Methanol Extracts from Cirsium japonicum DC. var. australe Kitam. and Their Active Components Reduce Intracellular Oxidative Stress in Caenorhabditis elegans.

Cirsium japonicum DC. var. australe Kitam. has been used as an herbal remedy and often involves using the whole plant or roots. However, the bioactivities of different parts of the plant have been far less explored. This study aimed to evaluate the antioxidative ability of methanol extracts from the flowers, leaves, stems, and roots of the Cirsium plant and their possible active components against juglone-induced oxidative stress in the nematode Caenorhabditis elegans. The results showed that the highest dry weight (12.3 g per plant) was observed in leaves, which was followed by stems (8.0 g). The methanol extract yields from the flowers, leaves, and roots were all similar (13.0-13.8%), while the yield from stems was the lowest (8.6%). The analysis of the silymarin contents in the extracts indicated that the flowers, leaves, stems, and roots contained silychristin and taxifolin; however, silydianin was only found in the leaves, stems, and roots. The flower, leaf, and stem extracts, at a concentration of 10 mg/L, significantly reduced juglone-induced oxidative stress in C. elegans, which was potentially due to the presence of silychristin and taxifolin. Overall, C. japonicum DC. var. australe Kitam. contains a significant amount of silymarin and exhibits in vivo antioxidative activity, suggesting that the prospects for the plant in terms of health supplements or as a source of silymarin are promising.

Potential anti-Parkinsonian's effect of S-(+)-linalool from Cinnamomum osmophloeum ct. linalool leaves are associated with mitochondrial regulation via gas-1, nuo-1, and mev-1 in Caenorhabditis elegans.

Parkinson's disease (PD) is one of the prevalent neurodegenerative diseases, and developing new treatments from natural products is of particular interest. Essential oils from Cinnamomum osmophloeum ct. linalool leaves contain high levels (~95%) of S-(+)-linalool. The neuroprotective effects of linalool have been previously described, yet the underlying molecular mechanisms remain largely unknown. This study aimed to investigate the potential anti-Parkinsonian's effect of S-(+)-linalool on mitochondrial regulation and decipher the underlying molecular mechanisms in Caenorhabditis elegans PD model. Essential oils at 20 mg/L and 20 mg/L S-(+)-linalool each significantly attenuated the damaging effects of 6-hydroxydopamine (6-OHDA) on dopaminergic (DA) neurons and decreased the mitochondrial unfolded protein response (UPRmt ) to antimycin. RNAi knockdown of mitochondrial complex I (gas-1, nuo-1), and complex II (mev-1) genes prevented the improvement of mitochondrial activity by S-(+)-linalool. The protective effects of S-(+)-linalool on 6-OHDA-induced behavior changes were absent in a DA-specific strain of C. elegans produced by gas-1, nuo-1, and mev-1 RNAi knockdown. These results suggest the potential anti-Parkinsonian's effect of S-(+)-linalool is associated with mitochondrial activity and regulated by gas-1, nuo-1, and mev-1 in C. elegans. Our findings suggest that S-(+)-linalool might be a promising candidate for therapeutic application to inhibit the progression of PD.

Parental CuO nanoparticles exposure results in transgenerational toxicity in Caenorhabditis elegans associated with possible epigenetic regulation.

Environmental nanomaterials contamination is a great concern for organisms including human. Copper oxide nanoparticles (CuO NPs) are widely used in a huge range of applications which might pose potential risk to organisms. This study investigated the in vivo transgenerational toxicity on development and reproduction with parental CuO NPs exposure in the nematode Caenorhabditis elegans. The results showed that CuO NPs (150 mg/L) significantly reduced the body length of parental C. elegans (P0). Only about 1 mg/L Cu2+ (~0.73%) were detected from 150 mg/L CuO NPs in 0.5X K-medium after 48 h. In transgenerational assays, CuO NPs (150 mg/L) parental exposure significantly induced developmental and reproductive toxicity in non-exposed C. elegans progeny (CuO NPs free) on body length (F1) and brood size (F1 and F2), respectively. In contrast, parental exposure to Cu2+ (1 mg/L) did not cause transgenerational toxicity on growth and reproduction. This suggests that the transgenerational toxicity was mostly attributed to the particulate form of CuO NPs. Moreover, qRT-PCR results showed that the mRNA levels of met-2 and spr-5 genes were significantly decreased at P0 and F1 upon only maternal exposure to CuO NPs (150 mg/L), suggesting the observed transgenerational toxicity was associated with possible epigenetic regulation in C. elegans.

