Mitigating Ni and Cu ecotoxicity in the ecological restoration material and ornamental Primula forbesii Franch. with exogenous 24-epibrassinolide and melatonin.

Nickel (Ni) and copper (Cu) contamination have become major threats to plant survival worldwide. 24-epibrassinolide (24-EBR) and melatonin (MT) have emerged as valuable treatments to alleviate heavy metal-induced phytotoxicity. However, plants have not fully demonstrated the potential mechanisms by which these two hormones act under Ni and Cu stress. Herein, this study investigated the impact of individual and combined application of 24-EBR and MT on the growth and physiological traits of Primula forbesii Franch. subjected to stress (200 µmol L-1 Ni and Cu). The experiments compared the effects of different mitigation treatments on heavy metal (HM) stress and the scientific basis and practical reference for using these exogenous substances to improve HM resistance of P. forbesii in polluted environments. Nickel and Cu stress significantly hindered leaf photosynthesis and nutrient uptake, reducing plant growth and gas exchange. However, 24-EBR, MT, and 24-EBR + MT treatments alleviated the growth inhibition caused by Ni and Cu stress, improved the growth indexes of P. forbesii, and increased the gas exchange parameters. Exogenous MT effectively alleviated Ni stress, and 24-EBR + MT significantly alleviated the toxic effects of Cu stress. Unlike HM stress, MT and 24-EBR + MT activated the antioxidant enzyme activity (by increasing superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT)), significantly reduced reactive oxygen species (ROS) accumulation, and regulated ascorbate and glutathione cycle (AsA-GSH) efficiency. Besides, the treatments enhanced the ability of P. forbesii to accumulate HMs, shielding plants from harm. These findings conclusively illustrate the capability of 24-EBR and MT to significantly bolster the tolerance of P. forbesii to Ni and Cu stress.

A comparative study of in vivo toxicity in zebrafish embryos synthesized CuO nanoparticles characterized from Salacia reticulata.

The Salacia reticulata, a medicinal woody climbing shrub, was utilized for our study, the green synthesis of CuO nanoparticles, which were analyzed through SEM, EDX, FTIR, XRD, and UV‒Vis spectroscopy. This study assessed the toxicity to zebrafish embryos and explored the antibacterial, cytotoxic, antidiabetic, and anti-inflammatory properties of the synthesized nanoparticles. In results, the UV absorption of the CuO NPs showed that the intensity of nanoparticle green colloidal suspension changed from blue to green, which also confirmed that the spectrum of the green CuO NPs changed from colorless to black. in FT-IR and XRD spectral analysis to identify functional groups and determine the particle size of CuO NPs prepared by green and chemical methods. Its showed that CuO NPs (green) had a size of approximately 42.2 nm, while CuO NPs (chemical) had a size of approximately 84 nm. The morphology of these NPs was analyzed using SEM-EDX. Compared with their chemically prepared counterparts, the green-synthesized CuO nanoparticles demonstrated superior dispersion. Additionally, both green and chemical CuO nanoparticles at a concentration of 200 µL/mL caused developmental anomalies and increased mortality in zebrafish embryos and larvae. The green and chemical CuO NPs inhibited α-glucosidase enzyme activity at concentrations between 10 and 50 µL/mL, with IC50 values of 22 µL/mL and 26 µL/mL, respectively. The extract exhibited anti-inflammatory activity, with IC50 values of 274 and 109 µL/mL. The authors concluded that this green nanoparticle method has potential as a more eco-friendly and cost-effective alternative to traditional synthetic methods. NPs are widely used in human contact fields (medicine and agriculture), hence synthesis methods that do not involve toxic substances are becoming increasingly important.

Drp1 Aggravates Copper Nanoparticle-Induced ER-Phagy by Disturbing Mitochondria-Associated Membranes in Chicken Hepatocytes.

