resulting in clear dose-dependent developmental defects, including shortened body length, reduced ocular size, and frequent pericardial and yolk sac edema, indicative of moderate to high embryotoxicity across the tested concentrations. In parallel, trietazine markedly enhanced intracellular reactive oxygen species levels and induced transcriptional activation of genes involved in inflammatory signaling and programmed cell death, supporting a central role for oxidative stress-driven apoptosis in its developmental toxicity. To delineate organ-level toxicity, we examined a panel of transgenic zebrafish lines. Embryos expressing cmlc2:dsRED and gata1a:dsRED exhibited pronounced cardiac malformations and impaired blood flow, while altered vascular organization was detected in the flk1:mCherry line. Disruption of cardiovascular development was further supported by aberrant expression patterns of the cardiac regulatory genes nkx2.5 and vmhc, as revealed by whole-mount in situ hybridization. Additionally, neurodevelopmental deficits and liver malformations were observed in olig2:dsRED, huC:EGFP, and fabp10a:dsRED embryos, demonstrating multi-organ developmental toxicity involving the nervous system and liver. Taken together, these results demonstrate that trietazine interferes with normal embryonic development across multiple organ systems by promoting oxidative stress-dependent inflammatory and apoptotic responses in both wild-type and transgenic zebrafish models. Our findings highlight the potential ecological hazards associated with trietazine contamination in aquatic ecosystems and provide mechanistic insight into the level and spectrum of its developmental toxicity.

Pesticides are essential for enhancing agricultural productivity and public health; however, their environmental residues can adversely affect non-target organisms, including humans. Alanycarb, a carbamate insecticide commonly used in households, has been detected in various food and environmental samples. However, its toxicological mechanisms remain unclear. In the present study, we explore the toxicity of alanycarb in bovine mammary gland epithelial (MAC-T) cells. Our results demonstrated that alanycarb treatment inhibited cell growth and proliferation, induced cell death, and altered the expression of apoptosis-involved genes. We also observed that alanycarb induced excessive intracellular reactive oxygen species (ROS) production, which triggered cell death and the activation of stress-responsive signaling pathways, suggesting that alanycarb exerts cytotoxicity via ROS production. Additionally, mitochondrial dysfunction was evident, characterized by impaired mitochondrial respiration (including basal respiration, ATP production, and spare respiratory capacity) and calcium accumulation in the mitochondria. These disturbances led to a depolarization of mitochondrial membrane potential and the increase of CASP3. Mitochondrial impairment led to increased ROS generation and triggered the activation of stress-responsive signaling cascades, such as the MAPK, PI3K, and NF-κB pathways. Dysregulation of these pathways induces inflammation and apoptosis in MAC-T cells. Collectively, our study provides new insights into the cytotoxic mechanisms of alanycarb in mammalian cells and contributes to a better understanding of the toxicological effects of carbamate insecticides on human health.

The development of spintronic emitters of broadband THz pulses relies on designing heterostructures where processes of laser-driven spin current generation and subsequent spin-to-charge current conversion are the most efficient. An interface between ferromagnetic and nonmagnetic layers in the emitter is one of the critical elements. Here, we study experimentally single-cycle THz pulse generation from a laser-pulse excited Pt/Co emitter with a composition gradient interface between Pt and Co and compare it with the emission from a conventional Pt/Co structure with an abrupt interface. We find that the gradient interface enhances the efficiency of optics-to-THz conversion by a factor of two in a wide range of optical fluences up to 3 mJ cm^-2. We reveal that this enhancement is caused by a pronounced increase in transmittance of the laser-driven spin-polarized current through the gradient interface compared to the abrupt one. Furthermore, we find that such a transmission deteriorates with laser fluence due to the spin accumulation effect.