Life cycle toxicity assessment of earthworms exposed to cadmium-contaminated soils.

Cadmium (Cd) is of great concern in the soil environment and it can damage terrestrial organisms. The purpose of this study was to employ a toxicokinetic/toxicodynamic (TK/TD) approach to investigate the effects of toxicologically relevant Cd accumulation on the life cycle growth of earthworms (Lumbricus rubellus and Eisenia fetida) and to assess potential terrestrial ecosystem risk. We reanalyzed growth toxicity and whole body and pellet accumulation data linked with TK/TD and life cycle growth models to estimate key rate constants. The growth risk of earthworms exposed to Cd was also assessed. This study found that the estimated whole body killing rate constant (0.114 g d µg-1) was much lower than that of pellet (0.248 g d µg-1). The recovery rate constant for whole body (6.02 d-1) was much higher than that of pellet (2.91 d-1). We also employed a life cycle-based probabilistic risk assessment model to estimate the growth inhibition risk for earthworms in response to environmentally relevant concentrations of Cd in Taiwan. Results showed that earthworms had a 90% growth inhibition probability risk of body weight, which was lower than 872.33 mg based on assessment of toxicologically relevant Cd accumulation. This study suggests that toxicologically relevant Cd accumulation could accurately reflect the capacity of Cd toxicity to earthworms. The integrated life cycle toxicity of earthworms exposed to Cd in this study provides a robust and applicable tool for the management of ecological risk assessment of Cd-contaminated soil.

Transgenerational Reproductive Effects of Arsenite Are Associated with H3K4 Dimethylation and SPR-5 Downregulation in Caenorhabditis elegans.

Arsenic is a prevalent environmental toxin. Arsenic is associated with a wide variety of adverse effects; however, studies on whether As-induced toxicities can be transferred from parents to offspring have received little attention. Caenorhabditis elegans has become an important animal model in biomedical and environmental toxicology research. In this study, transgenerational reproductive toxicity by arsenite exposure and the underlying mechanisms in C. elegans were investigated over six generations (F0-F5). Following arsenite maternal exposure of the F0 generation, subsequent generations (F1-F5) were cultured under arsenite-free conditions. We found that the brood size of C. elegans was significantly reduced by arsenite exposure in F0 and that this reduction in brood size was also observed in the offspring generations (F1-F5), after the toxicant had been removed from the diet. In addition, adult worms from F0 and F1 generations accumulated arsenite and arsenate when F0 L4 larvae were exposed to arsenite for 24 h. We found that the mRNA level of H3K4me2 demethylase LSD/KDM1, spr-5, was significantly reduced in the F0 exposed generation and subsequent unexposed generations (F1-F3). Likewise, the mRNA levels of spr-5 were also significantly decreased in the F1-F3 generations. Moreover, dimethylation of global H3K4 was increased in the F0-F3 generations. Our study demonstrates that maternal arsenite exposure causes transgenerational reproductive effects in C. elegans, which might be associated with H3K4 dimethylation and SPR-5 downregulation.

Assessment of selenium toxicity on the life cycle of Caenorhabditis elegans.

Selenium (Se) is a growing problem of global concern. Se can cause adverse effects on reproductive systems, which have been linked to declines in animal populations. The soil nematode Caenorhabditis elegans (C. elegans) is a ubiquitous soil organism that is increasingly utilized as a model organism in aquatic and soil toxicology. In the present study, the experimental data for individual body length, survival rate, brood size, and hatching rate were used to evaluate the possible effects of selenite [Se(IV)] on C. elegans. A stage-classified matrix model was applied to the experimental data to provide information on the population dynamics of C. elegans and to assess the Se(IV)-affected asymptotic population growth rate. Estimates of the survival probability showed significant decreases in survival at all stages when C. elegans was exposed to Se(IV). The growth probability of C. elegans in the L1 stage showed the most significant decline, from 0.11 h(-1) (for the control) to 0.04 h(-1) [for exposure to 3 mM Se(IV)]. These results showed that Se(IV) has a profound impact on C. elegans population dynamics. The asymptotic population growth rate (λ) was found to range from 1.00 to 0.64 h(-1) for increasing Se(IV) concentrations, implying a potential risk of population decrease for C. elegans exposure to a Se(IV)-contaminated environment. Our study shows how a mechanistic view based on the Se(IV) effects on the soil nematode C. elegans can promote a life cycle toxicity assessment. An important implication of this analysis is that mathematical models can be used to produce a population stage structure, to give clarity to the analysis of the key population-level endpoint (the asymptotic population growth rate) of population dynamics, and to evaluate the influences for the response of other species to environmental Se. These models sequentially provide candidate environmental criteria for the evaluation of the population impact of Se.