As an efficient alternative copper (Cu) source, copper nanoparticles (nano-Cu) have been widely supplemented into animal-producing food. Therefore, it is necessary to assess the effect of nano-Cu exposure on the biological health risk. Recently, the toxic effects of nano-Cu have been confirmed but the underlying mechanism remains unclear. This study reveals the impact of nano-Cu on endoplasmic reticulum autophagy (ER-phagy) in chicken hepatocytes and further identifies Drp1 and its downstream gene FAM134B as crucial regulators of nano-Cu-induced hepatotoxicity. Nano-Cu exposure can induce Cu ion overaccumulation and pathological injury in the liver, trigger excessive mitochondrial fission and mitochondria-associated membrane (MAM) integrity damage, and activate ER-phagy in vivo and in vitro. Interestingly, the knockdown of Drp1 markedly decreases the expression of FAM134B induced by nano-Cu. Furthermore, the expression levels of ATL3, CCPG1, SEC62, TEX264, and LC3II/LC3I induced by nano-Cu exposure are decreased by inhibiting the expression of Drp1. Simultaneously, the inhibition of FAM134B effectively alleviates nano-Cu-induced ER-phagy by downregulating the expression of ATL3, CCPG1, SEC62, TEX264, and LC3II/LC3I. Overall, these results suggest that Drp1-mediated impairment of MAM integrity leads to ER-phagy as a novel molecular mechanism involved in the regulation of nano-Cu-induced hepatotoxicity. These findings provide new ideas for future research on the mechanism of nano-Cu-induced hepatotoxicity.

MMP-3 mediates copper oxide nanoparticle-induced pulmonary inflammation and fibrosis.

BACKGROUND: The increasing production and usage of copper oxide nanoparticles (Nano-CuO) raise human health concerns. Previous studies have demonstrated that exposure to Nano-CuO could induce lung inflammation, injury, and fibrosis. However, the potential underlying mechanisms are still unclear. Here, we proposed that matrix metalloproteinase-3 (MMP-3) might play an important role in Nano-CuO-induced lung inflammation, injury, and fibrosis. RESULTS: Exposure of mice to Nano-CuO caused acute lung inflammation and injury in a dose-dependent manner, which was reflected by increased total cell number, neutrophil count, macrophage count, lactate dehydrogenase (LDH) activity, and CXCL1/KC level in bronchoalveolar lavage fluid (BALF) obtained on day 3 post-exposure. The time-response study showed that Nano-CuO-induced acute lung inflammation and injury appeared as early as day 1 after exposure, peaked on day 3, and ameliorated over time. However, even on day 42 post-exposure, the LDH activity and macrophage count were still higher than those in the control group, suggesting that Nano-CuO caused chronic lung inflammation. The Nano-CuO-induced pulmonary inflammation was further confirmed by H&E staining of lung sections. Trichrome staining showed that Nano-CuO exposure caused pulmonary fibrosis from day 14 to day 42 post-exposure with an increasing tendency over time. Increased hydroxyproline content and expression levels of fibrosis-associated proteins in mouse lungs were also observed. In addition, Nano-CuO exposure induced MMP-3 overexpression and increased MMP-3 secretion in mouse lungs. Knocking down MMP-3 in mouse lungs significantly attenuated Nano-CuO-induced acute and chronic lung inflammation and fibrosis. Moreover, Nano-CuO exposure caused sustained production of cleaved osteopontin (OPN) in mouse lungs, which was also significantly decreased by knocking down MMP-3. CONCLUSIONS: Our results demonstrated that short-term Nano-CuO exposure caused acute lung inflammation and injury, while long-term exposure induced chronic pulmonary inflammation and fibrosis. Knocking down MMP-3 significantly ameliorated Nano-CuO-induced pulmonary inflammation, injury, and fibrosis, and also attenuated Nano-CuO-induced cleaved OPN level. Our study suggests that MMP-3 may play important roles in Nano-CuO-induced pulmonary inflammation and fibrosis via cleavage of OPN and may provide a further understanding of the mechanisms underlying Nano-CuO-induced pulmonary toxicity.

