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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 (UPR

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.

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.

The widespread usage of ZnO nanoparticles (ZnO-NPs) and their potential to accumulate in sediment have raised great concerns regarding their chronic ecotoxicity in benthic ecosystems. This study investigated the effects of ZnO-NPs on the freshwater Asian clam Corbicula fluminea exposed to the nanoparticles through various routes in aquatic sediment environments. Significant amounts of Zn accumulated in the single-celled algae Chlorella ellipsoidea exposed to ZnO-NPs, resulting in foodborne exposure for C. fluminea. In addition, Zn was analyzed in overlaying water, pore water, and sediment in aquatic sediment environments and was found to accumulate mostly in sediment. Co-exposure to foodborne and waterborne ZnO-NPs significantly increased the mortality in C. fluminea compared to the mortality in clams exposed to untreated algae (about two-fold increase on day 28). Further evidence showed that bioaccumulation (about 1.5-fold increase), the expression of stress genes (about 1.5-fold increase), and DNA damage (about two-fold increase) were significantly enhanced in C. fluminea upon co-exposure to foodborne and waterborne ZnO-NPs compared with the levels in untreated algae on day 14. This study helps broaden the understanding of the ecotoxicity of ZnO-NPs and their interactions with sediment, algae, and bivalves in benthic ecosystems.

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

DEHP is commonly found in the environment, biota, food, and humans, raising significant health concerns. Whether developmental stage and exposure duration modify the obesogenic effects of DEHP is unclear, especially the underlying mechanisms by which chronic exposure to DEHP as well as its metabolites remain largely unknown. This study investigated the obesogenic effects of chronic DEHP exposure, with levels below environmentally-relevant amounts and provide the mechanism in Caenorhabditis elegans. We show that early-life DEHP exposure resulted in an increased lipid and triglyceride (TG) accumulation mainly attributed to DEHP itself, not its metabolite mono-2-ethylhexyl phthalate (MEHP). In addition, developmental stage and exposure timing influence DEHP-induced TG accumulation and chronic DEHP exposure resulted in the most significant effect. Analysis of fatty acid composition shows that chronic DEHP exposure altered fatty acid composition and TG, resulting in an increased ω-6/ω-3 ratio. The increased TG content by chronic DEHP exposure required lipogenic genes fat-6, fat-7, pod-2, fasn-1, and sbp-1. Moreover, chronic DEHP exposure induced XBP-1-mediated endoplasmic reticulum (ER) stress which might lead to up-regulation of sbp-1. This study suggests the possible involvement of ER stress and SBP-1/SREBP-mediated lipogenesis in chronic DEHP-induced obesogenic effects. Results from this study implies that chronic exposure to DEHP disrupts lipid metabolism, which is likely conserved across species due to evolutionary conservation of molecular mechanisms, raising concerns in ecological and human health.

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.

Di(2-ethylhexyl)phthalate (DEHP) is an ubiquitous and emerging contaminant that is widely present in food, agricultural crop, and the environment, posing a potential risk to human health. This study utilized the nematode Caenorhabditis elegans to decipher the toxic effects of early life exposure to DEHP on aging and its underlying mechanisms. The results showed that exposure to DEHP at 0.1 and 1.5 mg/L inhibited locomotive behaviors. In addition, DEHP exposure significantly shortened the mean lifespan of the worms and further adversely affected pharyngeal pumping rate and defecation cycle in aged worms. Moreover, DEHP exposure also further enhanced accumulation of age-related biomarkers including lipofuscin, lipid peroxidation, and intracellular reactive oxygen species in aged worms. In addition, exposure to DEHP significantly suppressed gene expression of hsp-16.1, hsp-16.49, and hsp-70 in aged worms. Further evidences showed that mutation of genes involved in insulin/IGF-1-like signaling (IIS) pathway (daf-2, age-1, pdk-1, akt-1, akt-2, and daf-16) restored lipid peroxidation accumulation upon DEHP exposure in aged worms, whereas skn-1 mutation resulted in enhanced lipid peroxidation accumulation. Therefore, IIS and SKN-1 may serve as an important molecular basis for DEHP-induced age-related declines in C. elegans. Since IIS and SKN-1 are highly conserved among species, the age-related declines caused by DEHP exposure may not be exclusive in C. elegans, leading to adverse human health consequences due to widespread and persistent DEHP contamination in the environment.