Life cycle exposure to titanium dioxide nanoparticles (TiO2-NPs) induces filial toxicity and population decline in the nematode Caenorhabditis elegans.

Titanium dioxide nanoparticle (TiO2-NP) exposure has raised significant concern due to their potential toxicity and adverse ecological impacts. Despite their ubiquitous presence in various environmental compartments, the long-term consequences of TiO2-NPs remain poorly understood. In this study, we combined data of in vivo toxicity and modeling to investigate the potential negative impacts of TiO2-NP exposure. We employed the nematode Caenorhabditis elegans, an environmental organism, to conduct a full life cycle TiO2-NP toxicity assays. Moreover, to assess the potential impact of TiO2-NP toxicity on population dynamics, we applied a stage-constructed matrix population model (MPM). Results showed that TiO2-NPs caused significant reductions in reproduction, survival, and growth of parental C. elegans (P0) at the examined concentrations. Moreover, these toxic effects were even more pronounced in the subsequent generation (F1) when exposed to TiO2-NPs. Furthermore, parental TiO2-NP exposure resulted in significant toxicity in non-exposed C. elegans progeny (TiO2-NPs free), adversely affecting their reproduction, survival, and growth. MPM analysis revealed decreased transition probabilities of surviving (Pi), growth (Gi), and fertility (Fi) in scenarios with TiO2-NP exposure. Additionally, the population growth rate (λmax) was found to be less than 1 in both P0 and F1, indicating a declining population trend after successive generations. Sensitivity analysis pinpointed L1 larvae as the most vulnerable stage, significantly contributing to the observed population decline in both P0 and F1 generations under TiO2-NP exposure. Our findings provide insight into the potential risk of an environmental organism like nematode by life cycle exposure to TiO2-NPs.

Nanoparticles in the Environment and Nanotoxicology.

Nanomaterials, including engineered nanoparticles and microplastics/nanoplastics, have attracted increasing concern as they might potentially release into the environment, leading to potential risks to ecosystems [...].

Nanoplastics exposure disrupts circadian rhythm associated with dysfunction of the endolysosomal pathway and autophagy in Caenorhabditis elegans.

Nanoplastics (NPs), an emerging pollutant, have raised great safety concerns due to their widespread applications and continuous release into the environment, which lead to potential human and environmental risks. Recently, polystyrene NPs (100 nm; 100 mg/L) exposure has been reported to disrupt circadian rhythms under five days temperature entrainment and be associated with stress resistance decline in Caenorhabditis elegans. This study explored the possible relationship between circadian rhythm disruption and endocytosis and autophagy under polystyrene NPs exposure in C. elegans. We show that the disrupted circadian rhythm induced by NPs exposure reduced stress resistance via endocytosis and autophagy impairment. Furthermore, we found that most NPs taken up by intestinal cells were localized to early endosomes, late endosomes, and lysosomes and delivered to autophagosomes. In addition, the disruption of circadian rhythm inhibited NPs localization to these organelles. These findings indicate that NPs exposure disrupts circadian rhythm and alters its subcellular trafficking, leading to enhanced toxicity in C. elegans. Our results shed light on the prominent role of NPs exposure in circadian rhythm disruption associated with endocytosis and autophagy impairments, which may be conserved in higher animals such as humans.

Sulfate-modified nanosized polystyrene impairs memory by inhibiting ionotropic glutamate receptors and the cAMP-response element binding protein (CREB) pathway in Caenorhabditis elegans.