Immunotoxicity and oxidative damage in Litopenaeus vannamei induced by polyethylene microplastics and copper co-exposure.

This study examines the combined effects of polyethylene microplastics (PE-MP) and copper (Cu2+) on the immune and oxidative response of Litopenaeus vannamei. PE-MP adsorbed with Cu2+ at 2.3, 6.8, and 16.8 ng (g shrimp)-1) were injected into L. vannamei. Over 14 days, survival rates were monitored, and immune and oxidative stress parameters were assessed. The results showed that combined exposure to PE-MP and Cu2+ significantly reduced the survival rate and decreased total haemocyte count. Immune-related parameters (phagocytic rate, phenoloxidase and superoxide dismutase (SOD)) and antioxidant-related parameters (SOD, catalase and glutathione peroxidase mRNA and enzyme) also decreased, while respiratory burst activity significantly increased, indicating immune and antioxidant system disruption. Additionally, there was a significant increase in oxidative stress, as measured by malondialdehyde levels. Histopathological analysis revealed severe muscle, hepatopancreas, and gill damage. These results suggest that simultaneous exposure to PE-MP and Cu2+ poses greater health risks to white shrimp.

Mitochondrial miR-12294-5p-Regulated Copper Exposure-Caused Mitochondrial-Dependent Ferroptosis by Targeted Inhibition of CISD1 in Chicken Hepatocytes.

Copper (Cu) is a common trace element additive in animal and human foods, and excessive intake of Cu has been shown to cause hepatotoxicity, but the underlying mechanism remains unclear. Our previous research found that Cu exposure dramatically upregulated mitochondrial miR-12294-5p expression and confirmed its targeted inhibition of CISD1 expression in chicken hepatocytes. Thus, we aimed to explore the potential role of mitomiR-12294-5p/CISD1 axis in Cu exposure-resulted hepatotoxicity. Here, we observed that Cu exposure resulted in Cu accumulation and pathological injury in chicken livers. Moreover, we found that Cu exposure caused mitochondrial-dependent ferroptosis in chicken hepatocytes, which were prominent on the increased mitochondrial Fe2+ and mitochondrial lipid peroxidation, inhibited levels of CISD1, GPX4, DHODH, and IDH2, and also enhanced level of PTGS2. Notably, we identified that inhibition of mitomiR-2954 level effectively mitigated Cu-exposure-resulted mitochondrial Fe2+ accumulation and mitochondrial lipid peroxidation and prevented the development of mitochondrial-dependent ferroptosis. However, increasing the mitomiR-12294-5p expression considerably aggravated the influence of Cu on these indicators. Meanwhile, the overexpression of CISD1 effectively alleviated Cu-caused mitochondrial-dependent ferroptosis, while silent CISD1 eliminated the therapeutic role of mitomiR-12294-5p inhibitor. Overall, our findings indicated that mitomiR-12294-5p/CISD1 axis played a critical function in Cu-caused hepatotoxicity in chickens by regulating mitochondrial-dependent ferroptosis.

Copper-induced renal toxicity controlled by period1 through modulation of Atox1 in mice.

Copper (Cu) is known to induce oxidative stress and apoptosis in the liver, kidney, and brain. We previously demonstrated the molecular mechanism underlying the Cu-induced hepatic diurnal variation. However, the cellular molecule(s) involved in Cu-induced renal chronotoxicity remain unknown. In this study, we aimed to elucidate the molecular mechanisms underlying Cu-induced diurnal toxicity in the kidneys. We evaluated cell viability and clock gene expression levels in mouse renal cortex tubular cells (MuRTE61 cells) after Cu treatment. We also examined the Cu homeostasis- and apoptosis-related gene levels after period 1 (Per1) overexpression in MuRTE61 cells. Cu treatment decreased MuRTE61 cell viability in a dose-dependent manner. It increased the Per1 expression levels after 24 h. Notably, Per1 overexpression alleviated the Cu-induced inhibition of MuRTE61 cell viability. Moreover, Per1 overexpression downregulated the cleaved caspase-3 and reduced Cu levels by upregulating the antioxidant 1 copper chaperone (Atox1) levels. These results suggest that Cu-induced renal toxicity is associated with Per1 expression via the regulation of the copper chaperone, Atox1.

