Perfluorobutane sulfonate (PFBS) is a synthetic organic molecule that belongs to the per and polyfluoroalkyl substances family. Due to its unique physicochemical characteristics, PFBS has been extensively used in consumer products and industries. However, its increasing usage and chemical stability cause environmental pollution and bioaccumulation. The toxicological effects of PFBS were not well studied. In this study, the impact of PFBS on zebrafish embryos was evaluated. PFBS (1000-1500 μM) exposure exhibited increased mortality and malformation in a concentration-dependent manner. After 96 hour post-fertilization of PFBS exposure, the LC50 was estimated to be 1378 μM. Furthermore, PFBS (1.4, 14, 140, 1400 μM) exposure significantly increases oxidative stress by suppressing antioxidant levels. Locomotor behavior analysis revealed that PFBS exposure caused locomotor changes in zebrafish larvae. Acetylcholine esterase activity was also reduced in the PFBS-exposed groups. Gene expression study showed that PFBS exposure downregulated the antioxidant gene expression in zebrafish larvae. Overall, the current study reveals that PFBS can trigger oxidative stress-induced apoptosis by reducing antioxidant activity in zebrafish larvae.

Non-invasive optical registration and subsequent analysis of heart rate (HR) and heart rate variability (HRV) in transparent aquatic animals have recently been proposed as convenient toxicological endpoints, well-suited for automation data acquisition and processing. This approach was evaluated in experiments involving juvenile Daphnia magna and zebrafish (Danio rerio) embryos exposed to glyphosate solutions (20 mg/L, 2 mg/L, 0.2 mg/L, and 0.02 mg/L) and imidacloprid solutions (30 mg/L, 3 mg/L, 0.3 mg/L, and 0.03 mg/L). The findings indicate that cardiac performance assessment is a promising approach for short-term toxicity evaluation. However, the sensitivity of this physiological endpoint to various external factors may limit its broader application. Results from the two model species highlight their differing sensitivities to the tested substances, emphasizing the need for thorough preliminary studies before establishing this method as a standardized toxicological tool. The potential development and improvement of techniques for assessing heart rate in zebrafish and daphnids are discussed.

β-Cypermethrin (β-CYP), a synthetic pyrethroid pesticide, is widely used for insect management. However, it also affects non-target organisms and pollutes aquatic ecosystems. Tetrahymena thermophila, a unicellular ciliated protist found in fresh water, is in direct contact with aquatic environments and sensitive to environmental changes. The proliferation of T. thermophila was inhibited and the cellular morphology changed under β-CYP stress. The intracellular ROS level significantly increased, and SOD activity gradually rose with increasing β-CYP concentrations. Under 25 mg/L β-CYP stress, 687 genes were up-regulated, primarily enriched in the organic cyclic compound binding and heterocyclic compound binding pathways. These include 8 ATP-binding cassette transporters (ABC) family genes, 2 cytochrome P450 monooxygenase genes, and 2 glutathione peroxidase related genes. Among of them, ABCG14 knockdown affected cellular proliferation under β-CYP stress. In contrast, overexpression of ABCG14 enhanced cellular tolerance to β-CYP. The results demonstrated that Tetrahymena tolerates high β-CYP concentration stress through various detoxification mechanisms, with ABCG14 playing a crucial role in detoxification of β-CYP.

Toxic emission from industrial activity is a serious problem, particularly with regard to the quality of water. Thus, the ISO 11348-3 standard for assessing water quality has been established. This method is used to determine solution toxicity from the bioluminescence inhibition of Aliivibrio fischeri. However, the accuracy of measurements is influenced by the selection of individual reaction time points. This study explores the utility of the area under the curve (AUC) method in water quality detection and evaluates how A. fischeri responds to three toxicants, namely ethanol, acetone, and zinc sulfate, over time. The half-maximal effective concentrations of these three substances were found to be 10.13 %, 5.02 %, and 19.49 mg/L, respectively. Compared with the results from individual reaction time point assessments, the results of AUC comprehensively captured the effects of the toxicants, including time-dependent effects and hormetic effects, by capturing dynamic changes under different toxicant concentrations and reaction times. Therefore, AUC analysis mitigates the pitfalls associated with individual reaction times and provides a more accurate and reliable assessment method for water quality detection, contributing to a better understanding of the impact of toxic substances on aquatic environments.