Nanoplastic contamination is an emerging environmental concern worldwide. In particular, sulfate anionic surfactants often appear along with nanosized plastic particles in personal care products, suggesting that sulfate-modified nanosized polystyrene (S-NP) may occur, remain, and spread into the environment. However, whether S-NP adversely affects learning and memory is unknown. In this study, we used a positive butanone training protocol to evaluate the effects of S-NP exposure on short-term associative memory (STAM) and long-term associative memory (LTAM) in Caenorhabditis elegans. We observed that long-term S-NP exposure impairs both STAM and LTAM in C. elegans. We also observed that mutations in the glr-1, nmr-1, acy-1, unc-43, and crh-1 genes eliminated the STAM and LTAM impairment induced by S-NP, and the mRNA levels of these genes were also decreased upon S-NP exposure. These genes encode ionotropic glutamate receptors (iGluRs), cyclic adenosine monophosphate (cAMP)/Ca2+ signaling proteins, and cAMP-response element binding protein (CREB)/CRH-1 signaling proteins. Moreover, S-NP exposure inhibited the expression of the CREB-dependent LTAM genes nid-1, ptr-15, and unc-86. Our findings provide new insights into long-term S-NP exposure and the impairment of STAM and LTAM, which involve the highly conserved iGluRs and CRH-1/CREB signaling pathways.

Assessing the ecological risk and ecotoxicity of the microbially mediated restoration of heavy metal-contaminated river sediment.

Anthropogenic activities such as mining, smelting industries, and the application of pesticides in agriculture might result in contamination of multiple heavy metals in the environment. Heavy metal contamination of sediment is a serious environmental problem, and thus the remediation of contaminated sediment is a worldwide challenge. Several strategies have been developed for the remediation of contaminated sediment, however the ecological risk and ecotoxicity of the restored sediment have rarely been evaluated. We assessed whether river sediment highly contaminated with heavy metals could be restored using microbial bioleaching followed by evaluating the residual toxicity and ecological risk of the microbially remediated sediment. Sequential extraction revealed that the bioavailable levels of Cu, Ni, and Zn in the contaminated sediment exceeded sediment quality guideline (SQG) thresholds. It was consequently found that acidophilic sulfur-oxidizing Acidicaldus sp. SV5 effectively bioleached Cu, Ni, and Zn from the contaminated sediment, reducing the bioavailable fraction of these elements below SQG thresholds. The ecological risk assessment indicated that SV5-driven remediation significantly reduced the potential ecological risk of the contaminated sediment. The residual ecotoxicity of the microbially remediated sediment was also tested with the soil nematode Caenorhabditis elegans. There was a significant decrease in the body burden of Cu, Ni, and Zn in C. elegans and a reduction in the toxicological effect on survival, growth, and reproduction in the microbially remediated sediment. Our study suggests that a combination of chemical analysis, chemical-based ecological risk assessment, and ecotoxicity tests would be helpful for the development of efficient and eco-friendly strategies for the restoration of contaminated sediment, which could be incorporated into sediment quality management practices.

Chronic exposure to di(2-ethylhexyl) phthalate (DEHP) weakens innate immunity and leads to immunosenescence in C. elegans.

Di(2-ethylhexyl) phthalate (DEHP), a widespread contaminant, has numerous adverse impacts on human health and ecosystems. Chronic DEHP exposure has been found to accelerate aging; however, its potential threat to age-dependent innate immune decline remains unknown. This study aims to evaluate the effects of chronic DEHP exposure on innate immunosenescence in Caenorhabditis elegans. We show that the length of the exposure period significantly impacts DEHP-induced age-related declines, which is linked to immunosenescence and oxidative stress. We found that the DEHP-caused immunosenescence is accompanied with downregulation of an antimicrobial gene lys-7 as well as an enhancement of the nuclear translocation of HLH-30, an orthologue of mammalian transcription factor EB (TFEB). Moreover, DEHP exposure increases the expression of riok-1, a human RIO kinase homolog, which is associated with DEHP-induced HLH-30/TFEB translocation. Our findings suggest that early-life and chronic exposure to DEHP, mostly due to parent compound rather than its metabolite mono(2-ethylhexyl) phthalate (MEHP), may weaken the innate immunity in C. elegans and may enhance susceptibility to infections or promote immunosenescence in aged populations.

Co-contaminants of ethinylestradiol and sulfamethoxazole in groundwater exacerbate ecotoxicity and ecological risk and compromise the energy budget of C. elegans.