Combined Effects of Tetracycline and Copper Ion on Microorganisms During the Biological Phosphorus Removal.

Tetracycline and copper ion are common pollutants in wastewater, and the effects of mixed pollutants on microorganisms in wastewater biological treatment have been less studied. In order to reveal the effects of mixed pollutants of tetracycline and copper ion on the microorganisms during the biological phosphorus removal, three ratios of tetracycline and copper ions were designed by the direct equipartition ray method. The relative abundance and diversity of microbial community were investigated, and the microbial interactions were revealed through microbiological methods. The results demonstrated that, for three different ratios, the inhibitory effect of specific phosphorus uptake rate became more significant with the increase of the tetracycline-copper ions concentration and the reaction time. The microbial community decreased with the increase of the proportion of tetracycline in different ratios. The relative abundance of Acinetobacter decreased with the increase of the proportion of tetracycline, while the relative abundance of Ca.Competibacter was higher under the conditions of low mixtures concentrations. Positive interactions and symbiotic relationships among microorganisms were predominant for three different ratios. However, as the proportion of tetracycline increased, the community structure of microorganisms shifted from phosphate-accumulating organisms to glycogen accumulating organisms and denitrifying bacteria. This study can provide a reference for the effect of mixed pollutants on microorganisms and the mechanism of wastewater treatment.

Copper-Nanoparticle-Induced Neurotoxic Effect and Oxidative Stress in the Early Developmental Stage of Zebrafish (Danio rerio).

Copper nanoparticles (CuNPs) are extensively used in electronics, cosmetics, fungicides, and various other fields due to their distinctive qualities. However, this widespread usage can contribute to environmental contamination and heightened health risks for living organisms. Despite their prevalent use, the ecological impacts and biosafety of CuNPs remain inadequately understood. The present study aims to delve into the potential toxic effects of CuNPs on zebrafish (Danio rerio) embryos, focusing on multiple indexes such as embryonic development, neurotoxicity, oxidative stress, and inflammatory response. The results revealed a notable increase in the death rate and deformity rate, alongside varying degrees of decrease in hatching rate and heart rate following CuNPs exposure. Particularly, the frequency of spontaneous tail coiling significantly declined under exposure to CuNPs at concentrations of 500 µg/L. Furthermore, CuNPs exposure induced alterations in the transcriptional expression of GABA signaling pathway-related genes (gabra1, gad, abat, and gat1), indicating potential impacts on GABA synthesis, release, catabolism, recovery, and receptor binding. Additionally, CuNPs triggered oxidative stress, evidenced by disruption in superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, along with elevated malondialdehyde (MDA) levels. This oxidative stress subsequently led to a proinflammatory cascade, as demonstrated by the increased transcriptional expression of inflammatory markers (il-1ß, tnf-α, il-6, and il-8). Comparative analysis with copper ion (provided as CuCl2) exposure highlighted more significant changes in most indexes with CuCl2, indicating greater toxicity compared to CuNPs at equivalent concentrations. In conclusion, these findings provide valuable insights into the toxic effects of CuNPs on zebrafish embryo development and neurotransmitter conduction. Furthermore, they present technical methodologies for assessing environmental and health risks associated with CuNPs, contributing to a better understanding of their biosafety and ecological impact.

Effect of ultraviolet aged polytetrafluoroethylene microplastics on copper bioavailability and Microcystis aeruginosa growth.