Concerns have arisen regarding potential environmental risks from the increased usage and widespread development of engineered nanomaterials (ENMs). Zinc oxide nanoparticles (ZnO-NPs) are emerging materials that tend to accumulate in sediment after being released into aquatic environments, potentially leading to chronic toxicity in aquatic ecosystems. In this study, the nematode Caenorhabditis elegans was used to evaluate the chronic toxicity of ZnO-NPs in sediment and the underlying molecular mechanisms. Following long-term sediment exposure to ZnO-NPs, growth and reproduction defects were not observed in C. elegans at the examined concentrations, whereas locomotive behaviours (frequency of body bends and head thrashes) and ATP levels were adversely affected. In addition, significant increases in intracellular reactive oxygen species and lipid peroxidation were induced by long-term sediment exposure to ZnO-NPs. Furthermore, long-term sediment exposure to ZnO-NPs triggered translocation of the transcription factor DAF-16/FOXO from the cytoplasm to the nuclei and further activated the targeted expression of the corresponding stress-responsive genes (mtl-1 and sod-3). This study demonstrates that long-term sediment exposure to ZnO-NPs results in oxidative stress in the benthic organism C. elegans, mediated by the transcription factor DAF-16 triggering stress-responsive gene activation.

Triadimenol, an agricultural fungicide, is an emerging environmental concern due to its wide usage, detection in the environment, and its chemical persistency. Triadimenol has been found to disrupt endocrine signaling and alter function of several transcription factors, yet its age-related toxicity effects remain unclear. This study used Caenorhabditis elegans as an in vivo model organism to elucidate the age-related effects of triadimenol and its underlying mechanisms. The results showed that chronic exposure to triadimenol at environmentally relevant concentrations (3, 30, and 300 μg/L) adversely affected several toxicity endpoints including growth, total brood size, and locomotive behaviors. In addition, triadimenol (300 μg/L) significantly reduced the mean lifespan of wild-type N2 C. elegans from 17.9 to 16 days. Chronic exposure to triadimenol (300 μg/L) also significantly affected age-related behavioral changes, with a decreased pharyngeal pumping rate and an increased defecation cycle. Moreover, an increased accumulation of aging biomarkers including lipofuscin, lipid peroxidation, and reactive oxygen species (H2O2 and O2 −) level upon chronic triadimenol exposure was observed in aged worms. Furthermore, chronic triadimenol exposure increased the transcriptional factor DAF-16 nuclear localization. Finally, mutation of daf-2, age-1, pdk-1, akt-1, or akt-2 restored the accumulation of lipofuscin in aged worms upon chronic triadimenol exposure, while mutation of daf-16 led to more enhanced lipofuscin accumulation. Therefore, the insulin/IGF-1 signaling pathway may serve as an important molecular basis for triadimenol induced aging declines in C. elegans.

Background: Parkinson's disease (PD) is a common neurodegenerative disease, yet fundamental treatments for the disease remain sparse. Thus, the search for potentially efficacious compounds from medicinal plants that can be used in the treatment of PD has gained significant interest. Purpose: In many medicinal plants, selenium is primarily found in an organic form. We investigated the neuroprotective potential of an organic form of selenium, N-γ-(L-glutamyl)-L-selenomethionine (Glu-SeMet) in a Caenorhabditis elegans PD model and its possible molecular mechanisms. Methods: We used a C. elegans pharmacological PD strain (BZ555) that specifically expresses green fluorescent protein (GFP) in dopaminergic neurons and a transgenic PD strain (NL5901) that expresses human α-synuclein (α-syn) in muscle cells to investigate the neuroprotective potential of Glu-SeMet against PD. Results: We found that Glu-SeMet significantly ameliorated 6-hydroxydopamine (6-OHDA)-induced dopaminergic neuron damage in the transgenic BZ555 strain, with corresponding improvements in slowing behavior and intracellular ROS levels. In addition, compared with clinical PD drugs (L-DOPA and selegiline), Glu-SeMet demonstrated stronger ameliorated effects on 6-OHDA-induced toxicity. Glu-SeMet also triggered the nuclear translocation of SKN-1/Nrf2 and significantly increased SKN-1, GST-4, and GCS-1 mRNA levels in the BZ555 strain. However, Glu-SeMet did not increase mRNA levels or ameliorate the damage to dopaminergic neurons when the BZ555 strain was subjected to skn-1 RNA interference (RNAi). Glu-SeMet also upregulated the mRNA levels of the selenoprotein TRXR-1 in both the BZ555 and BZ555; skn-1 RNAi strains and significantly decreased α-syn accumulation in the NL5901 strain, although this was not observed in the NL5901; trxr-1 strain. Conclusion: We found that Glu-SeMet has a neuroprotective effect against PD in a C. elegans PD model and that the anti-PD effects of Glu-SeMet were associated with SKN-1/Nrf2 and TRXR-1. Glu-SeMet may thus have the potential for use in therapeutic applications or supplements to slow the progression of PD.