Dimethyl sulfoxide (DMSO) is a solvent used to dissolve a variety of organic compounds. It is presumed to be non-toxic at concentrations below 1 % v/v, although several studies have demonstrated that low dose DMSO exposure can alter cellular biochemistry. This study evaluated the toxicity of DMSO at 0.0002 % v/v to the Sydney Rock oyster, Saccostrea glomerata, following 7d of exposure. Metabolites were chosen as the toxicity endpoints because they can be used as energy sources and counteract contaminant-induced stress. Relative to seawater controls, exposure to DMSO caused a 74 % significant change in metabolites in the female digestive gland, including decreases in most amino acids, carbohydrates, nicotinamides, and lipids. The female gonad showed a 43 % significant change in metabolites, with decreases in amino acids and carbohydrates, but increases in lipids. The male digestive gland showed a 29 % significant change in metabolites, with increases in lipids. The decline in metabolites in the female digestive gland, but not in the male digestive gland, may be due to their differential metabolic demands. Furthermore, pathway impact analysis revealed that DMSO exposure altered energy metabolism, disturbed osmotic balance, and induced oxidative stress in oysters. Because the effects of DMSO are not uniform across gender and tissue, use of DMSO as a solvent will confound metabolomic experimental results when comparisons among sexes and/or tissues are integral to the experimental design. There is a risk of incomplete dissolution of contaminants unless carrier solvents are used. Therefore, in practice, a solvent control along with a water control is recommended for experimentation.

Antioxidant indices and hemocytes apoptosis in the 6th instar larvae of Hermetia illucens., and their correlation with larval growth were evaluated by exposing larvae to different concentrations of Cu for 1, 3 and 5 generations. Cu accumulated in larval hemolymph showed significant dose-dependent relationship with Cu concentrations in diets within a generation. Larval growth was only promoted after low concentrations of Cu exposure for 1 generation, while seriously affected after high concentrations of Cu exposure. Though total antioxidant capacity activity in larval hemolymph in treatment groups was all higher than that in control, it was increased at lower levels of Cu, while decreased with increasing Cu concentrations at higher levels of Cu exposure. The catalase (CAT) activity and metallothioneins (MTs) levels were also characterized as improved at lower levels of Cu, and inhibited at higher levels of Cu exposure. However, CAT activity and MTs levels at higher Cu treatments were significantly lower than that in control. Apoptosis rate of hemocytes was increased with increasing Cu concentrations. Annexin V - fluorescein isothiocyanate (FITC)/ propidium iodide (PI) staining was in accordance with the results exhibited in flow cytometer. Results from transmission electron microscope and comet assay further confirmed that membrane blebbing, nuclear condensation, and DNA fragmentation were gradually apparent with increasing Cu concentration. All parameters in different generation had similar dose-dependent trends, but the effects were strongest in the fifth generation. This study indicated that at some extent growth of H. illucens were associated with antioxidant responses and apoptosis induced by Cu.

Ammonia nitrogen, a common aquaculture pollutant, harms crustaceans by causing intestinal inflammation, though its exact mechanisms are unclear. Thus, we exposed shrimp to 0, 2, 10 and 20 mg/L NHCl exposure for 0, 3, 6, 12, 24, 48, 72 h, and explored the intestinal stress, apoptosis, proliferation, inflammation and its histopathological changes. This research indicated that ammonia nitrogen exposure heightens plasma dopamine (DA), 5-hydroxytryptamine (5-HT), norepinephrine (NE), and acetylcholine (ACh) levels, alters gene expression of neurotransmitter receptors in the intestine, triggering the PLCCa pathway and induces endoplasmic reticulum stress. Additionally, mitochondrial fission-related genes (Drp1, FIS1) significantly increase, the level of reactive oxygen species (ROS) was significantly elevated in the intestine, which induced DNA damage effects and initiated the DNA repair function, mainly through the base excision repair pathway, but with a low repair efficiency. By determining the expression of key genes of caspase-dependent and non-caspase-dependent apoptotic pathways, it was found that ammonia nitrogen exposure induced apoptosis in intestinal cells, proliferation key signaling pathways such as Wnt, EGFR and FOXO signaling showed an overall decrease after ammonia nitrogen exposure, combined with the gene expression of cell cycle proteins and proliferation markers, indicated that the proliferation of intestinal cells was inhibited. Performing pearson correlation analysis of intestinal cell damage, proliferation, and inflammatory factors, we hypothesized that ammonia nitrogen exposure induces intestinal endoplasmic reticulum stress and mitochondrial fission, induces elevated ROS, leads to DNA damage, and causes inflammation and damage in intestinal tissues by the underlying mechanism of promoting apoptosis and inhibiting proliferation.

