The increased use of agrochemicals to enhance crop production has had detrimental environmental effects including implication in the sharp decline of North American farmland-breeding birds. Here, using a combination of deep shotgun metatranscriptomics and pesticide exposure data, we sought to assess whether exposure to cotton (Gossypium spp.) production had a differential effect on ileum multi-kingdom microbial activity, metabolism, anti-microbial resistance, and virulence factors of sedentary northern mockingbirds (Mimus polyglottos) sampled from two cotton-producing areas (16 birds in total) and one uncultivated area (7 birds) in Texas, USA. Both Shannon Index values (Adj. r2 = 0.174, F(1,21) = 5.633, p = 0.027) and a Mantel test (Spearman ρ = 0.184, p = 0.013) supported a relationship between metabolically active microbiota Bray-Curtis dissimilarities and differences in pesticide mixtures among study areas. Virulence factor richness (Adj. r2 = 0.182, F(1,21) = 5.890, p = 0.024), Shannon Index (Adj. r2 = 0.231, F(1,21) = 7.612, p = 0.012), and load (sum of virulence factor abundances; Adj. r2 = 0.160, F(1,21) = 5.194, p = 0.033) were related to total pesticide load (total quantity of pesticides). We found no pesticide effects on expression of either antimicrobial resistance genes or metabolic pathways.
Antibiotics are a common contaminant of freshwaters, yet surprisingly understudied compared to other classes of drugs. Even trace concentrations of antibiotics can alter the gut microbiome, in turn affecting multiple systems including physiology, biochemistry, and behavior. Concurrently, climate change is leading to higher average temperatures and more frequent temperature spikes. The microbiome of poikilotherms is also highly sensitive to temperature. Little is known of how these two stressors interact. In this study we investigated the effects of amoxicillin, an antibiotic that is widely used in human and veterinary medicine, on the swimming behavior and predatory avoidance responses of zebrafish at two temperatures, 28°C (normal) and 32°C (heat-stressed). Additionally, we investigated the effects of the two stressors on the gut microbiome and heat shock protein expression. Both temperature and amoxicillin affected key behaviors including boldness, sociability, and swimming speed, with fish exposed to low-dose amoxicillin having higher swimming velocity suggesting a possible hormesis response. Amoxicillin exposure also increased fish boldness, while temperature had the opposite effect. A high temperature also reduced fish sociability. Both stressors also altered zebrafish responses to a conspecific alarm cue and induced heat shock protein gene expression. Heat stress and amoxicillin both altered the fish gut microbiome at the genus level with heat stress alone increasing several genera (e.g., Nordella, Nocardia, Reyranella), while heat stress plus high amoxicillin (20 μg/L) further increased others (e.g., Bradyrhizobium, Legionella, Xanthobacter). Overall alpha diversity (Shannon) changed little, but community composition (ANOSIM) shifted most clearly under high amoxicillin and under heat combined with amoxicillin, indicating dose- and temperature-dependent restructuring of the gut microbiome. Overall, the microbiome is emerging as an important regulator of physiology and behavior that is vulnerable to multiple stressors.