Fenoxycarb, a carbamate insecticide, functions as a juvenile hormone agonist to inhibit pests, and its detection in aquatic environments is concerning because of its widespread application. These concerns have led to ecotoxicological studies on aquatic crustaceans; however, research on the effects of fenoxycarb on the developmental processes of organisms is limited. In the present study, the deleterious effects of fenoxycarb on zebrafish development and the related cellular mechanisms mediating this toxicity were addressed. Exposure to sublethal concentrations of fenoxycarb (0, 0.5, 1, and 2 mg/L) resulted in morphological defects in zebrafish larvae, particularly in the heart region, eyes, and body length. These defects were accompanied by an increase in the number of apoptotic cells and the upregulation of related gene expression. Moreover, fenoxycarb increased ROS production and the number of macrophages, and altered the expression of immune-related genes, thereby inducing inflammation. These results revealed various abnormalities in the heart, vasculature, liver, and pancreas, as confirmed by transgenic models, such as cmlc2:DsRed, fli1a:EGFP, and fabp10a:DsRed;elastase:GFP. These developmental impairments were associated with the altered expression levels of genes involved in the development and function of each organ. These results suggest that fenoxycarb can affect multiple organs through excessive inflammation during development and highlight its potent toxic effects on other non-target organisms.

Pesticides are increasingly the focus as a prominent factor in environmental pollution. Fenpropimorph, a widely utilized morpholine fungicide, is a significant water pollutant. Because of its extensive usage, fenpropimorph is readily detected in diverse aquatic ecosystems. Despite its well-known toxicity to aquatic organisms, its toxicity to zebrafish development and accompanying mechanics remain unexplored. To assess fenpropimorph's toxicity and potential mechanism, we employed the zebrafish model, a representative tool in toxicological studies. Our results showed that exposure to fenpropimorph reduced embryonic viability during the early stages of development and reduced head and body size. Moreover, fenpropimorph triggered apoptosis, DNA fragmentation, and inflammation. Aberrations in the vascular network were observed in the fli1:eGFP transgenic zebrafish model. Additionally, neurotoxic impacts were further assessed using transgenic olig2:dsRed zebrafish, accompanied by a reduction of liver size and fluorescence intensity of fabp10a:dsRed zebrafish. mRNA expression analysis related to corresponding organ development further supported our data. Overall, our research suggests that fenpropimorph may cause aberrations in aquatic organisms.

Bendiocarb, a carbamate insecticide, is widely applied in various circumstances; however, it poses a potential threat to various non-target organisms. Although many researchers have focused on defining the toxic effects of bendiocarb, those associated with early and organ development remain poorly understood. In this study, we evaluated the developmental and organ-specific toxic mechanisms of bendiocarb in a zebrafish model. Exposure of bendiocarb decreased viability of zebrafish larvae by changing morphology and inducing production of reactive oxygen species with a decrease of the expression of antioxidant genes cat and sod2. In addition, bendiocarb affected mitochondrial bioenergetics and plasticity with reduction of mitochondrial complexes I, III, and V related genes leading to suppression of ATP generation. To investigate multi-organ toxic effects of bendiocarb, various transgenic zebrafish were utilized, for example, cardiac toxicity, impaired vasculature, and interfered blood flow were confirmed using cmlc2:dsRed, fli1a:EGFP, and gata1a:dsRed. Hepatotoxicity was examined using the fabp10a:dsRed model, and pancreatic toxicity was elucidated using the elastase:EGFP and insulin:EGFP models. Additionally, abnormal neuronal development was observed following treatment with olig2:dsRed and gad1b:EGFP. Moreover, changes at the molecular level by whole mount in situ hybridization and qPCR analyses were consistent with our observations. Furthermore, N-acetylcysteine (NAC) co-treatment substantially ameliorated developmental toxicity across multiple organ systems, including the cardiovascular, metabolic, and nervous systems. Taken together, this study provides novel perspectives on the system-level toxicity of bendiocarb and its molecular mechanisms of action in zebrafish.

Carbamate pesticides are derivatives of carbamic acid and are widely used in agriculture to enhance crop productivity by controlling pests and weeds. However, with the development of agriculture, the increasing use of carbamate pesticides has raised concerns regarding their environmental persistence and potential toxicity to non-target organisms, including humans. This review explores the negative effects of carbamate pesticides with a particular focus on their effects on embryonic development using a zebrafish animal model which is a well-recognized model for toxicity studies. Zebrafish share genetic similarities with humans and have many comparable organs, making them a valuable model to use toxicity results and to predict potential effects in humans. It has been reported that various carbamate pesticides can exhibit toxicity in different organs, as demonstrated using the zebrafish model. They induce oxidative stress and apoptosis, affecting the structure and function of various organs. Morphological defects, including shortened body length, reduced eye size, and pericardial and yolk sac edema, were observed. Moreover, the mRNA expression of angiogenesis-related genes was inhibited by carbamate pesticides, leading to impaired cardiac and vessel formation. They negatively affect neurodevelopment by reducing the expression of neurodevelopment-related genes, suggesting that the toxicity observed in target organisms can also be identified in non-target organisms. Immunotoxicity and hepatotoxicity are also notable concerns because carbamate exposure diminishes immune cell function and causes liver damage. These findings highlight the potential risks posed by carbamate pesticides during embryonic development. Therefore, it is essential to assess the toxicity of these chemicals to understand their long-term impact on human health and environmental safety.