Microplastics (MPs) are ubiquitous in aquatic environments, which can act as carriers to affect the bioavailability of heavy metals. The aging process in the environment changes the physicochemical properties of MPs, thereby affecting their environmental behavior and co-toxicity with other pollutants. However, relevant research is limited. In this study, we compared the properties and Cu2+ adsorption capacity of pristine and aged polytetrafluoroethylene (PTFE) MPs and further explored the influence on copper bioavailability and bio-effects on Microcystis aeruginosa. Aging process induced surface oxidation and cracks of PTFE MPs, and decreased the stability of MPs in water by increasing zeta potential. PTFE MPs had a strong adsorption capacity for Cu2+ and increased the bioavailability of copper to microalgae, which was not affected by the aging process. Pristine and aged PTFE MPs adhered to cyanobacterium surfaces and caused shrinkage and deformation of cells. Inhibition of cyanobacterium growth, photosynthesis and reduction of total antioxidant capacity were observed in the treatment of PTFE MPs. Combined exposure of pristine MPs and Cu2+ had stronger toxic effects to cyanobacterium, and increased Microcystin-LR release, which could cause harm to aquatic environment. Aging reduced the toxic effects of PTFE MPs on microalgae. Furthermore, soluble exopolysaccharide (EPS) content was significantly higher in co-exposure of aged MPs and Cu2+, which could reduce the toxicity to cyanobacterium cells. These results indicate that aging process alleviates the toxicity to microalgae and environmental risks caused by PTFE MPs. This study improves understanding of the combined toxicity of aged MPs and metals in freshwater ecosystems.

Physiological and multi-omics analysis reveals the influence of copper on Halophila beccarii Asch.

High concentrations of copper can pollute coastal waters, primarily from agricultural runoff and mining activities, which can harm marine organisms, including seagrasses. The molecular mechanism of copper toxicity to seagrass currently remains unclear. To determine the response to copper, physiological and multi-omic analyses were conducted to explore the molecular mechanism by which copper affects the global threatened seagrass Halophila beccarii Asch. Excessive copper stress causes oxidative damage and stimulates the activity of the antioxidant enzyme system to remove excess reactive oxygen species (ROS), thereby reducing the damage caused by copper stress. Cu increases the activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), peroxidase (EC 1.11.1.7), ascorbate peroxidase (EC 1.11.1.11), glutathione peroxidase (EC 1.11.1.9), ascorbate oxidase (EC 1.10.3.3), glutathione reductase (EC 1.6.4.2), and dehydroascorbate reductase (EC 1.8.5.1) and the content of malondialdehyde and reduces the activity of monodehydroascorbate reductase (EC 1.6.5.4). Under copper stress, H. beccarii upregulates the metabolic pathways of steroid biosynthesis and cutin, suberin, and wax biosynthesis, downregulates the metabolic pathways of arginine and proline metabolism and fructose and mannose metabolism; the levels of expression of the ribosome-related genes; upregulates the levels of expression of circadian rhythm-related proteins and downregulates the levels of glutathione metabolism and the proteins related to carbon fixation. This study provides new insights into the response of seagrass to copper stress and reports potential candidate metabolites, genes, and proteins that can be considered as biomarkers to improve the protection and management of seagrass meadows.

Effect of different sizes of nanocopper particles on rainbow trout (Oncorhynchus mykiss W.) spermatozoa motility kinematics.

In recent years, nanocopper (Cu NPs) has gained attention due to its antimicrobial properties and potential for industrial, agricultural, and consumer applications. But it also has several effects on the aquatic environment. Widespread use of various nanoproducts has raised concerns about impacts of different nanoparticle size on environment and biological objects. Spermatozoa is a model for studying the ecotoxic effects of pollutants on cells and organisms. This study aimed to investigate the effects of different sizes of copper nanoparticles on rainbow trout spermatozoa motility, and to compare their effects with copper ionic solution. Computer assisted sperm analysis (CASA) was used to detect movement parameters at activation of gametes (direct effect) with milieu containing nanocopper of primary particle size of 40-60, 60-80 and 100 nm. The effect of the elements ions was also tested using copper sulfate solution. All products was prepared in concentration of 0, 1, 5, 50, 125, 250, 350, 500, 750, and 1000 mg Cu L-1. Six motility parameters were selected for analysis. The harmful effect of Cu NPS nanoparticle was lower than ionic form of copper but the effect depends on the motility parameters. Ionic form caused complete immobilization (MOT = 0 %, IC100) at 350 mg Cu L-1 whilst Cu NPs solution only decreased the percentage of motile sperm (MOT) up to 76.4 % at highest concentration tested of 1000 mg Cu L-1 of 40-60 nm NPs. Cu NPs of smaller particles size had more deleterious effect than the bigger one particularly in percentage of MOT and for curvilinear velocity (VCL). Moreover, nanoparticles decrease motility duration (MD). This may influence fertility because the first two parameters positively correlate with fertilization rate. However, the ionic form of copper has deleterious effect on the percentage of MOT and linearity (LIN), but in some concentrations it slightly increases VCL and MD.