Ethinylestradiol (EE2) and sulfamethoxazole (SMX) are among pharmaceuticals and personal care products (PPCPs) and regarded as emerging contaminants in groundwater worldwide. However, the ecotoxicity and potential risk of these co-contaminants remain unknown. We investigated the effects of early-life long-term co-exposure to EE2 and SMX in groundwater on life-history traits of Caenorhabditis elegans and determined potential ecological risks in groundwater. L1 larvae of wild-type N2 C. elegans were exposed to measured concentrations of EE2 (0.001, 0.75, 5.1, 11.8 mg/L) or SMX (0.001, 1, 10, 100 mg/L) or co-exposed to EE2 (0.75 mg/L, no observed adverse effect level derived from its reproductive toxicity) and SMX (0.001, 1, 10, 100 mg/L) in groundwater. Growth and reproduction were monitored on days 0 - 6 of the exposure period. Toxicological data were analyzed using DEBtox modeling to determine the physiological modes of action (pMoAs) and the predicted no-effect concentrations (PNECs) to estimate ecological risks posed by EE2 and SMX in global groundwater. Early-life EE2 exposure significantly inhibited the growth and reproduction of C. elegans, with lowest observed adverse effect levels (LOAELs) of 11.8 and 5.1 mg/L, respectively. SMX exposure impaired the reproductive capacity of C. elegans (LOAEL = 0.001 mg/L). Co-exposure to EE2 and SMX exacerbated ecotoxicity (LOAELs of 1 mg/L SMX for growth, and 0.001 mg/L SMX for reproduction). DEBtox modeling showed that the pMoAs were increased growth and reproduction costs for EE2 and increased reproduction costs for SMX. The derived PNEC falls within the range of detected environmental levels of EE2 and SMX in groundwater worldwide. The pMoAs for EE2 and SMX combined were increased growth and reproduction costs, resulting in lower energy threshold values than single exposure. Based on global groundwater contamination data and energy threshold values, we calculated risk quotients for EE2 (0.1 - 123.0), SMX (0.2 - 91.3), and combination of EE2 and SMX (0.4 - 341.1). Our findings found that co-contamination by EE2 and SMX exacerbates toxicity and ecological risk to non-target organisms, suggesting that the ecotoxicity and ecological risk of co-contaminants of pharmaceuticals should be considered to sustainably manage groundwater and aquatic ecosystems.

Early developmental nanoplastics exposure disturbs circadian rhythms associated with stress resistance decline and modulated by DAF-16 and PRDX-2 in C. elegans.

Plastics pollution is an emerging environmental problem and nanoplastics (NPs) toxicity has received great concern. This study investigated whether early developmental exposure to polystyrene NPs influence the circadian rhythms and the possible underlying mechanisms in C. elegans. We show that early developmental NPs exposure disturbs circadian rhythms in C. elegans and ASH neurons and G protein-coupled receptor kinase (GRK-2) are involved in the level of chemotaxis response. A higher bioconcentration factor in entrained worms was observed, suggesting that circadian interference results in increased NPs bioaccumulation in C. elegans. In addition, we show that reactive oxygen species produced by NPs exposure and peroxiredoxin-2 (PRDX-2) are related to the disturbed circadian rhythms. We further show that the NPs-induced circadian rhythms disruption is associated with stress resistance decline and modulated by transcription DAF-16/FOXO signaling. Because circadian rhythms are found in most living organisms and the fact that DAF-16 and PRDX-2 are evolutionarily conserved, our findings suggest a possible negative impact of NPs on circadian rhythms and stress resistance in higher organisms including humans.

Chronic di(2-ethylhexyl) phthalate exposure leads to dopaminergic neuron degeneration through mitochondrial dysfunction in C. elegans.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is frequently detected in the environment due to the abundance of its use. These levels might be hazardous to human health and ecosystems. Phthalates have been associated with neurological disorders, yet whether chronic DEHP exposure plays a role in Parkinson's disease (PD) or its underlying mechanisms is unknown. We investigated the effects of chronic DEHP exposure less than an environmentally-relevant dose on PD hallmarks, using Caenorhabditis elegans as a model. We show that developmental stage and exposure timing influence DEHP-induced dopaminergic neuron degeneration. In addition, in response to chronic DEHP exposure at 5 mg/L, mitochondrial fragmentation became significantly elevated, reactive oxygen species (ROS) levels increased, and ATP levels decreased, suggesting that mitochondrial dysfunction occurs. Furthermore, the data show that mitochondrial complex I (nuo-1 and gas-1) and complex II (mev-1) are involved in DEHP-induced dopaminergic neuron toxicity. These results suggest that chronic exposure to DEHP at levels less than an environmentally-relevant dose causes dopaminergic neuron degeneration through mitochondrial dysfunction involving mitochondrial complex I and II. Considering the high level of genetic conservation between C. elegans and mammals, chronic DEHP exposure might elevate the risk of developing PD in humans.