This study assessed the contamination levels, bioaccessibility, and potential health risks of As, Cd, Cu, Pb, and Zn in sediments from three dry riverbeds (El Beal-EB, Las Matildes-LM, and Ponce-PN) impacted by historical mining activities in the Cartagena-La Unión Mining District. Sediment samples (20 samples from EB, 13 samples from LM, and 19 samples from PN) were collected and analyzed for total and bioaccessible metal(loid) concentrations, and physicochemical properties. Spatial distribution for the contamination factor (Cf), pollution load index (PLI), and correlation analyses were employed to evaluate sediment pollution status. Bioaccessibility was determined using the Solubility Bioaccessibility Research Consortium (SBRC) method. Human health risks were assessed using hazard quotients (HQ) and carcinogenic risk (CR) for children, considering total (scenario 1) and bioaccessible (scenario 2) concentrations. The PLI indicated severe contamination, with maximum values of 66, 78, and 80 for EB, LM, and PN, respectively. Bioaccessible fractions varied widely across all metals and sites, ranging from 0.04% for As to 98.4% for Cd in Las Matildes; in El Beal, Pb bioaccessibility varied between 22.0% and 92.1%, while in Ponce, Pb bioaccessibility ranged from 5.6% to 96.3%. In addition, PN exhibited that pH and inorganic carbon collectively govern metal(loid) bioaccessibility, with strongly acidic conditions enhancing the solubility of Cd, Pb, and Zn. The correlations between total and bioaccessible metal(loid) concentrations were strong and significant in EB-PN, but no correlation in LM was found, emphasizing the importance of site-specific geochemical factors in assessing human health risks. Health risk assessments revealed that total Pb concentration posed the highest non-carcinogenic risk (non-carcinogenic risk was considered significant when HQ > 1), with HQ reaching a mean value of 2.43 in LM and 1.09 in EB. However, when non-carcinogenic risk was evaluated via bioaccessible fraction, mean HQ values decreased by 58% for Pb, remained above the safety threshold (HQ > 1) in specific samples. Additionally, total As concentrations contributed to carcinogenic risk, with values exceeding the threshold (CR > 10-5) across the riverbeds. However, when bioaccessible concentrations were considered, carcinogenic risk was substantially reduced (CR < 10-5), indicating no significant carcinogenic risk. This study highlights the importance of considering bioaccessibility in risk assessment studies of mining-impacted areas.
Thiram is an agricultural fungicide known to disrupt cellular calcium homeostasis by inducing endoplasmic reticulum (ER) stress and mitochondrial calcium overload in hepatic and growth plate (GP) tissues. Current study investigated thiram-induced alterations at mitochondria-associated membranes (MAMs) and their impact on inter-organ calcium signaling. Following thiram exposure in chickens, hepatic ER stress markers GRP78 and CHOP, along with key calcium-transfer proteins mediating ER-mitochondrial coupling, including inositol 1,4,5-trisphosphate receptor 1 (IP3R1) and voltage-dependent anion channel 1 (VDAC1), were significantly upregulated. Importantly, hepatic ER stress driven hyperactivation of IP3R1/VDAC1 signaling was accompanied by parallel calcium dysregulation and mitochondrial stress responses in the tibial growth plate, providing direct evidence that liver ER stress acts upstream of skeletal calcium imbalance. These findings establish a previously unrecognized liver-bone axis in which thiram-induced hepatic ER stress propagates calcium signaling disturbances to the growth plate, thereby disrupting chondrocyte calcium homeostasis and bone development. Collectively, this study elucidates a mechanistic framework linking MAM-mediated calcium-transfer, ER stress, and cross-organ communication, offering new insights into how toxicant-induced hepatic stress orchestrates systemic calcium metabolism and skeletal pathology.
Cephalosporin is increasingly recognized as an emerging aquatic pollutant capable of inducing systemic toxicity in non-target organisms. This study investigated the comparative toxic effects of three commonly used cephalosporins-cefepime, ceftriaxone, and cefotaxime-on African catfish (Clarias gariepinus), with emphasis on hematological, cytotoxic, genotoxic, hepatorenal, and metabolic alterations, as well as the potential protective role of dietary Chlorella vulgaris (50 g/kg feed). Fish were allocated into seven experimental groups: control, cefepime (0.5 mg/L), cefepime + C. vulgaris, ceftriaxone (1 mg/L), ceftriaxone + C. vulgaris, cefotaxime (1 mg/L), and cefotaxime + C. vulgaris, and exposed for 15 days. Exposure to cephalosporin induced significant hematological disturbances, including reductions in erythrocyte count, hemoglobin concentration, hematocrit, and total leukocyte count, together with marked changes in differential leukocyte profiles. In addition, all tested cephalosporin significantly increased erythrocyte apoptosis and DNA damage, as evidenced by elevated apoptotic cell percentages and increased comet assay tail moment values, confirming marked cytotoxic and genotoxic stress. Serum biochemical analyses revealed significant elevations in liver enzymes, renal function markers, total protein, total cholesterol, and glucose, indicating substantial hepatic, renal, and metabolic impairment, with cefepime generally exerting the most pronounced biochemical toxicity, whereas ceftriaxone produced the highest genotoxic response. Dietary supplementation with Chlorella vulgaris partially but significantly ameliorated many of these adverse effects by improving hematological indices, reducing erythrocyte apoptosis, attenuating DNA damage, and modulating hepatorenal and metabolic disturbances, although complete restoration to control levels was not consistently achieved. Collectively, these findings demonstrate that cephalosporin residues can induce multi-system toxicity in C. gariepinus, while C. vulgaris represents a promising natural dietary strategy for mitigating cephalosporin-induced physiological and cellular damage in aquatic organisms.