Transcriptomic-metabolomic analysis reveals the effect of copper toxicity on fermentation properties in Saccharomyces cerevisiae.

Copper is one of the unavoidable heavy metals in wine production. In this study, the effects on fermentation performance and physiological metabolism of Saccharomyces cerevisiae under copper stress were investigated. EC1118 was the most copper-resistant among the six strains. The ethanol accumulation of EC1118 was 26.16-20 mg/L Cu2+, which was 1.90-3.15 times higher than that of other strains. The fermentation rate was significantly reduced by copper, and the inhibition was relieved after 4-10 days of adjustment. Metabolomic-transcriptomic analysis revealed that amino acid and nucleotide had the highest number of downregulated and upregulated differentially expressed metabolites, respectively. The metabolism of fructose and mannose was quickly affected, which then triggered the metabolism of galactose in copper stress. Pathways such as oxidative and organic acid metabolic processes were significantly affected in the early time, resulting in a significant decrease in the amount of carboxylic acids. The pathways related to protein synthesis and metabolism under copper stress, such as translation and peptide biosynthetic process, was also significantly affected. In conclusion, this study analyzed the metabolite-gene interaction network and molecular response during the alcohol fermentation of S. cerevisiae under copper stress, providing theoretical basis for addressing the influence of copper stress in wine production.

Copper exposure induces trophoblast cell cuproptosis by up-regulating lnc-HZ11.

Copper pollution has attracted global environmental concern. Widespread Cu pollution results in excessive Cu accumulation in human. Epidemiological studies and animal experiments revealed that Cu exposure might have reproductive toxicity. Cuproptosis is a recently reported Cu-dependent and programmed cell death pattern. However, the mechanism by which copper exposure might cause cell cuproptosis is largely unknown. We chose trophoblast cells as cell model and found that copper exposure causes trophoblast cell cuproptosis. In mechanism, copper exposure up-regulates lnc-HZ11 expression levels, which increases intracellular Cu2+ levels and causes trophoblast cell cuproptosis. Knockdown of lnc-HZ11 efficiently reduces intracellular Cu2+ levels and alleviate trophoblast cell cuproptosis, which could be further alleviated by co-treatment with DC or TEPA. These results discover novel toxicological effects of copper exposure and also provide potential target for protection trophoblast cells from cuproptosis in the presence of excessive copper exposure.

CuO nanoparticles elicit intestinal immunotoxicity in zebrafish based on intestinal microbiota dysbiosis.

Copper II oxide nanoparticles (CuO NPs), a kind of widely used nanomaterial, have been detected in food and the environment, which has aroused widespread public concern. Recently, increasing data have suggested that intestinal microecology is closely related to immune homeostasis. However, the intestinal immunotoxicity induced by CuO NPs through intestinal microbiota is still unknown. Therefore, in this study, zebrafish were exposed to CuO NPs to explore intestinal immunotoxicity by evaluating physiological indicators, intestinal tissue injury, antioxidant enzyme activities, gene expression of immune factors, and changes in intestinal microbiota and its metabolites (short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS)). The results revealed that the intestinal immunotoxicity of CuO NPs was mediated by the impact on intestinal microbiota and its metabolite levels. Specifically, changes were observed in the abundance of microbes that participated in the metabolism of SCFAs and LPS. The reduction in acetic acid, propionic acid and valeric acid upregulated GPR84 expression, and the decline in LPS levels further resulted in the suppression of the key immune regulatory pathways TLR4/MyD88/NF-κB, ultimately leading to intestinal immunotoxicity. This study would provide a scientific basis for the risk assessment of CuO NPs and a new perspective for research on the immunotoxicity of nanoparticles.