Methomyl, a widely used carbamate pesticide, is frequently detected in aquatic ecosystems, due to its high water solubility and long environmental half-life. Although carbamate pesticides have been implicated in cardiovascular toxicity, the specific effects of methomyl on cardiovascular development remain largely unknown. In this study, we investigated the environmental and developmental effects of methomyl using Danio rerio (zebrafish) as an in vivo model. Methomyl exposure lowered cell viability and morphological abnormalities. Impaired cardiac development and disrupted vascular formation in zebrafish were confirmed using cmlc2:dsRed and fli1a:EGFP transgenic models. Furthermore, blood flow defects and erythrocyte accumulation were observed in gata1:dsRed transgenic model, suggesting compromised circulation. In addition, mpeg1:EGFP model revealed that methomyl activates the innate immune response in zebrafish. Molecular analyses revealed that methomyl exposure altered the expression of key genes involved in cardiac development, angiogenesis, and erythropoiesis, implicating oxidative stress and immune activation as potential underlying mechanisms. Human umbilical vein endothelial cells (HUVECs) were used as an in vitro model. We found that methomyl exhibited vascular toxicity in HUVECs, further supporting its role as a cardiovascular disruptor. These findings provide novel insights into the environmental and toxicological effects of methomyl and highlight its potential risk of accumulation in aquatic systems.

Fenoxycarb is a carbamate pesticide that negatively affects the environment and harms various non-target organisms. Despite its common use in controlling fleas and mosquitoes that are often found in cattle feedlots, the toxic effects of fenoxycarb on cattle have not yet been studied. Considering the pivotal role of cattle in milk production, this study examined the effect of fenoxycarb on bovine mammary epithelial cells (MAC-T) to assess its potential risks for the lactation system. Fenoxycarb reduced cell viability and growth in both 2D and 3D cultures and increased apoptosis. Furthermore, it triggered sub-G1 phase arrest of the cell cycle, accompanied by a pronounced decrease in CCND1 and PCNA expression. Disruption of calcium homeostasis was demonstrated by a marked decline in calcium levels in both the cytosol and the mitochondria. This reduction ultimately led to the collapse of the overall calcium balance, which in turn is closely associated with a decrease in mitochondrial respiration. In addition, fenoxycarb triggered endoplasmic reticulum stress while suppressing the unfolded protein response, especially by inhibiting the EIF2A-GADD153 signaling pathway. Moreover, decreased expression of autophagy-related proteins and diminished formation of acidic vesicular organelles confirmed the occurrence of autophagy. This study highlights the potential adverse effects of fenoxycarb on the dairy industry by elucidating its toxicity mechanisms in bovine mammary glands.

There has been growing emphasis on environmental pollutants, including heavy metals, pesticides, and nanoplastics, owing to the escalating significance of environmental pollution as a major global issue. Various toxicities induced by these compounds have been consistently reported, and many cell lines and animal models have been used in toxicity studies. Zebrafish are one of the most widely used animal models for verifying the toxic effects of environmental pollutants, owing to their many advantages. In this study, we provide brief guidelines for zebrafish maintenance and mating methods, toxicant treatments, survival measurements, and morphological abnormalities.