Despite the frequent co-occurrence of glyphosate and arsenic in agricultural freshwater systems, the biochemical mechanisms underlying their combined toxicity in fish remain poorly understood. Here, we evaluated the acute (96 h) individual and joint effects of glyphosate (0.5 mg/L) and arsenic [As(III), 0.5 mg/L] on the Neotropical fish Cnesterodon decemmaculatus using an integrated biomarker approach. Endpoints related to oxidative balance, DNA integrity, neurotoxicity, and energy metabolism were assessed across multiple tissues. Glyphosate exposure induced marked oxidative and metabolic disturbances, including increased catalase activity, glutathione levels, and mitochondrial electron transport system activity, along with reduced cellular energy allocation and glutathione-S-transferase activity. In contrast, arsenic decreased glutathione content, superoxide dismutase activity, lipids, and carbohydrates. Comparable DNA damage levels were observed across single and combined exposures. Co-exposure resulted in non-additive interactions, with mixture effects deviating from the sum of individual responses, leading to either reduced (antagonistic) or enhanced (potentiation) effects depending on the biomarker and its direction of change. Antagonistic interactions predominated for genotoxic and several oxidative stress biomarkers, whereas potentiation was observed for selected metabolic endpoints. Multivariate analysis revealed distinct physiological profiles among treatments, with partial overlap between glyphosate and mixture responses. These findings underscore the complexity of pollutant mixture effects and highlight the need to incorporate combined exposures into ecotoxicological risk assessment.
The intensification of agricultural practices has led to an increase in the use of insecticides, raising concerns about the exposure of non-target organisms, particularly pollinators. In this context, plant-derived essential oils have been proposed as environmentally friendlier alternatives due to their low persistence; however, their toxicological effects on bees remain insufficiently characterized, especially with respect to different exposure routes. This study evaluated the toxicity of Melaleuca alternifolia essential oil to Africanized Apis mellifera worker bees under three exposure pathways: indirect spraying, direct spraying, and ingestion. The essential oil was tested at a concentration of 0.75% (v/v). Bee survival was analyzed using Cox proportional hazards models, while potential sublethal behavioral effects were assessed through vertical displacement and flight resumption assays. Indirect spraying and ingestion did not significantly affect worker survival compared with the control, indicating low toxicity under conditions simulating residual environmental or dietary exposure. In contrast, direct spraying caused an approximately 20% reduction in survival over the experimental period, demonstrating route-dependent toxicity, although mortality remained substantially lower than that observed for the positive control (fipronil). Behavioral assays showed no significant impairment of flight performance in surviving bees. Overall, the results indicate that the toxicity of M. alternifolia essential oil to A. mellifera is strongly influenced by the route of exposure, underscoring the importance of exposure pathways in environmental risk assessment. These findings contribute to understanding the physiological selectivity of botanical insecticides and provide relevant information for evaluating the safety of essential oils for pollinator protection in agroecosystems.