Perillaldehyde (PAE), a prevalent flavoring agent, has raised safety concerns due to conflicting evidence regarding its toxicity. This study provides a comprehensive assessment of the developmental and neurotoxic effects of PAE in zebrafish, elucidating the underlying mechanisms of its toxicity. Results showed that PAE affected the viability and hatching rate of zebrafish at 96 h postfertilization with the 50 % lethal concentration (LC50) of 7.975 mg/L. Furthermore, exposed‌ to a non-lethal concentration of 4 mg/L PAE induced a spectrum of morphological abnormalities, such as pericardial edema, delayed yolk sac absorption, reduced body length, and microphthalmia. Behavioral observations revealed that PAE reduced motor ability, and was accompanied by an increase in spontaneous turning angle and angular velocity. Using the TG(elav13:EGFP) transgenic model, we observed the number of newborn neurons was reduced, indicating that PAE induced obvious neurotoxic effects. Additionally, this concentration facilitated the accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), concomitantly decreasing the activity of antioxidant enzymes. QRT-PCR analysis revealed that PAE down-regulated Nestin and Neurogenin1 gene expression, up-regulated Glipr1a and Nox1 gene expression, and inhibited the Nrf2/HO-1 pathway. Notably, co-administration of N-acetylcysteine (NAC), an inhibitor of oxidative stress, mitigated oxidative stress levels and partially ameliorated the neurotoxicity. These findings suggest that oxidative stress is the primary mediator of PAE-induced neurotoxicity. This study provides crucial insights for the safe application of PAE.

Amitriptyline (AMI), one of the widely used tricyclic antidepressants (TCAs), has become a pharmaceutical contaminant frequently detected in aquatic ecosystems. However, the impacts of AMI exposure and underlying mechanisms on fish are still limited. In this study, adult zebrafish (F0) were exposed to AMI at 0 (control), 0.8, and 8 μg/L for 14 days. Subsequently, the exposed zebrafish were paired for spawning, and their offspring (F1) were reared in an AMI-free medium until 5 days post-fertilization (dpf). This study aimed to assess variations in behaviors and neurotransmitter levels in both the F0 (at the end of the 14-day exposure) and F1 generations (at 5 dpf). As a result, waterborne AMI exposure significantly reduced the locomotor activity, frequency of body contact, and duration of chase in F0 zebrafish, and resulted in notable changes in monoamine neurotransmitter levels in their brains. Parental exposure to AMI significantly elevated the heart rate and eye movement but reduced the locomotor activity in the F1 zebrafish, also along with significant changes in monoamine neurotransmitters and acetylcholine. Furthermore, significant correlations between the changes in behavioral traits and neurotransmitter levels were identified in both F0 and F1 generations. Our findings confirm the critical role of monoamine modulation in the neurobehavioral toxicity of AMI on zebrafish and their offspring, and emphasize the importance of paying attention to its multigenerational effects on fish.

