Microplastics (MPs) are newly emerged pollutants found in water and soil, while microcystin-leucine arginine (MC-LR) is often detected in drinking water and water products, both posing serious threats to aquatic environment and food safety. MPs can serve as carriers of MC-LR. These pollutants are often found together, rather than separately. This study focused on assessing the neurotoxicity of co-exposure to MC-LR and PS in Caenorhabditis elegans (C. elegans) after combined exposure to these two pollutants. Exposure to varying concentrations of polystyrene (PS) and MC-LR individually caused a dose-dependent decrease in the locomotion behaviors of C. elegans. Exposure to either of these substances alone caused damage to the phenotypic indicators of the C. elegans. To further explore the additional damage caused by the combined exposure of PS and MC-LR, the low, medium, and high combined dose groups were selected based on the locomotion behaviors and survival results. Combined exposure increased the level of oxidative stress indicators and resulted in neuronal loss. It also reduced serotonin, glutamate, GABA, and dopamine neurotransmitters levels, without affecting cholinergic neurons. The expression of neurotransmitter-related genes also decreased. The high-dose group showed the most significant effects. This article is the first to study the combined effect of PS and MC-LR on C. elegans nervous systems, offering novel insights into the risks posed by co-occurring contaminants and their implications for aquatic ecosystems and food safety.

Crops produced using the practice of continuous cropping can become seriously damaged by plant-parasitic nematodes, an important indicator of continuous cropping obstacles. As a typical and important perennial economic crop, dragon fruit is prone to serious plant-parasitic nematode infestation; however, whether it encounters continuous cropping obstacles remains unclear. Here, we studied plant-parasitic nematodes (Meloidogyne spp. and Tylenchorhynchus sp.) in the soil and roots, soil nematode communities, metabolic footprint, soil integrated fertility, and the yield of intensively planted dragon fruit under non-continuous cropping (Y1) and 3 years (Y3) and 5 years (Y5) of continuous cropping, to determine potential continuous-cropping obstacles and factors that affect the yield of this fruit. The largest numbers of plant-parasitic nematodes in the soil and roots were observed in Y5; the associated yield was reduced, and the dragon fruit was severely stressed. Further analysis of the composition, diversity, and ecological function indices of soil nematodes showed that the soil ecological environment deteriorated after 3 years of continuous cropping, with Y5 having the worst results. Similarly, the soil at Y5 had a significant inhibitory effect on the growth and reproduction of Caenorhabditis elegans. Mantel test analysis and a random forest model showed that soil available phosphorus, soil exchange calcium, and soil nematode abundance and diversity were related significantly to yield. Partial least squares path modeling revealed that soil fertility and soil nematode diversity directly impacts the yield of continuously cropped dragon fruit. In summary, continuous cropping obstacles occurred in Y5 of intensive dragon fruit cultivation, with soil nematode diversity and soil fertility determining the crop's yield.

Soil worms are among the most abundant and functionally diverse soil animals. However, they have been largely overlooked in studies on microplastic (MP) toxicity. MPs and plant secondary metabolites (PSMs) are ubiquitous in soil due to plant litter decomposition and heavy MP contamination, inevitably interacting and exerting combined toxicity on soil organisms. However, little research has been conducted on their joint effects. This study investigates the individual and combined toxic effects of polyethylene (PE) MPs and three PSMs (glycyrrhizic acid, tannic acid, and matrine) on the model organism Caenorhabditis elegans. Physiological and biochemical responses were assessed using fluorescence microscopy, image analysis, and statistical methods. After 42 h of exposure to PE MPs and/or PSMs, worm growth and development were negatively impacted. Under experimental conditions, matrine and PE MPs synergistically inhibited worm growth, exacerbated neurological damage, and induced oxidative stress. In contrast, glycyrrhizic acid and tannic acid alleviated PE MP-induced growth inhibition, mitigated oxidative stress, and demonstrated antioxidant properties that counteracted oxidative damage. This study offers new insights into the combined effects of MPs and PSMs in soil ecosystems, contributing to ecological risk assessments and pollution management strategies.