Fluorine-free foam (F3) alternatives that lack per- and polyfluoroalkyl substances (PFAS) are rapidly being adopted for firefighting operations and will be entering ecosystems. Despite this, little is known about their impact on freshwater communities. This knowledge gap is concerning for zooplankton, which are highly sensitive to F3 exposure and serve a keystone role as phytoplankton grazers and prey items for fish and invertebrates. Additionally, it is unknown how resource availability, which widely fluctuates in nature, influences the toxicity of F3s to zooplankton. Using varying algae feeding levels, we investigated how exposure to two F3s, National Foam Avio F3 Green KHC 3% (Avio) and Bio-Ex ECOPOL A 3% FFF (ECOPOL), impacts life history tradeoffs in a freshwater zooplankton, Daphnia magna. At high food levels, sublethal exposure to F3s caused earlier onset of reproduction and increased growth with no apparent tradeoffs, consistent with cases of fecundity compensation or hormesis. In contrast, when no food was provided, individuals exposed to Avio starved earlier, indicating an energetic cost of toxic exposure. This work shows F3s can substantially alter the life history of D. magna, possibly leading to altered freshwater community dynamics and trophic cascades. Additionally, this work highlights that toxic responses, and therefore ecological consequences, can vary based on food availability.
Metal contamination in estuarine environments poses environmental and public health concerns, particularly where surface waters support domestic and subsistence uses. This study assessed the seasonal distribution, controlling mechanisms, and non-carcinogenic health risks of selected metals (Mg, Al, Ba, Fe, Mn, and Zn) in the Buffalo River Estuary, Eastern Cape, South Africa. Water samples were collected from 11 stations during wet and dry seasons and analyzed using standard methods. Descriptive statistics, Pearson's correlation analysis, and principal component analysis (PCA) were applied to evaluate metal distribution, inter-element relationships, and dominant controlling processes. Marked seasonal variability was observed, with higher concentrations of Al (97-1708 μg/L), Ba (7.4-29 μg/L), Fe (54-1751 μg/L), Mn (4-116 μg/L), and Zn (4-23 μg/L) during the wet season, while Mg concentrations were elevated in the dry season (10686-851 382 μg/L) relative to the wet season (1056-1313 μg/L). PCA indicated that wet-season metal dynamics were governed by lithogenic and hydrological processes linked to runoff and suspended sediments, whereas dry-season variability reflected sedimentary geochemical controls, redox processes, conservative mixing, and secondary anthropogenic inputs. Non-carcinogenic health risk assessment for Al, Ba, Fe, Mn, and Zn showed Mn as the largest contributor to risk, although cumulative hazard indices for adults (2.19 × 10-2-1.39 × 10-1) and children (8.10 × 10-2-5.01 × 10-1) remained below unity, indicating low health risk. These findings highlight the dominance of seasonal geochemical processes, providing essential baseline data for water-quality management, and underscore the need for continued monitoring to support effective water-resource management.
Triclosan (TCS) is an antimicrobial compound widely used in pharmaceutical and personal care products (PPCPs). It is classified as a contaminant of emerging concern (CEC) due to its environmental health implications. However, significant knowledge gaps remain regarding the toxic effects of environmentally relevant concentrations of TCS in coastal and marine species, such as bivalves. In this study, the impact of triclosan on the primary heart cell cultures derived from the euryhaline coastal bivalve, Magallana bilineata, was investigated. The heart cells were exposed to various concentrations of TCS, and the IC50 value was determined to be 2.1494 mg L-1. Following this, sub-lethal toxicity tests based on cellular and molecular parameters were conducted using environmentally relevant TCS concentrations. The results demonstrated that TCS induces ROS (reactive oxygen species) production at environmentally relevant levels and also alters gene expression, as evident from the mRNA profiling of superoxide dismutase (Cu/Zn sod), catalase (cat), glutathione peroxidase (gpx), calmodulin (calm), and heat shock protein 70 (hsp70). Furthermore, cardiomyocyte beating patterns varied (contraction impairment, arrhythmic activity, or absence of cardiomyocyte clusters) depending on the TCS concentrations. The results point to ROS-mediated disruptions in excitation-contraction coupling as a likely contributor, and further studies will strengthen mechanistic understanding. Overall, these findings provide critical insights into the cellular and molecular toxicity of environmentally relevant TCS concentrations and support the utility of M. bilineata heart cell cultures for advancing aquatic toxicology research.