Autophagy is an essential response mechanism to environmental stress during the evolution of organisms. DRAM2 (Damage-regulated autophagy regulator 2) is recognized as necessary for the process of p53-mediated cell apoptosis. Although the role of DRAM2 in apoptosis has been confirmed, the mechanism of its relationship with autophagy is still unclear. Here we describe PvDRAM2 features and functions. We found that nitrite stress induced autophagy accumulation and ROS production. A novel DRAM-homologous protein, DRAM2, was cloned, and its expression is significantly up-regulated under nitrite stress conditions. PvDRAM2 primarily localizes within the cytoplasmic lysosome.Loss of PvDRAM2 increased sensitivity response to nitrite stress of Pacific white shrimp. And silenced of PvDRAM2 promoted ROS production and inhibited autophagy accumulation. In addition, silenced of PvDRAM2 decreased the autophagy-related protein of p62, Beclin 1, and LC3 expression under nitrite stress of Pacific white shrimp. Collectively, these studies uncover a novel critical role for PvDRAM2 in regulating autophagy under nitrite stress. Specifically, PvDRAM2 is essential for the induction of autophagy, enabling Pacific white shrimp to adapt to environmental stress. This provides mechanistic insight into how autophagy functions as a way for Pacific white shrimp to cope with environmental challenges.

Copper excess has been tested as an anticancer therapy, due to its properties to generate oxidative stress resulting in tumoral cell death. Thus, this study aimed to evaluate the impact of copper excess on oxidative stress and antioxidant responses in glioma cells, establishing the antioxidant system as a target of copper toxicity in tumoral cells. C6 and U-87 MG cells were exposed to CuSO (0-600 μM) for 24-48 h. SOD, CAT, GPx, GR, and CK activities, protein and non-protein thiol levels (PSH and NPSH), and O production were assessed, alongside SOD1, GPx1, and GR gene expression. Results revealed a decrease in GPx, GR, and CAT activity after CuSO exposure in both cell lines over 24-48 h, while SOD activity initially increased, then declined after 48 h. CK activity was also decreased in C6 cells. NPSH and PSH levels dropped after 24 h, and O production was observed in all CuSO concentrations. GR mRNA was reduced in both cell lines, contrasting with increased GPx1 mRNA in C6. U-87 MG cells exhibited higher levels of SOD1 mRNA, while C6 cells displayed lower expression. Our findings suggest that copper excess limits antioxidant enzyme activity and thiol levels, particularly in the C6 cells, likely attributable to oxidative stress or direct copper-enzyme interactions. Moreover, our results imply differences in copper toxicity regarding the cell lineage used, highlighting the importance of analyzing high copper levels effects in different models. Moreover, it could be proposed that the antioxidant system is a target of copper toxicity, contributing to glioma cell death.

Crustaceans often encounter the occurrence of various hypoxic situations, and in order to cope with this situation, they have evolved a series of antioxidant defenses against hypoxic stress. The present study was conducted to investigate the physiological and molecular regulation of hypoxic stress in the Chinese mitten crab (Eriocheir sinensis). We used the method of reducing dissolved oxygen in water to treat the juvenile E. sinensis with hypoxia. The results showed that total antioxidant capacity, superoxide dismutase, catalase and malondialdehyde contents in the gills of juvenile crabs were significantly elevated under hypoxia. In addition, gill tissues from normoxic control (NC), hypoxia-sensitive (HS) and hypoxia-tolerant (HT) groups were analysed using transcriptomic sequencing. The results revealed that 2124, 2946 and 2309 differentially expressed genes (DEGs) were found in NC vs. HS, NC vs. HT and HS vs. HT, respectively. The analysis of KEGG pathway enrichment indicated DEGs were predominantly enriched in oxidative phosphorylation, adipocytokine signaling pathway, and protein processing in endoplasmic reticulum in HS vs. HT. Enrichment of the MAPK signaling pathway, apoptosis, glucagon signaling pathway, and arachidonic acid metabolism was also found in the comparisons of NC vs. HS and NC vs. HT. The DEGs in these pathways may play a key role in gill tolerance to hypoxia. These results provide new insights and references for the oxidative defense and adaptive regulatory mechanisms of gill tissues of juvenile E. sinensis in response to hypoxic stress.