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.

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.

Manganese occurs naturally in sediment, yet anthropogenic sources, such as industrial wastewater and mining, increases Mn concentration. However, the environmental risk of bioavailable Mn is often overlooked and infrequently addressed. A probabilistic risk assessment was conducted to determine the effects of bioavailable Mn in river sediments on reproduction in model organism Caenorhabditis elegans using in utero egg counts and germline apoptosis as biomarkers. The lowest-observed-adverse-effect level (LOAEL) of sediment Mn that decreases in utero egg counts or increases germline apoptosis in C. elegans was 50 or 10 mg of Mn(II) per kg of dry weight sediment, respectively. Effect and exposure analyses were conducted using Hill model-simulated concentration-response curves and Mn concentrations of Laojie River sediment. Risk quotients (RQs) and exceedance risk (ER) analyses showed that bioavailable levels of Mn in Laojie River sediments from downstream sites collected during the dry season elevate reproductive risk as measured by germline apoptosis. These findings suggest that bioavailable levels of Mn in sediment exert negative impacts, and germline apoptosis is a sensitive biomarker for reproductive risk assessment. Our results also suggest that the anthropogenic Mn pollution in river sediment and spatial-seasonal bioavailability of Mn should be considered to improve sediment quality control.

Contamination by heavy metals and metalloids is a serious environmental and health concern. Acidic wastewaters are often associated with toxic metals which may enter and spread into agricultural soils. Several biological assays have been developed to detect toxic metals; however, most of them can only detect toxic metals in a neutral pH, not in an acidic environment. In this study, an acidophilic iron-oxidizing bacterium (IOB) Strain Y10 was isolated, characterized, and used to detect toxic metals toxicity in acidic water at pH 2.5. The colorimetric acidophilic IOB biosensor was based on the inhibition of the iron oxidizing ability of Strain Y10, an acidophilic iron-oxidizing bacterium, by metals toxicity. Our results showed that Strain Y10 is acidophilic iron-oxidizing bacterium. Thiobacillus caldus medium (TCM) (pH 2.5) supplied with both S4O62- and glucose was the optimum growth medium for Strain Y10. The optimum temperature and pH for the growth of Strain Y10 was 45 °C and pH 2.5, respectively. Our study demonstrates that the color-based acidophilic IOB biosensor can be semi-quantitatively observed by eye or quantitatively measured by spectrometer to detect toxicity from multiple toxic metals at pH 2.5 within 45 min. Our study shows that monitoring toxic metals in acidic water is possible by using the acidophilic IOB biosensor. Our study thus provides a novel approach for rapid and cost-effective detection of toxic metals in acidic conditions that can otherwise compromise current methods of chemical analysis. This method also allows for increased efficiency when screening large numbers of environmental samples.

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.

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.

The widespread use of di(2-ethylhexyl) phthalate (DEHP) has resulted in its ubiquitous presence in the environment, which has led to serious health concerns. One of these concerns is its possible link to Alzheimer’s disease (AD), which is the most common neurodegenerative disease in aged individuals. This study investigated whether early-life and chronic exposure to DEHP affects AD via the toxicity of amyloid-β (Aβ), which has been implicated in the pathogenesis of AD, using Caenorhabditis elegans AD models (strains CL4176 and CL2006). We show that early-life DEHP exposure increased Aβ toxicity in C. elegans strains CL4176 and CL2006. Early-life and chronic exposure to DEHP also significantly increased intracellular ROS levels and Aβ deposition in aged CL2006 nematodes. Moreover, it was found that DEHP-induced Aβ toxicity does not require transcription factors DAF-16 or SKN-1, while early-life and chronic exposure to DEHP significantly increased the accumulation of lysosome-related organelles and the mRNA levels of the autophagy-related gene bec-1 in aged CL2006 nematodes. Our findings suggest that early-life and chronic exposure to DEHP enhances Aβ toxicity, which may be associated with the autophagy–lysosomal degradation pathway in C. elegans.