Climate change and anthropogenic ignitions are intensifying wildfire frequency worldwide, elevating the risk of freshwater contamination by ash. In water, dissolved ash releases ions and other toxic constituents that increase pH and alter physicochemical conditions, while suspended ash particles may impose mechanical stress, disrupt behavior, and increase exposure through ingestion. However, the relative contributions of these distinct ash exposure pathways to ecological toxicity remain poorly understood. Here, we investigated whether wildfire ash alters crustacean behavior and whether suspended macroparticles and ash-induced pH shifts differentially shape these responses. The freshwater crab Aegla jarai and the cladoceran Daphnia magna were exposed to aqueous ash extracts without suspended macroparticles (dissolved fraction) or containing suspended macroparticles (dissolved plus particulate fractions), alongside a control. For D. magna, treatments with and without pH correction disentangled intrinsic ash toxicity from the effects of alkalinization. In A. jarai, ash did not affect agonistic responsiveness, refuge use, or food consumption. However, locomotor activity increased during the food detection test, particularly in treatments containing macroparticles, consistent with reduced search efficiency without impairing ingestion. In contrast, D. magna exhibited concentration-dependent immobilization (a proxy for mortality), intensified by elevated pH and the presence of macroparticles. Effects on distance traveled were weaker and mainly associated with pH shifts. Together, these findings show that wildfire ash affects freshwater crustaceans through chemical and physical pathways. Ash-induced pH shifts primarily drive ash toxicity, while suspended macroparticles amplify this effect, underscoring the need to consider both dissolved and particulate fractions in postwildfire risk assessments.
Organophosphate esters (OPEs) are found ubiquitously in the environment and exposure to these chemicals has induced behavioral, developmental, and morphological impairments in several model organisms. Yet there is still a lack of understanding of how sub-lethal exposure disrupts organism function at the molecular-level, especially for Daphnia magna. To address this knowledge gap, D. magna responses after exposure to three sub-lethal concentrations consisting of 23.5 mg/L, 59 mg/L, and 118 mg/L for tris(2-chloroethyl) phosphate (TCEP); 2.5 mg/L, 6.25 mg/L, and 12.5 mg/L for tris(2-chloro-1-methylethyl) phosphate (TCPP); 0.125 mg/L, 0.312 mg/L, and 0.625 mg/L for triphenyl phosphate (TPhP) were examined. These OPEs were selected as they are frequently detected in aquatic ecosystems. Targeted mass spectrometry metabolomics was used to measure the molecular-level regulation of key metabolites after 48 h of exposure. Metabolomics technologies can capture changes of metabolite levels in model organisms exposed to sub-lethal concentrations where key metabolic pathways responsible for vital biological functions can be elucidated. Metabolic perturbations in amino acid levels were observed after exposure to OPEs with higher octanol-water partition coefficients (TCPP and TPhP). In addition to the perturbed metabolites shared across all tested OPEs, each OPE resulted in unique perturbations to select metabolites. Most metabolite concentrations exhibited non-monotonic responses following exposure to TCEP and TPhP. In contrast, after TCPP exposure, both non-monotonic and monotonic responses were observed across the measured metabolites. This study distinguishes specific metabolic disturbances that are unique to the side chains attached to the phosphate center when exposed to D. magna. Hence, these metabolites are most sensitive to OPE sub-lethal exposure. Providing novel insights into the diverse modes of action from sub-lethal OPE exposure to a sentinel species allows for more effective risk assessment and water monitoring strategies to be implemented for the protection of freshwater ecosystems.