Propanil, an anilide herbicide, has frequently been detected in surface waters in Europe and the United States, largely due to its use in paddy cultivation areas. Particularly in specific regions like Sri Lanka, propanil is considered a potential cause of certain diseases and toxicities due to its high environmental runoff; however, there has been little research on its developmental toxicity. In the present study, we confirmed the developmental toxicity of propanil in zebrafish embryos exposed to 0, 2, 5, and 6 mg/L based on the LC50 value. Propanil exposure in embryos induced morphological changes, including decreased body length and eye size, and increased the heart and yolk sac edema. It increased the number of apoptotic cells in the brains and eyes of zebrafish larvae by 214 % and 184 %, respectively. Propanil-treated embryos exhibited altered mitochondrial metabolism, reducing basal respiration by 28 %, maximal respiration by 24 %, and ATP production by 38 %. These alterations induced organ defects in transgenic zebrafish models (cmlc2:DsRed, flk1:EGFP, olig2:DsRed, lfabp:DsRed;elastase:EGFP, and insulin:EGFP). It induced cardiovascular toxicity, as confirmed by the reduced atrial area, cerebrovascular intensity, and intersegmental vessels. Additionally, propanil decreased the fluorescence intensity of neurons, liver, and pancreas. Collectively, this study indicates that propanil causes early developmental toxicity through apoptosis and mitochondrial dysfunction. It presents a new perspective on how mitochondrial dysfunction, previously unreported in toxicity studies of other anilide herbicides, may affect developmental toxicity.

There is increasing global concern about environmental pollutants, such as heavy metals, plastics, pharmaceuticals, personal care products, and pesticides, which have been detected in a variety of environments and are likely to be exposed to nontarget organisms, including humans. Various animal models have been utilized for toxicity assessment, and zebrafish are particularly valuable for studying the toxicity of various compounds owing to their similarity to other aquatic organisms and 70% genetic similarity to humans. Their development is easy to observe, and transgenic models for organs such as the heart, liver, blood vessels, and nervous system enable efficient studies of organ-specific toxicity. This suggests that zebrafish are a valuable tool for evaluating toxicity in specific organs and forecasting the potential impacts on other nontarget species. This review describes organ toxicity caused by various toxic substances and their mechanisms in zebrafish.

Dynamic interactions between organelles are responsible for a variety of intercellular functions, and the endoplasmic reticulum (ER)–mitochondrial axis is recognized as a representative interorganelle system. Several studies have confirmed that most proteins in the physically tethered sites between the ER and mitochondria, called mitochondria-associated ER membranes (MAMs), are vital for intracellular physiology. MAM proteins are involved in the regulation of calcium homeostasis, lipid metabolism, and mitochondrial dynamics and are associated with processes related to intracellular stress conditions, such as oxidative stress and unfolded protein responses. Accumulating evidence has shown that, owing to their extensive involvement in cellular homeostasis, alterations in the ER–mitochondrial axis are one of the etiological factors of tumors. An in-depth understanding of MAM proteins and their impact on cell physiology, particularly in cancers, may help elucidate their potential as diagnostic and therapeutic targets for cancers. For example, the modulation of MAM proteins is utilized not only to target diverse intracellular signaling pathways within cancer cells but also to increase the sensitivity of cancer cells to anticancer reagents and regulate immune cell activities. Therefore, the current review summarizes and discusses recent advances in research on the functional roles of MAM proteins and their characteristics in cancers from a diagnostic perspective. Additionally, this review provides insights into diverse therapeutic strategies that target MAM proteins in various cancer types.

Mevinphos, an organophosphate insecticide, is widely used to control pests and enhance crop yield. Because of its high solubility, it can easily flow into water and threaten the aquatic environment, and it is known to be hazardous to non-target organisms. However, little is known about its developmental toxicity and the underlying toxic mechanisms. In this study, we utilized zebrafish, which is frequently used for toxicological research to estimate the toxicity in other aquatic organisms or vertebrates including humans, to elucidate the developmental defects induced by mevinphos. Here, we observed that mevinphos induced various phenotypical abnormalities, such as diminished eyes and head sizes, shortened body length, loss of swim bladder, and increased pericardiac edema. Also, exposure to mevinphos triggered inflammation, apoptosis, and DNA fragmentation in zebrafish larvae. In addition, MAPK and Akt signaling pathways, which control apoptosis, inflammation, and proper development of various organs, were also altered by the treatment of mevinphos. Furthermore, these factors induced various organ defects which were confirmed by various transgenic models. We identified neuronal toxicity through transgenic olig2:dsRed zebrafish, cardiovascular toxicity through transgenic fli1:eGFP zebrafish, and hepatotoxicity and pancreatic toxicity through transgenic lfabp:dsRed;elastase:GFP zebrafish. Overall, our results elucidated the developmental toxicities of mevinphos in zebrafish and provided the parameters for the assessment of toxicities in aquatic environments.