Growing evidence suggests that a flavonoid-rich diet can prevent or reverse the effects of stressors, although the underlying mechanisms remain poorly understood. One common and abundant flavonoid found in numerous foods is quercetin. This study utilizes the pond snail Lymnaea stagnalis, a valid model organism for learning and memory, and a simple but robust learning paradigm-operant conditioning of aerial respiration-to explore the behavioral and transcriptional effects of different stressors on snails' cognitive functions and to investigate whether quercetin exposure can prevent stress effects on learning and memory formation. Our findings demonstrate that three different stressors-severe food deprivation, lipopolysaccharide injection (an inflammatory challenge), and fluoride exposure (a neurotoxic agent)-block memory formation for operant conditioning and affect the expression levels of key targets related to stress response, energy balance, and immune response in the snails' central ring ganglia. Remarkably, exposing snails to quercetin for 1 h before stress presentation prevents these effects at both the behavioral and transcriptional levels, demonstrating the potent stress-preventive properties of quercetin. Despite the evolutionary distance from humans, L. stagnalis has proven to be a valuable model for studying conserved mechanisms by which bioactive compounds like quercetin mitigate the adverse effects of various stressors on cognitive functions across species. Moreover, these findings offer insights into quercetin's potential for mitigating stress-induced physiological and cognitive impairments.

Although the measurement of short-chain chlorinated paraffins (SCCPs) in aquatic ecosystems has increased, limited information is available on their toxic effects on aquatic animals. To evaluate the harmful effects of SCCPs, we assessed their acute impact on 24-h survival and biochemical parameters, as well as their chronic effects on growth and reproduction over three generations in the harpacticoid copepod Tigriopus japonicus. Dose-dependent increases in mortality were observed, with an LC50 value of 74.6 μg L for 24 h. Acute exposure to the LC10 value for 24 h significantly reduced feeding behavior, accompanied by a notable decrease in acetylcholinesterase enzymatic activity. Simultaneously, the intracellular levels of reactive oxygen species increased, along with elevated malondialdehyde contents. Glutathione level was increased by the LC10 value of SCCPs with the induction of enzymatic activities of antioxidant defense components, including glutathione S-transferase, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. When T. japonicus was continuously exposed to 1/10 of the NOEC and NOEC values for 12 days across three generations (F0-F2), growth retardation was observed in the F2 generation, with delay in the developmental periods from nauplius to adult. Although the total number of nauplii per brood was not significantly altered across generations, a significant delay in the onset of reproduction was observed in the F2 generation. Our findings suggest that even sublethal concentrations of SCCPs can negatively affect the health of copepod populations with consistent exposure.

Spintor® (SPIT®) is a commercial formulation of a bioinsecticide with the active ingredient Spinosad (SPIN). Despite the efforts of regulatory agencies, there still is a lack of information regarding short- and long-term exposures to soil-dwellers, as well as effects at environmentally relevant concentrations. This work aimed to evaluate the effects of SPIT® and SPIN, on the oligochaete Eisenia fetida, and the arthropod Folsomia candida. For this, natural soil was spiked with environmentally relevant concentrations (0.00-1.49 mg of the active ingredient·kg of dry soil) to assess avoidance behaviour in E. fetida and reproduction effects on both species. Further, in E. fetida adults exposed for 2- and 28-day biomarkers of oxidative stress, energetic reserves, neurotoxicity and genotoxicity were evaluated. A significant reduction in juvenile production for F. candida was observed for SPIT® at ≥0.66 mg kg and SPIN at ≥0.13 mg kg, and although no effect was observed on E. fetida reproduction, the oligochaeta revealed a tendency to avoid soil spiked with SPIT® at 0.44, 0.66 and 1.49 mg kg. The sub-individual responses of E. fetida demonstrate genotoxicity upon exposure to SPIT® and SPIN for 2 days. The 2-day exposures of SPIT® and SPIN seem to induce defence mechanisms, and in general, SPIN exerted higher effects than SPIT® on the oligochaetes. Overall, the pro-oxidant performance and energy metabolism pathways were disrupted in both exposures to SPIT® and SPIN. The results suggest that spinosyns-based products can have an impact on soil arthropods F. candida and oligochaete's health, possibly affecting their essential functions in terrestrial ecosystems.