Malathion (MAL) is a widely used organophosphate pesticide associated with hepatotoxicity through oxidative stress and apoptosis. Morin, a naturally occurring flavonoid, exhibits potent antioxidant and anti-inflammatory properties. This study investigated oxidative stress, inflammatory, and apoptotic alterations induced by acute and subacute MAL exposure in rats and evaluated the potential protective effects of morin. Fifty 3-month-old male Sprague Dawley rats were randomly assigned to six groups: control, morin (200 mg/kg), subacute MAL (150 mg/kg), acute MAL (300 mg/kg), subacute MAL + morin, and acute MAL + morin. At the end of the experimental period, liver tissues and plasma samples were analyzed. Hepatic malondialdehyde (MDA) and glutathione (GSH) levels; catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and glutathione S-transferase (GST) activities; plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) activities; and tissue acetylcholinesterase (AChE), butyrylcholinesterase (BChE), tumor necrosis factor-α (TNF-α), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Bax/Bcl-2 ratio and caspase-3 levels were determined. MAL exposure significantly increased MDA, TNF-α, Bax, Bax/Bcl-2 ratio, caspase-3, and liver enzyme activities, while decreasing GSH levels, antioxidant enzyme activities, AChE, BChE, and Bcl-2 levels (p < 0.001). Histopathological findings included hepatocellular swelling, focal necrosis, sinusoidal congestion, periportal infiltration, and bile duct proliferation, with more pronounced lesions in the subacute MAL group. Morin administration markedly attenuated biochemical alterations and improved histopathological damage. These findings demonstrate that MAL induces hepatotoxicity by promoting oxidative stress, inflammation, and apoptosis, whereas morin exerts significant hepatoprotective effects, likely through modulation of antioxidant defense systems and apoptotic pathways.
Cadmium (Cd) is a persistent environmental heavy metal and a major public health concern because it persists in the body for long periods and gradually accumulates in vital organs, particularly the liver, kidneys, and brain. Chronic Cd exposure promotes the excessive production of reactive oxygen species (ROS), which ultimately leads to oxidative stress, inflammatory responses, organ dysfunction, and neurobehavioral alterations. Apis mellifera bee venom (BV) consists of a diverse mixture of biologically active peptides, including key components such as melittin and apamin with documented antioxidant, anti-inflammatory, and neuroprotective properties. However, to date, no studies have directly investigated its potential to mitigate Cd-induced multi-organ toxicity. Therefore, the present study aimed to evaluate the protective effects of BV against Cd-induced hepatorenal injury, oxidative imbalance, and anxiety-like behavior in a rat model, and to investigate its potential as a natural therapeutic strategy against heavy metal-induced systemic toxicity. Male Wistar rats were assigned to control, BV (1 mg/kg/day, subcutaneous route), Cd (40 mg/L in drinking water), and Cd + BV for 14 days. Anxiety-like behavior was investigated using two behavioral tests, namely the elevated plus maze (EPM) and the open field test (OFT), while hepatic and renal function markers and oxidative stress parameters were quantified in plasma and tissue samples. BV composition was verified by RP-HPLC ESI-MS analysis, confirming melittin as the predominant peptide component. Cd exposure induced anxiety-like behavior, elevated plasma ALT, AST, and urea levels, increased lipid peroxidation, and reduced antioxidant enzyme activities in brain, liver, and kidney. Co-administration of BV markedly attenuated these behavioral and biochemical alterations, reducing MDA levels and restoring SOD and CAT activities. Collectively, these findings highlight the potential of BV to protect against Cd-induced hepatorenal and neurobehavioral toxicity, likely through modulation of oxidative stress pathways, thereby underscoring its promise as a natural therapeutic candidate for mitigating oxidative damage induced by heavy metals.
ABSTRACT Particulate matter (PM) in the air, classified as PM 2.5 and PM 10 , enters the body through the nose and mouth during breathing and reaches the lungs. PM is linked to respiratory damage, lung cancer, and the activation of immune system cells, including inflammation and metastasis. Previously, our work group showed that PM upregulates the expression of adhesion molecules and their ligands in lung cancer cells (A549), favoring their adhesion to monocytes; however, its role in cancer progression remains unclear. Therefore, this study examined whether PM exposure promotes a pro‐migratory behavior and cell death in A549 cells and monocytes (U937). PM uptake was detected in cells by transmission electron microscopy (TEM) and flow cytometry; cell migration was measured by wound‐healing and transwell assays in cocultures of U937 and A549 cells; and cell death was measured by Annexin‐V‐FLUOS/propidium iodide‐mediated flow cytometry. In A549 cells, both PM exposures led to cellular uptake, morphological changes, and increased cell migration. In cocultures of U937 and A549 cells, treatment of both cells with 10 μg/cm 2 of PM 2.5 and PM 10 resulted in the most significant increase in monocyte migration, and PM 10 had the maximum effect compared to PM 2.5 . High PM concentrations (30 μg/cm 2 ) induced necrosis in A549 cells, with rates of 17.7% for PM 2.5 and 63.3% for PM 10 . Therefore, these results suggest that PM exposure in lung cancer cells and monocytes could promote an inflammatory environment and tumor cell progression.