Pyridaben is a widely used pyridazinone insecticide used to protect crops against insects and mites. The toxicity of pyridaben has been reported in mice, zebrafish, the human reproductive system, nervous system, and respiratory system. Pyridaben can also be ingested by dairy cattle through feed. However, the toxicity of pyridaben in cattle has not been investigated on. Thus, this study focuses on demonstrating the toxicity of pyridaben in the bovine mammary glands and with the generation milk in the bovine mammary epithelial cells, as it is crucial to the continuance of the amount and the quality of the milk produced. We started by analyzing the intracellular toxicity along with the impact of pyridaben on the cell cycle distribution and the transcription of associated genes. Pyridaben treatment induced cell cycle arrest accompanied the disruption in G1 and S phases with imbalanced cytosolic and mitochondrial calcium ion homeostasis, and caused a destruction of mitochondrial membrane potential. This eventually led to apoptosis of MAC-T cells. We also investigated in the impact that pyridaben has on MAPK signaling proteins, where phosphorylation of ERK1/2, JNK, and p38 were upregulateed. Moreover, examination of the effect of pyridaben in the inflammatory genes revealed hyperactivation of the inflammatory gene transcription. This is the first research to assess the negative outcomes that pyridaben could impose on dairy cattle and milk production.

Existing evidence shows that currently used pesticides pose toxicological risks to exposed wildlife. Chemically, bifenox belongs to diphenyl ethers, a well-known group of herbicides. Its mechanism of action primarily involves inducing lipid peroxidation and blocking protoporphyrinogen oxidases. Toxicity of diphenyl ether herbicides has been elucidated in animal cells; however, in vivo toxicological evaluations of bifenox are required to determine its unexpected effects. This study aimed to determine the negative effects of bifenox, and its effects on higher eukaryotes. We found that early stages of zebrafish embryo exposed to bifenox demonstrated increased mortality and physiological defects, based on the LC50 value. Bifenox severely inhibited blood vessel growth by reducing key elements of complex connectivity; fluorescently tagged transgenic lines (fli1a:EGFP) showed morphological changes. Additionally, transgenic lines that selectively identified hepatocytes (fabp10a:DsRed) showed reduced fluorescence, indicating that bifenox may inhibit liver development. To evaluate the level of oxidative stress, we used 2 ',7 '-dichlorofluorescein diacetate (DCFH-DA) probes in zebrafish embryos to identify the underlying mechanisms causing developmental damage. Our findings demonstrate that exposure to bifenox causes abnormalities in the hepatic and cardiovascular systems during zebrafish embryogenesis. Therefore, this study provides new information for the evaluation of toxicological risks of bifenox in vertebrates.

Resmethrin, a type I pyrethroid insecticide, is frequently used globally in residential and farmland areas to control pests. Owing to the repeated administration of resmethrin, and particularly because of its lipophilic nature, residues have been detected in various environments, crops, and livestock. Previous studies have shown the adverse effects of resmethrin, including neurotoxicity and hepatotoxicity. However, the toxic effects of resmethrin on the female reproductive system have rarely been investigated. In the present study, we used two cell types, porcine trophectoderm (pTr) and porcine uterine luminal epithelial (pLE) cells, to examine the toxic effects of resmethrin on implantation and its mechanisms. Our study showed that resmethrin exposure induced apoptosis and inhibited cell cycle progression, thereby reducing the viability of both cell types. In addition, calcium homeostasis was disrupted following resmethrin treatment, and disrupted calcium homeostasis impaired the mitochondrial membrane potential and mitochondrial respiration. In addition to mitochondrial dysfunction, GRP75 and ER stress-related proteins were upregulated. Furthermore, the AKT and MAPK cascades were altered, and reactive oxygen species production and inflammation occurred after resmethrin treatment. Ultimately, through various mechanisms, resmethrin decreased the migratory abilities, and it could diminish the crosstalk between the two cell lines and lower the probability of successful implantation. Overall, we demonstrated that resmethrin interfered with the implantation process by triggering various toxic mechanisms. This study presents, for the first time, evidence regarding the mechanisms through which resmethrin exerts toxic effects on the female reproductive system, thereby raising awareness regarding the potential implications of its widespread use.