Fluoride, a naturally occurring element found in water, soil, food, and atmospheric precipitation, can lead to fluorosis and various health issues when consumed excessively. However, the mechanism of fluorosis is still under investigation. This study utilizes Caenorhabditis elegans as a model organism to investigate the effects of fluoride exposure on biological systems and to explore the mechanisms by which curcumin mitigates fluoride- induced toxicity. Three groups were established: a blank control, a sodium fluoride (NaF) exposure group (concentration 5 mmol/L), and a curcumin intervention group (concentration 25 mu mol/L). Physiological parameters, lipofuscin levels, intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential, and mitochondrial copy numbers were measured to assess the effects of fluoride toxicity and curcumin protection. RNA-seq and qRT-PCR were utilized to investigate the molecular mechanisms underlying fluoride- induced damage and curcumin's mitigating effects. Results indicated that fluoride-exposed nematodes displayed physiological abnormalities, increased ROS production, higher lipofuscin levels, altered mitochondrial membrane potential and mitochondrial copy number, and activated MAPK signaling pathway genes. Curcumin exhibited protective effects on these parameters, suggesting its potential in preventing fluoride-induced harm by modulating oxidative stress and preserving mitochondrial function. This research enhances our understanding of the mechanisms of fluoride toxicity and highlights the potential benefits of curcumin.

Sediment is the ultimate sink of environmental pollutants. A total of 128 surface sediment samples were collected from 8 rivers and 3 reservoirs in Maoming City, Guangdong Province. This study assessed the content and distribution of brominated flame retardants in sediments. The acute toxicity effects of tetrabromobisphenol A (TBBPA) and hexabromocyclododecane (HBCDs) in sediments were evaluated using Caenorhabditis elegans as model organisms. The concentration of TBBPA in sediments ranged from not detected (ND) to 12.59 pg/kg and was mainly distributed in the central area, which was affected by the emission of TBBPA from residential and factory. The concentration of HBCDs ranged from ND to 6.31 pg/kg, and the diastereoisomer distribution was consistent, showing a trend close to the South China Sea. The composition pattem of HBCDs in the surface sediments from rivers were 41.73%62.33%, 7.89%-25.54%, and 18.76%-40.65% for a-, /3-, and y-HBCD, respectively, and in the sediments from reservoirs were 26.15%-45.52%, 7.44%-19.23%, and 47.04%-61.89% for a-, /3-, and y-HBCD, respectively. When the sum of concentrations of TBBPA and HBCD in sediments were above high levels, reactive oxygen species in nematodes significantly increased, resulting in an oxidative stress response. Intestinal permeability was also enhanced, causing intestinal damage. In addition, in terms of this study, TBBPA had a greater impact on biotoxicity compared to HBCDs, and more attention should be paid to the toxic effects of the river ecosystem organisms in Maoming City, Guangdong Province. This study can complement the pollution database in the study area and provide basic data for pollution control. (c) 2024 The Research Center for Eco-Environmental Sciences, Chinese Academy of

Alzheimer's disease (AD) is a complex neurodegenerative disorder that is classically defined by the extracellular deposition of senile plaques rich in amyloid-beta (A beta) protein and the intracellular accumulation of neurofibrillary tangles (NFTs) that are rich in aberrantly modified tau protein. In addition to aggregative and proteostatic abnormalities, neurons affected by AD also frequently possess dysfunctional mitochondria and disrupted mitochondrial maintenance, such as the inability to eliminate damaged mitochondria via mitophagy. Decades have been spent interrogating the etiopathogenesis of AD, and contributions from model organism research have aided in developing a more fundamental understanding of molecular dysfunction caused by A beta and toxic tau aggregates. The soil nematode C. elegans is a genetic model organism that has been widely used for interrogating neurodegenerative mechanisms including AD. In this review, we discuss the advantages and limitations of the many C. elegans AD models, with a special focus and discussion on how mitochondrial quality control pathways (namely mitophagy) may contribute to AD development. We also summarize evidence on how targeting mitophagy has been therapeutically beneficial in AD. Lastly, we delineate possible mechanisms that can work alone or in concert to ultimately lead to mitophagy impairment in neurons and may contribute to AD etiopathology.