ABSTRACT Copper (Cu 2+ ), hexavalent chromium (Cr 6+ ), and cadmium (Cd 2+ ) are pervasive heavy metal pollutants in aquatic ecosystems, often coexisting and posing potential risks to aquatic organisms. While the individual toxicity of these metals is well documented, their combined effects at environmentally relevant concentrations remain poorly understood. This study investigated the chronic toxicity of a ternary mixture of Cu 2+ , Cr 6+ , and Cd 2+ in adult zebrafish ( Danio rerio ) across multiple biological endpoints. In the chronic toxicity test, the toxicity of Cu 2+ , Cr 6+ , and Cd 2+ was set up in five concentration groups, namely the control group, 1/40 (Cu 2+ 0.013 mg/L, Cr 6+ 4.610 mg/L, and Cd 2+ 0.471 mg/L), 1/30 (Cu 2+ 0.017 mg/L, Cr 6+ 6.147 mg/L, and Cd 2+ 0.628 mg/L), 1/20 (Cu 2+ 0.026 mg/L, Cr 6+ 9.220 mg/L, and Cd 2+ 0.942 mg/L), and 1/10 (Cu 2+ 0.052 mg/L, Cr 6+ 18.440 mg/L, and Cd 2+ 1.884 mg/L) of the 96 h‐LC50 values. Each group had three replicates, with 25 fish in each replicate. Under the exposure of different concentrations of Cu 2+ , Cr 6 + , and Cd 2+ , the liver, intestine, and gill tissue induced different degrees of pathological damage, and caused oxidative damage and immune system disorder in liver and gill tissue. In the 1/10 and 1/20 concentration group, the relative abundance of Bacteroidetes and Firmicutes in intestinal tissue increased, while the relative abundance of Actinobacteriota and Proteobacteria decreased. The residual amounts of Cd 2+ and Cr 6+ in muscle tissue are positively correlated with their concentrations, while the residual amounts of Cu 2+ are negatively correlated with their concentrations.
Microplastic (MP) pollution is widely recognized as an emerging environmental threat. Yet, most studies still rely on controlled experimental conditions that poorly reflect environmental complexity, potentially underestimating risks under realistic scenarios, particularly during short-term exposures. Here, we tested whether acute oral exposure to an environmentally relevant mixture of MPs (PE, PS, PP, and PVC) induces physiological changes in Swiss mice under contrasting climate regimes. Males and females were exposed for 7 days to two MP doses (8 and 80 mg/kg/day) under a realistic thermal regime with gradual, predictable fluctuations and a pessimistic regime characterized by abrupt, unpredictable temperature shifts. MPs accumulated in the liver primarily as a function of exposure group and sex, with scenario-related differences detected in specific sex/exposure contrasts, alongside alterations in oxidative stress and biotransformation biomarkers, including ROS, MDA, SOD, CAT, and GST. Behavioral alterations, including changes in locomotion and anxiety-like responses, also varied according to the interaction between dose and thermal regime. Multivariate analyses (Permutational Multivariate Analysis of Variance, Principal Coordinates Analysis, multivariate trajectories, and Distance to Control) showed clear separation among groups and greater deviation from controls, particularly in males under the pessimistic regime. Partial Least Squares Discriminant Analysis identified key biomarkers linked to redox balance, energy metabolism, and neurochemical regulation. At the same time, network analysis suggested correlation-based changes in physiological integration under more stressful conditions. Together, our results show that acute MP exposure can induce measurable systemic physiological shifts under dynamic environmental conditions. The findings indicate that MP toxicity is strongly context-dependent and may be underestimated by conventional approaches, underscoring the need for more integrative and ecologically realistic ecotoxicological frameworks.