Microplastics (MPs) have become a major focus of environmental toxicology, raising concerns about their potential adverse effects on animal organs and body systems. As these tiny particles infiltrate ecosystems, they may pose risks to the health of organisms across diverse species. In this study, we attempted to examine the neurotoxic effects of MPs exposure on avian hypothalamus by using an animal model-Japanese quail (Coturnix japonica). The quails of 7-day-old were exposed to 0.02 mg/kg, 0.4 mg/kg and 8 mg/kg polystyrene microplastic (PS-MPs) of environmental relevance for 35 days. The results showed PS-MPs exposure did damages to hypothalamic structure characterized by neuron malformation, irregular arrangement and cellular vacuolation after 5-week exposure. PS-MPs exposure also induced Nissl body reduction and dissolution in the hypothalamus. Moreover, the decrease of acetylcholinesterase (AchE) activity and increasing acetylcholine (Ach) indicated that PS-MPs exposure caused hypothalamic neurotransmission disturbance. PS-MPs exposure also led to neuroinflammation by disrupting the balance between proinflammatory and anti-inflammatory cytokines. Moreover, increasing reactive oxygen species (ROS) and malondialdehyde (MDA) generation with reducing antioxidants indicated PS-MPs led to hypothalamic oxidative stress. Additionally, RNA-Seq analysis found that both transforming growth factor-β (TGF-β) signaling and forkhead box O (FoxO) signaling were disturbed in the hypothalamus by PS-MPs exposure. Especially, the increasing ROS led to TGF-β activation and then induced hypothalamic inflammation by nuclear factor κB (NF-κB) activation. The present study concluded that oxidative stress might be an important mechanistic signaling involved in MPs neurotoxicology.

Avermectin (AVM) is a broad-spectrum antibiotic from the macrolide class, extensively employed in fisheries and aquaculture. Nevertheless, its indiscriminate utilisation has resulted in a substantial accumulation of remnants in the aquatic ecosystem, potentially inflicting significant harm to the cardiovascular system of aquatic species. Ferulic acid (FA) is a naturally occurring compound in wheat grain husks. It possesses potent anti-inflammatory and antioxidant properties, which can help reduce cardiovascular damage. Additionally, its affordability makes it an excellent option for aquaculture usage as a feed additive. This article explored the potential of FA as a feed additive to protect against AVM-induced heart damage in carp. We subjected carp to AVM for 30 days and provided them with a diet of 400 mg/kg of FA. FA substantially reduced the pathogenic damage to heart tissue caused by AVM, as shown through hematoxylin-eosin staining. The biochemical analysis revealed that FA markedly enhanced the activity of antioxidant enzymes catalase (CAT), glutathione (GSH), and total antioxidant capacity (T-AOC) while reducing the malondialdehyde (MDA) content. Furthermore, qPCR analysis demonstrated a substantial increase in the mRNA levels of transforming growth factor-β1 (tgf-β1) and interleukin-10 (il-10) simultaneously, significantly reducing the expression levels of interleukin-10 (il-6), interleukin-1β (il-1β), tumor necrosis factor-α (tnf-α) and inductible nitric oxide synthase (inos). Through the mitochondrial apoptotic route, FA reduced AVM-induced cell death in carp heart cells by upregulating bcl-2 while downregulating the mRNA expression levels of bax, fas, caspase8 and caspase9. In summary, FA alleviated cardiac injury by inhibiting AVM-induced oxidative stress, inflammatory response, and apoptosis in carp heart tissue.

Air exposure stress can induce stress response of Eriocheir sinensis and affect its normal life activities. The goal of this study was to investigate the effects of water immersion on the recovery of hepatopancreas immune-related enzyme activity, intestinal microbial diversity and metabolic level of Chinese mitten crabs after exposure to air. The results show that immersion can effectively alleviate the adverse effects of air exposure on the antioxidant capacity and immune capacity of Chinese mitten crabs, and the longer the time of immersion, the more obvious the recovery effect. Among them, the levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and acid phosphatase significantly increased after exposure to air (P < 0.05), reached a peak at 3 h, began to decline after immersion, and returned to a level close to the initial value at 24 h (P < 0.05). In addition, after exposure to air, the glucose and total cholesterol in haemolymph of Eriocheir sinensis were significantly different from the initial values (P < 0.05), gradually recovered to the initial level after re-immersion. However, changes in intestinal flora and hepatopancreas metabolism caused by air exposure did not fully recover after water exposure, and its negative effects did not completely disappear. The sequencing results showed that the species composition and diversity of intestinal microorganisms of Chinese mitten crab changed after air exposure and immersion treatment. The relative abundance of Actinomycetes increased significantly, while that of Proteobacteria and Firmicutes decreased significantly. Metabolomics analysis showed that air exposure and immersion destroyed the metabolic balance of amino acids and carnitine, reduced the level of carnitine metabolism, hindered the absorption of nutrients, and led to the accumulation of harmful substances.