Removal of nano-sized polystyrene plastic from aqueous solutions using untreated coffee grounds.

Nanoplastic (NP) pollution is an emerging global concern due to its adverse impact on aquatic ecosystems. Nevertheless, the removal of aqueous NPs from aquatic environments remains a significant challenge. This study aims to investigate whether polystyrene NP in aqueous solutions can be removed using coffee grounds. Due to the difficulty associated with directly measuring NP levels and monitoring the biosorption process, we used fluorescent-orange amine-modified polystyrene beads (fluo-NP, 100 nm) to evaluate the efficacy of the biosorption process. The factors including pH, coffee grounds concentration, initial fluo-NP concentration, and contact time were optimized on batch experiments. In addition, the isotherm and kinetic models were employed to clarify the adsorption behaviors and mechanisms. It was found that aqueous fluo-NP particles were effectively adsorbed onto the coffee grounds over a wide pH range (pH 2-12), with a coffee ground concentration of 25 g/L leading to the maximum adsorption efficiency (74%). The equilibrium adsorption capacity of the coffee grounds was 4 mg/g for a reaction time of 40 min. Coffee grounds demonstrated the highest removal efficiency when the initial fluo-NP concentration was 100-125 mg/L. The Dubinin-Radushkevich model and pseudo-second-order model described the adsorption isotherm and kinetics well, respectively, and the adsorption at high fluo-NP concentration range was favorable. Moreover, the results suggest that the mechanism lies in the electrostatic interactions and hydrogen bonding between surface functional groups of the coffee grounds and the fluo-NP particles. Given that there is an urgent need to remove NPs from aqueous systems, this study illustrates that it is possible to use coffee ground biowaste for this purpose.

Nanoplastic exposure in soil compromises the energy budget of the soil nematode C. elegans and decreases reproductive fitness.

Environmental nanoplastics (NPs) can accumulate in soils, posing a potential risk to soil ecosystems. However, the ecotoxicity of NPs for soil organisms has received little research attention. This study investigated whether NP exposure in soil leads to reproductive decline in the soil nematode Caenorhabditis elegans and sought to determine the mechanisms by which it may occur. Wild-type N2 C. elegans L1 larvae were exposed to various concentrations of nano-sized polystyrene (100 nm) in soil (0, 1, 10, 100, and 1000 mg/kg dry weight) for 96 h. We show that nano-sized polystyrene (100 nm) labeled with red fluorescence significantly accumulated in the intestine of C. elegans in a dose-dependent fashion via soil exposure (8%-47% increase). In addition, NP soil exposure led to 7%-33% decline in the number of eggs in utero and 2.6%-4.4% decline in the egg hatching percentage. We also find that the number of germ cell corpses (31%-55% increase) and the mRNA levels of germline apoptosis marker gene ced-3 (14%-31% increase) were significantly higher with greater NP soil exposure (10, 100, and 1000 mg/kg), while intracellular ATP levels were significantly reduced. Finally, the DEBtox model, which is based on the dynamic energy budget theory, was applied to show that the increased reproductive costs for C. elegans caused by NPs in soil are associated with energy depletion and reproductive decline. The threshold value (4.18 × 10-6 mg/kg) for the energy budget also highlighted the potential high reproductive risk posed by NPs in terrestrial ecosystems. Our study provides new insights into how soil organisms interact with NPs in soil ecosystems.

A combined approach to remediate cadmium contaminated sediment using the acidophilic sulfur-oxidizing bacterial SV5 and untreated coffee ground.