Excessive nanoplastics not only pose a direct threat to the environment but also have the propensity to adsorb and interact with other pollutants, exacerbating their impact. The coexistence of nanoplastics and heavy metals in soils is a prevalent phenomenon. However, limited research existed about the joint effects of the two contaminants on soil organisms. In this paper, we ascertained the combined toxicity of polystyrene nanoplastics (PSNPs) and copper (Cu2+) on soil organisms (Caenorhabditis elegans) at quantities that were present in the environment, further exploring whether the two toxicants were synergistic or antagonistic. The outcomes manifested that single exposure to low-dose PS-NPs (1 mu g/L) would not cause significant damage to nematodes. After treatment with PS-NPs and Cu2+, the locomotion ability of nematode was impaired, accompanied by an elevation in reactive oxygen species (ROS) level and a biphasic response in antioxidant enzyme activity. Moreover, combined exposure to PS-NPs and Cu2+ induced the mRNA up-regulation of vit-6, cyp-35a2, hsp-16.2, age-1, and cep-1, both of which were stress-related genes. The comparative analysis between groups (with or without PSNPs) revealed that the combined exposure group resulted in significantly greater toxic effects on nematodes compared with Cu2+ exposure alone. Furthermore, the addition of PS-NPs influenced the metabolic profiles of Caenorhabditis elegans under Cu2+ stress, with numerous differential metabolites associated with oxidative damage or defense mechanism. Overall, these findings manifested that PS-NPs at the expected environmental concentration elevated Cu2+ toxicity on nematodes.

Polymer chain extenders, commonly used in plastic production, have garnered increasing attention due to their potential environmental impacts. However, a comprehensive understanding of their ecological risks remains largely unknown. In this study, we employed the model organism Caenorhabditis elegans to investigate toxicological profiles of ten commonly -used chain extenders. Exposure to environmentally relevant concentrations of these chain extenders (ranging from 0.1 mu g L-1 to 10 mg L-1) caused significant variations in toxicity. Lethality assays demonstrated the LC50 values ranged from 92.42 mu g L-1 to 1553.65 mg L-1, indicating marked differences in acute toxicity. Sublethal exposures could inhibit nematodes' growth, shorten lifespan, and induce locomotor deficits, neuronal damage, and reproductive toxicity. Molecular analyses further elucidated the involvement of the DAF-16 and SKN-1 signaling pathways, as evidenced by upregulated expression of genes including ctl-1,2,3, sod -3, gcs-1, and gst-4. It implicates these pathways in mediating oxidative stress and toxicities induced by chain extenders. Particularly, hexamethylene diisocyanate and diallyl maleate exhibited markedly high toxicity among the chain extenders, as revealed through a comparative analysis of multiple endpoints. These findings demonstrate the potential ecotoxicological risks of polymer chain extenders, and suggest the need for more rigorous environmental safety assessments.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) is commonly used in rubber compounds as antioxidants to protect against degradation from heat, oxygen, and ozone exposure. This practice extends the lifespan of rubber products, including tires, by preventing cracking, aging, and deterioration. However, the environmental consequences of waste generated during rubber product use, particularly the formation of 6PPD-quinone (6PPD-Q) through the reaction of 6PPD with ozone, have raised significant concerns due to their detrimental effects on ecosystems. Extensive research has revealed the widespread occurrence of 6PPD and its derivate 6PPDQ in various environmental compartments, including air, water, and soil. The emerging substance of 6PPD-Q has been shown to pose acute mortality and long-term hazards to aquatic and terrestrial organisms at concentrations below environmentally relevant levels. Studies have demonstrated toxic effects of 6PPD-Q on a range of organisms, including zebrafish, nematodes, and mammals. These effects include neurobehavioral changes, reproductive dysfunction, and digestive damage through various exposure pathways. Mechanistic insights suggest that mitochondrial stress, DNA adduct formation, and disruption of lipid metabolism contribute to the toxicity induced by 6PPD-Q. Recent findings of 6PPD-Q in human samples, such as blood, urine, and cerebrospinal fluid, underscore the importance of further research on the public health and toxicological implications of these compounds. The distribution, fate, biological effects, and underlying mechanisms of 6PPD-Q in the environment highlight the urgent need for additional research to understand and address the environmental and health impacts of these compounds.