ABSTRACT Triclosan (TCS) is a micropollutant frequently detected in biosolids applied to agricultural soils. In soil solution—where it is potentially bioavailable to roots—it occurs at residual concentrations (ng L −1 ). Nevertheless, the ecotoxicological implications of TCS exposure in agricultural crops at these concentrations are still not fully elucidated. In this context, the present study investigated the effects of TCS (25–200 ng L −1 ) on seed germination and root development in Cucumis sativus , Solanum lycopersicum , Lactuca sativa , and Raphanus sativus , as well as its phytotoxic, cytotoxic, and genotoxic potential in Allium cepa root systems. All concentrations induced H 2 O 2 accumulation in the roots and consumption of nonenzymatic antioxidants, and, under specific conditions, triggered lipid peroxidation, indicating oxidative stress as the primary mechanism associated with the observed adverse effects. In A. cepa , TCS induced a mitodepressive effect and morphological alterations in the roots at all tested concentrations, in addition to significant aneugenic effect at concentrations of 50–200 ng L −1 . In contrast, TCS concentrations of 25–100 ng L −1 stimulated root growth in cucumber, tomato, lettuce, and radish; however, the resulting radicles were more susceptible to breakage and morphological changes, suggesting that root elongation may have been associated more with cell expansion than with coordinated proliferative growth. In these species, concentrations of 200 ng L −1 caused a significant reduction in root growth and intensified morphological damage. These findings demonstrate that trace levels of TCS can impair early plant establishment by compromising root structural integrity, potentially affecting agronomic performance under environmentally realistic conditions.
ABSTRACT Mold growth in damp indoor environments is a widespread problem associated with respiratory health effects, though causal mechanisms remain incompletely understood. We established a human cell‐based in vitro test system using bronchial epithelial cells (NuLi‐1) and macrophages (THP‐1) to assess inhalation toxicity and immunomodulatory effects of indoor molds, focusing on cellular responses and mycotoxin patterns from contaminated building materials. The system integrates endpoints and impedance‐based real‐time cell viability analysis, quantification of released cytokines, and targeted mycotoxin profiling for comprehensive toxicological insights. Methanolic extracts from plasterboard, woodchip wallpaper, and malt extract agar (sterile PBS‐treated or contaminated with Alternaria botrytis , Aspergillus versicolor , Penicillium chrysogenum , and Stachybotrys chartarum ) were prepared via direct extraction of the material or surface swabs of the contaminated material. The system detected fungus‐ and material‐specific effects, with pronounced cytotoxicity and immunomodulation, especially in Stachybotrys chartarum‐contaminated samples. This material increased cytotoxicity in both tested cell types, decreased GM‐CSF release from NuLi‐1 cells, as well as increased interleukin‐1 β release from THP‐1 macrophages. Therefore, mycotoxin composition and concentration were analyzed and confirmed elevated levels of the mycotoxins Roridin L2, Verrucarin J, and Stachybotrylactam. These findings reveal a substantial inhalation toxicity potential from Stachybotrys chartarum ‐contaminated indoor materials, highlighting health risks in damp environments and necessitating further in vivo and epidemiological studies.
Triclosan (TCS) persists as a contaminant of concern in the Anthropocene, despite regulatory actions. Environmental dissemination continues through wastewater effluents, biosolid application, and improper disposal practices. This narrative review synthesizes current evidence regarding triclosan's environmental fate, transformation pathways, and toxicological impacts, drawing upon findings from environmental chemistry, ecotoxicology, and molecular health sciences. Emphasis is placed on persistence in sediments and aquatic environments, transformation via photochemical and chlorination processes into more toxic derivatives, and bioaccumulation across trophic levels. Mechanistically, it interferes with endocrine signaling, mitochondrial function, lipid metabolism, and microbial community structure, thereby promoting antibiotic resistance and metabolic dysregulation. This review systematically connects exposure pathways to ecological disruption and potential human health outcomes, specifically endocrine and cardiometabolic effects. Integrating environmental monitoring data, mechanistic toxicology, and epidemiological trends, this analysis presents triclosan as a model contaminant for elucidating the long-term propagation of ecological imbalance and chronic disease risk by legacy antimicrobials in modern industrial societies.