A rapid and multi-endpoint ecotoxicological test using Mychonastes afer for efficient screening of metals and herbicides.

Microalgal growth-based tests are international standards for ecotoxicity assessment; however, their long exposure times, large sample volumes, and reliance on a single growth-endpoint make them inadequate for rapid toxicity screening. Here, we aimed to develop a rapid and simple ecotoxicological test using the fast-growing green alga Mychonastes afer, with multiple endpoints-growth, lipid content, and photosynthesis. We exposed M. afer to two metals-silver and copper-and two herbicides-atrazine and diuron-for 24 h and identified the most sensitive and reliable endpoints for each toxicant: the maximum electron transport rate (ETRmax) for Ag, Cu and atrazine, and the lipid content for diuron. Lipid content was found to be both a sensitive and reliable biomarker, meeting the effluent limit guidelines in both the Republic of Korea and the USA. The sensitivity of M. afer to Ag and atrazine also closely matched the HC5 values derived from the species sensitivity distribution approach, confirming its reliability for setting regulatory concentrations of these contaminants. Our calculated predicted no-effect concentration (PNEC) values were similar to established European Union PNECs for Ag, Cu, atrazine, and diuron, underlining the utility of these biological endpoints for ecological risk assessment and regulatory decision making. This method required lower sample volume (2 mL vs 100 mL) and exposure time (24 h vs 72-120 h) than conventional green algal tests, and eliminated the need for labour-intensive cell counting, expensive equipment, and chlorophyll fluorescence measurement expertise. Overall, this M. afer test can be a valuable tool for the rapid screening of wastewater for metals and herbicides, contributing to environmental protection and management practices.

Combined toxicity of polyvinyl chloride microplastics and copper to marine jacopever (Sebastes schlegelii).

Marine organisms commonly encounter co-stress resulting from the coexistence of microplastics (MPs) and heavy metals pollution in marine environments. Nevertheless, the combined effects and toxicity mechanisms of MPs and heavy metals on marine organisms remain unclear. This study integrated growth, physiological, morphological, and biochemical markers to assess the individual and combined toxicity of polyvinyl chloride MPs (PVC MPs, 1 × 104 particles/L) and copper (Cu, 200 µg/L) on marine jacopever (Sebastes schlegelii). The results revealed that co-exposure to MPs and Cu had a more detrimental impact on jacopever compared to the single-exposure groups, as evidenced by the enhanced growth inhibition, respiratory stress, and hepatotoxicity. This phenomenon may be attributed to PVC MPs accelerating the accumulation of Cu in jacopever liver. Therefore, peroxidation damage occurred in the co-exposed liver and may result in liver dysfunction. These findings contribute valuable insights into the risks associated with the coexistence of MPs and heavy metal pollution in marine ecosystems.

Construction of an in vitro simulated one compartment extravascular administration model and its comparison with classic in vitro administration model in copper chloride induced HepG2 cell death.

In this study, we designed an in vitro administration device based on compartment model theory and utilized it to construct an in vitro simulated one compartment extravascular administration model of copper chloride. Within the Cmax range of 3.91-1000.00 µM, the measured concentration-time curves of the simulated one compartment extravascular administration model almost coincide with the corresponding theoretical curves. The measured values of toxicokinetic parameters, including ke, T1/2, ka, T1/2a, Tmax, Cmax, CL, and AUC0-∞ are close to the corresponding theoretical values. The fitting coefficients are >0.9990. In simulated one compartment extravascular administration and classic in vitro administration, copper chloride dose-dependently induced HepG2 cell death. When Cmax/administration concentration is equal, classic in vitro administration induces a higher cell death rate than simulated one compartment extravascular administration. However, there is no significant difference in inducing cell death between the two administration models when area under the curve is equal. In conclusion, the device designed in this study can be used to in vitro simulate one compartment extravascular administration, making in vitro toxicity testing more similar to in vivo scenarios. There are differences in copper chloride induced HepG2 cell death between simulated one compartment extravascular administration and classic in vitro administration.