The in vitro and in vivo antioxidant activities and its potential to protect against amyloid-P toxicity of essential oils from Zelkova serrata (Thunb.) Makino were investigated in the model organism Caenorhabditis elegans. The results revealed that the essential oil of Z serrata heartwood exhibited great radical scavenging activities and high total phenolic content. In vivo assays showed significant inhibition of oxidative damage in wild-type C. elegans under juglone- indueed oxidative stress and heat shock. Based on results from both in vitro and in vivo assays, the major compound in essential oil of heartwood, (-)-(S, 4S)- 7-hydroxycalamenene (IS, 4S-7HC), may contribute significantly to the observed antioxidant activity. Further evidence showed that IS, 4S-7HC significantly delayed the paralysis phenotype in amyloid beta-expressing transgenic C. elegans. These findings suggest that IS, 4S-7HC from the essential oil of Z serrata heartwood has potential as a source for antioxidant or Alzheimer's disease treatment.

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.

River sediment is the ultimate sink for heavy metal pollution. Copper (Cu) and zinc (Zn) are consistently found at environmentally significant levels in sediments worldwide. We hypothesized that the bioavailability and potential ecological risk of Cu and Zn in river sediments may be affected by seasonal variations and spatial distribution. In this study, we tested our hypothesis using highly industrialized river sediments (Laojie River) as an example. The concentration of heavy metals, pollution indexes, and risk indexes were evaluated and multivariate statistical analyses were performed. We found that seasonal variations affect heavy metal contamination, pollution indexes, and potential ecological risk in sediments and this effect was more severe in the dry season. In addition, higher levels of metal contamination, pollution indexes, and potential ecological risk were observed midstream and downstream of the Laojie River. We found that Cu and Zn were the primary contaminants in Laojie River sediments and may originate from common anthropogenic sources. Analysis of the chemical fractions further revealed that Cu and Zn exhibited high mobility and potential bioavailability risk. In addition, a high percentage and amount of Cu and Zn were found in exchangeable fractions, suggesting they pose a great risk to aquatic organisms. Our results indicate that seasonal variations and spatial distribution affect the bioavailability and potential ecological risk of Cu and Zn in river sediments. These findings suggest that seasonal variations and spatial distribution are important parameters to consider for environmental monitoring and environmental management in aquatic environments.

Arsenic (As) is a human carcinogen, and arsenic contamination in groundwater is a worldwide public health concern. Arsenic-affected areas are found in many places but are reported mostly in agricultural farmlands, yet the interaction of fertilizers, microorganisms, and arsenic mobilization in arsenic-contaminated aquifers remains uncharacterized. This study investigates the effects of fertilizers and bacteria on the mobilization of arsenic in two arsenic-contaminated aquifers. We performed microcosm experiments using arsenic-contaminated sediments and amended with inorganic nitrogenous or phosphorus fertilizers for 1 and 4 months under aerobic and anaerobic conditions. The results show that microcosms amended with 100 mg/L phosphorus fertilizers (dipotassium phosphate), but not nitrogenous fertilizers (ammonium sulfate), significantly increase aqueous As(III) release in arsenic-contaminated sediments under anaerobic condition. We also show that concentrations of iron, manganese, potassium, sodium, calcium, and magnesium are increased in the aqueous phase and that the addition of dipotassium phosphate causes a further increase in aqueous iron, potassium, and sodium, suggesting that multiple metal elements may take part in the arsenic release process. Furthermore, microbial analysis indicates that the dominant microbial phylum is shifted from α-proteobacteria to β- and γ-proteobacteria when the As(III) is increased and phosphate is added in the aquifer. Our results provide evidence that both phosphorus fertilizers and microorganisms can mediate the release of arsenic to groundwater in arsenic-contaminated sediments under anaerobic condition. Our study suggests that agricultural activity such as the use of fertilizers and monitoring phosphate concentration in groundwater should be taken into consideration for the management of arsenic in groundwater.

Using arsenic (As) contaminated groundwater for drinking or irrigation has caused major health problems for humans around the world, raising a need to monitor As level efficiently and economically. This study developed a color-based bacterial biosensor which is easy-to-use and inexpensive for measuring As and could be complementary to current As detecting techniques. The arsR-lacZ recombinant gene cassette in nonpathogenic strain Escherichia coli DH5α was used in the color-based biosensor which could be observed by eyes or measured by spectrometer. The developed bacterial biosensor demonstrates a quantitative range from 10 to 500μgL(-1) of As in 3-h reaction time. Furthermore, the biosensor was able to successfully detect and estimate As concentration in groundwater sample by measuring optical density at 595nm (OD595). Among different storage methods used in this study, biosensor in liquid at 4°C showed the longest shelf life about 9d, and liquid storage at RT and cell pellet could also be stored for about 3-5d. In conclusion, this study showed that the As biosensor with reliable color signal and economical preservation methods is useful for rapid screening of As pollutant, providing the potential for large scale screening and better management strategies for environmental quality control.