Cadmium (Cd) contamination in sediment is an emerging concern for the sustainability of aquatic ecosystem due to the toxicity of Cd is correlated to different trophic levels. An effective and inexpensive remediation strategy for Cd-contaminated sediment is desirable. The feasibility of using a newly isolated acidophilic sulfur-oxidizing bacterium and untreated coffee ground to remediate Cd-contaminated sediment was evaluated. The bioleaching approach was firstly conducted with the acidophilic sulfur-oxidizing bacterial SV5, resulting in Cd(II) release from Cd(II)-contaminated sediment. Subsequently, Cd(II) in the acidic leachate was further removed using untreated agricultural wastes. Untreated coffee ground exhibited about 2-fold Cd(II) removal efficiency comparing to that of rice husk and peanut shell. Scanning electron microscope (SEM) and Fourier-transform infrared spectroscopy (FTIR) analysis were conducted to characterize the coffee ground after the adsorption of 0 or 200 mg/L Cd(II). At pH 4, the optimal coffee ground concentration was 30 g/L along with 100 mg/L Cd(II) concentration. Adsorption of Cd(II) by coffee ground was rapid and the adsorption kinetic followed pseudo-second order model. Cd(II) sorption by coffee ground was a favorable process and Langmuir isotherm model well described the experimental data. Taken together, even at pH 4, coffee ground still showed good biosorption capacity for Cd(II) with short equilibrium time. This study suggests that acidophilic sulfur-oxidizing bacterial SV5 and untreated coffee ground could be used as inexpensive and environment-friendly biomaterial and agricultural waste for the remediation of Cd-contaminated sediment.

Early-life chronic di(2-ethylhexyl)phthalate exposure worsens age-related long-term associative memory decline associated with insulin/IGF-1 signaling and CRH-1/CREB in Caenorhabditis elegans.

The ubiquitous contamination of di(2-ethylhexyl)phthalate (DEHP) in the environment, biota, and food poses potential ecological and human health risks. DEHP exposure can adversely affect learning and memory, yet the underlying mechanisms remain unclear. In this study, Caenorhabditis elegans was used to investigate the effect of early-life DEHP exposure on age-related long-term associative memory (LTAM) decline, as well as the associations with the cAMP-responsive element-binding protein (CREB) transcription factor and insulin/IGF-1 signaling (IIS). We showed that early-life exposure to DEHP reduced LTAM in wild-type worms at day-0 adulthood. Chronic exposure to DEHP from the L1 stage to day-5 adulthood worsened the age-dependent decline of LTAM. Moreover, the effect of DEHP on age-related LTAM requires CRH-1, a homolog of CREB. Mutations in daf-2, the sole receptor of C. elegans IIS, ameliorated the inhibition of LTAM by DEHP, and the effect depended on daf-16. In addition, daf-2 mutation restored the CRH-1 level in DEHP-exposed worms, and the effect required daf-16. Our study suggests that early-life chronic exposure to DEHP worsens age-related LTAM decline and the effect is associated with CRH-1 and IIS in C. elegans. The evolutionary conservation of IIS and CREB implies possible adverse effects by DEHP across species.

Long-term nanoplastics exposure results in multi and trans-generational reproduction decline associated with germline toxicity and epigenetic regulation in Caenorhabditis elegans.

The environmental risk from long-term plastic pollution is growing. We investigated the multi and trans-generational reproductive toxicity of nanoplastics (NPs) in Caenorhabditis elegans and the underlying mechanisms over five generations. Following a single maternal exposure (F0) to NPs (100 nm; 1, 10, 50, or 100 mg/L) for 72 h, the subsequent generations (F1-F4) were cultured under NPs-free conditions. We showed that the total brood size was significantly reduced across all offspring generations (F1-F4). NPs accumulated in the intestine of C. elegans in the F0 generation, but not in the germline system, and not observed in subsequent generations. Chromosomal aberrations in oocytes and germline cell apoptosis were significantly elevated in the NPs-exposed F0 generation and in subsequent unexposed generations. Likewise, the expression of ced-3 was increased across generations, regulated by hypomethylation in the promoter region of ced-3 after maternal NPs exposure. Finally, NPs exposure reduced the expression of epigenesis-related genes met-2, set-2, and spr-5 and the trans-generational effects of maternal NPs exposure were not observed in met-2, set-2, and spr-5 RNAi worms. We demonstrate that a single long-term maternal NPs exposure can cause multi and trans-generational reproduction decline in C. elegans, which may be associated with germline toxicity and epigenetic regulation.