Environmental efficacy of polyethylene microplastics: Enhancing the solidification of CuO nanoparticles and reducing the physiological toxicity to peanuts.

Microplastics and metal-based nanoparticles (NPs) are environmental pollutants that have attracted significant attention. However, there have been relatively few studies on the combined pollution of these substances in the soil-plant system. To investigate the environmental impact and interaction mechanisms of these two pollutants, a pot experiment was conducted to examine the effects of soil exposure on peanut growth. The experiment results revealed that polyethylene (PE) had a minimal effect on peanut growth, while CuO NPs significantly inhibited peanut growth. Peanut biomass decreased by over 50 % in all Cu treatments. The presence of PE significantly impacted the dissolution and absorption of CuO NPs. When 0.5 % PE was present, the dissolution and transformation of CuO NPs were limited, resulting in a total Cu concentration of 458 mg/kg. Conversely, when 5 % PE was present, the dissolution and transformation of CuO NPs were promoted, leading to a DTPA-Cu concentration of 141 mg/kg, the highest level observed. The distribution of trace elements in peanut stems also responded to the differences in Cu concentration. Both pollutants significantly disrupted soil bacteria, with CuO NPs having a more pronounced effect than PE. Throughout the entire growth cycle of peanuts, no chemical adsorption occurred between PE and CuO NPs, and CuO NPs had no significant impact on the aging rate of PE. In summary, this study provides insights into the environmental impact and transport mechanisms of composite pollution involving microplastics and metal-based nanoparticles in the soil-peanut system.

Copper, Iron, Cadmium, and Arsenic, All Generated in the Universe: Elucidating Their Environmental Impact Risk on Human Health Including Clinical Liver Injury.

Humans are continuously exposed to various heavy metals including copper, iron, cadmium, and arsenic, which were specifically selected for the current analysis because they are among the most frequently encountered environmental mankind and industrial pollutants potentially causing human health hazards and liver injury. So far, these issues were poorly assessed and remained a matter of debate, also due to inconsistent results. The aim of the actual report is to thoroughly analyze the positive as well as negative effects of these four heavy metals on human health. Copper and iron are correctly viewed as pollutant elements essential for maintaining human health because they are part of important enzymes and metabolic pathways. Healthy individuals are prepared through various genetically based mechanisms to maintain cellular copper and iron homeostasis, thereby circumventing or reducing hazardous liver and organ injury due to excessive amounts of these metals continuously entering the human body. In a few humans with gene aberration, however, liver and organ injury may develop because excessively accumulated copper can lead to Wilson disease and substantial iron deposition to hemochromatosis. At the molecular level, toxicities of some heavy metals are traced back to the Haber Weiss and Fenton reactions involving reactive oxygen species formed in the course of oxidative stress. On the other hand, cellular homeostasis for cadmium and arsenic cannot be provided, causing their life-long excessive deposition in the liver and other organs. Consequently, cadmium and arsenic represent health hazards leading to higher disability-adjusted life years and increased mortality rates due to cancer and non-cancer diseases. For unknown reasons, however, liver injury in humans exposed to cadmium and arsenic is rarely observed. In sum, copper and iron are good for the human health of most individuals except for those with Wilson disease or hemochromatosis at risk of liver injury through radical formation, while cadmium and arsenic lack any beneficial effects but rather are potentially hazardous to human health with a focus on increased disability potential and risk for cancer. Primary efforts should focus on reducing the industrial emission of hazardous heavy metals.