This review explores the increasing impact of microplastics and nanoplastics on the reproductive system of various organisms. As the use of plastics continues to increase, research has progressively focused on how these particles disrupt both male and female reproductive systems, leading to impaired reproductive cell function, reduced fertility, and increased offspring abnormalities. This review emphasizes the importance of understanding the underlying mechanisms of reproductive toxicity from microplastic and nanoplastic exposure, while addressing the current lack of effective treatments and the need for further investigation, particularly in humans. This review highlights the significant progress in our understanding of the reproductive toxicity caused by microplastics and nanoplastics. Previous studies have demonstrated that exposure to these particles can lead to oxidative stress, inflammation, and endocrine disruption, affecting both male and female reproductive systems. Research on animal models has shown that microplastics and nanoplastics impair reproductive cell function, decrease sperm quality, disrupt ovarian function, and reduce fertility. Additionally, there is growing evidence of transgenerational effects, whereby the reproductive damage caused by plastic exposure can be passed down to subsequent generations. Collectively, these findings underscore the urgent need for continued investigation into the mechanisms underlying reproductive toxicity and potential therapeutic interventions to mitigate these harmful effects.

Hexaconazole is a highly effective triazole fungicide that is frequently applied in various countries to elevate crop productivity. Given its long half-life and high water solubility, this fungicide is frequently detected in the environment, including water sources. Moreover, hexaconazole exerts hazardous effects on nontarget organisms. However, little is known about the toxic effects of hexaconazole on animal development. Thus, this study aimed to investigate the developmental toxicity of hexaconazole to zebrafish, a valuable animal model for toxicological studies, and elucidate the underlying mechanisms. Results showed that hexaconazole affected the viability and hatching rate of zebrafish at 96 h postfertilization. Hexaconazole-treated zebrafish showed phenotypic defects, such as reduced size of head and eyes and enlarged pericardiac edema. Moreover, hexaconazole induced apoptosis, DNA fragmentation, and inflammation in developing zebrafish. Various organ defects, including neurotoxicity, cardiovascular toxicity, and hepatotoxicity, were observed in transgenic zebrafish models olig2: dsRed, fli1:eGFP, and l-fabp:dsRed. Furthermore, hexaconazole treatment altered the Akt and MAPK signaling pathways, which possibly triggered the organ defects and other toxic mechanisms. This study demonstrated the developmental toxicity of hexaconazole to zebrafish and elucidated the underlying mechanisms.

Acifluorfen, a selective herbicide from the diphenyl ether family, targets broad leaf weeds. Diphenyl ether inhibits chlorophyll production in green plants by inhibiting protoporphyrinogen oxidase (PPO), causing cellular damage. Despite its known impacts on plants, the influence of acifluorfen on zebrafish embryo development remains unclear. In this study, we explored the LC50 of acifluorfen in early-stage wild-type zebrafish, determining it to be 54.99 mg/L. Subsequent examinations revealed morphological changes in zebrafish, including reduced body length. Using the cmlc2:dsRED transgenic model, we observed heart dysfunction in acifluorfen-exposed zebrafish, marked by an enlarged heart area, edema, and decreased heart rate. In response to dose-dependent acifluorfen exposure, the inhibition of angiogenesis in the brain was observed in transgenic zebrafish models (fli1a:eGFP). Organ malformations, specifically in the liver and pancreas, were noted, in lfabp:dsRED;elastase:eGFP transgenic models, indicating reduced organ size in acifluorfen-exposed zebrafish. Furthermore, acifluorfen heightened the expression of apoptosis-related genes (casp8, casp9, and tp53) in zebrafish embryos. We then determined whether acifluorfen affected the viability of zebrafish liver (ZFL) cells based on its effects on liver development in vivo. The results indicated that the proliferation of ZFL cells decreased significantly in a dose-dependent manner. Additionally, acifluorfen-treated ZFL cells exhibited a slight increase in apoptotic cells stained with annexin V and propidium iodide. In summary, these findings establish a baseline concentration for acifluorfen's effects on aquatic ecosystems and non-target organisms.