The presence of antibiotic residues in the aquatic environments poses great potential risks to the aquatic organisms, and even human health. Elucidating the interaction mechanisms between antibiotics and biomacromolecules is crucial for accurately assessing and preventing their potential risks. Therefore, the toxicity of three beta-lactam antibiotics on Escherichia coli (E. coli) was investigated by using the time-dependent toxicity microplate analysis method in this study. Then, molecular docking and molecular dynamics simulation technologies were used to elucidate the potential molecular interactions between β-lactam antibiotics and penicillin-binding proteins of E. coli, and their correlation with the physical and chemical behaviors observed in the physiological and biochemical experiments. The results show that three antibiotics exert inhibitory effects on E. coli cells by modifying their membrane permeability, and even more severe cell damage including rupture, wrinkling, adhesion, indentation, elongation and size alterations. But, toxic effect of the three antibiotics on E. coli varies, and toxicity order is followed by meropenem > cefoperazone > amoxicillin. Van der Waals forces play a vital role in the molecular interactions between the three antibiotics penicillin binding protein of E. coli and the sequence of binding free energy is consistent with the observed toxicity order. Shape compensation is the principal determinant for the binding of antibiotics to penicillin binding proteins, which pertains to the drug-induced alteration in the three-dimensional conformation of penicillin binding proteins.

Over the past decades, the concern about lead pollution in marine environments has increased due to its remarkable toxicity, even at low concentrations. Lead is one of the significant contaminants arising from human activities in Antarctica. However, its effects on polar photosynthetic organisms are poorly known. This work aims to evaluate the effects of two different environmental concentrations of lead (10 μg/L and 50 μg/L) on pigment content, antioxidant enzyme activities (catalase, superoxide dismutase, ascorbate peroxidase and glutathione-S-transferase), metabolome, thalli morphology and cell ultrastructure of the red seaweed Iridaea cordata (Turner) Bory from Terra Nova Bay (Ross Sea, Antarctica). The results highlighted that lead exposure decreased phycocyanin and phycoerythrin content, starting from 10 μg/L, while induced carotenoid accumulation at 50 μg/L. Catalase, ascorbate peroxidase, and superoxide dismutase activities generally increased after lead exposure and distinct biochemical features were identified in the control and treatment groups. Further lead-related effects on cell ultrastructure comprised floridean starch accumulation and plastoglobuli formation. Overall, our results suggested that the enhanced formation of reactive oxygen species in response to lead altered the photosynthetic pigment pattern, antioxidant defenses, metabolome and ultrastructure of I. cordata.

The increasing release of tire-derived particles, particularly those containing N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), into the environment has raised concerns regarding their ecological impact. This study aims to elucidate the toxicological effects of 6PPD on the metabolism in early developmental stage of zebrafish. Larval zebrafish were exposed to 10 and 100 μg/L 6PPD, and some endpoints in biochemical parameters, gene expression, and metabolism were analyzed. The results showed that 6PPD exposure disrupted glucolipid metabolism in zebrafish larvae, evidenced by increased triglyceride (TG) levels and decreased glucose content. Nile red staining indicated significant lipid accumulation in the liver and intestines. Additionally, RT-qPCR analysis revealed the upregulation of genes involved in lipid synthesis and metabolism, such as ppar-γ and fas, and downregulation of glycolysis-related genes like pk and gk. Furthermore, the untargeted metabolomics technique was used to identify a total of 220 differentially expressed metabolites (DEMs) with changes in amino acid metabolism, lipid metabolism, and the TCA cycle. KEGG pathway enrichment analysis highlighted disruptions mainly in Taurine and hypotaurine metabolism, Arginine and proline metabolism, and Histidine metabolism, which played very important roles on energy metabolism in zebrafish. The results provided some critical insights into the ecological risks associated with 6PPD.