The widespread use of zinc oxide nanoparticles (ZnO-NPs) has led to their release into the environment, and they thus represent a potential risk for both humans and ecosystems. However, the negative impact of ZnO-NPs on the immune system, especially in relation to host defense against pathogenic infection and its underlying regulatory mechanisms, remains largely unexplored. This study investigated the effects of early-life long-term ZnO-NPs exposure (from L1 larvae to adults) on innate immunity and its underlying mechanisms using a host–pathogen Caenorhabditis elegans model, and this was compared with the effect of ionic Zn. The results showed that the ZnO-NPs taken up by C. elegans primarily accumulated in the intestine and that early-life long-term ZnO-NPs exposure at environmentally relevant concentrations (50 and 500 μg/L) decreased the survival of wild-type C. elegans when faced with pathogenic Pseudomonas aeruginosa PA14 infection. Early-life long-term ZnO-NPs (500 μg/L) exposure significantly increased (by about 3-fold) the accumulation of live P. aeruginosa PA14 colonies in the intestine of C. elegans. In addition, ZnO-NPs (500 μg/L) inhibited the intestinal nuclear translocation of SKN-1 and also downregulated gcs-1 gene expression, which is an SKN-1 target gene. Further evidence revealed that early-life long-term exposure to ZnO-NPs (500 μg/L) did not increase susceptibility to mutation among the genes (pmk-1, sek-1, and nsy-1) encoding the p38 mitogen-activated protein kinase (MAPK) cascade in response to P. aeruginosa PA14 infection, though ZnO-NPs significantly decreased the mRNA levels of pmk-1, sek-1, and nsy-1. This study provides regulatory insight based on evidence that ZnO-NPs suppress the innate immunity of C. elegans and highlights the potential health risks of certain environmental nanomaterials, including ZnO-NPs, in terms of their immunotoxicity at environmentally relevant concentrations.

There is growing need and interest in finding specific compounds in natural products that have health benefits. Despite ongoing efforts to discover such compounds, the scientific evidence lags behind the vision, and it is important to find an effective paradigm for discovering such compounds. The model organism Caenorhabditis elegans offers a promising solution for studying the potential bioactivity and molecular mechanisms of natural compounds in vivo. This perspective discusses its use to study potential human health benefits, with focus on antioxidative, anti-aging, antimetabolic disorders (diabetes and obesity), and antineurodegenerative activities (Alzheimer’s disease and Parkinson’s disease), with practical examples. Finally, future directions in using a C. elegans-based model for discovering bioactive compounds for health promotion are discussed.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is an emerging organic contaminant that has represented a risk for organisms present in the environment. However, there is still limited information regarding DEHP-induced multigenerational toxicity and the underlying mechanisms. In this study we investigated the multigenerational toxic effects including locomotive behaviors and reproduction upon prolonged DEHP exposure (from larval L1 to adult) and the underlying mechanisms in the nematode Caenorhabditis elegans. The multigenerational effects were examined over 6 generations (F0-F5) with only parental C. elegans (F0) was exposed to DEHP from larval L1 to adults (72h), and the subsequent offsprings (F1-F5) were grown under DEHP-free conditions. The results showed that prolonged exposure (72h) to various concentrations of DEHP caused dose-dependent locomotive impairments and reproduction defects in C. elegans and that a concentration of 0.2mg/L DEHP was enough to cause such sublethal effects. The results showed that after prolonged exposure to DEHP in the F0 generation, abnormal locomotive behaviors such as reduced body bends and head thrashes were observed from generations F0 to F5. Additionally, prolonged exposure to DEHP (20mg/L) in F0 significantly reduced total brood size in F0, and this parental exposure was sufficient to cause multigenerational reproductive toxicity in the offspring generations (F1-F5) as well. Furthermore, the expressions of reproduction-related genes such as vit-2 and vit-6 were down-regulated by about 20% until F3, and the expression of H3Kme2 demethylase, spr-5, was downregulated in F1 by about 40%. Results from this study demonstrate that prolonged exposure to DEHP only at F0 adversely affected reproduction and locomotive behaviors in C. elegans across generations and might be associated with inadequate vitellogenin production and malfunction of H3Kme2 demethylase. This study implies that parentally prolonged exposure to DEHP caused multigenerational defects in both reproduction and locomotive behaviors raising the potential health and ecological risk.

Iron (Fe) is an essential element for many organisms, but high concentrations of iron can be toxic. The complex relation between iron, arsenic (As), bacteria, and organic matter in sediments and groundwater is still an issue of environmental concern. The present study addresses the effects of humic acids and microorganisms on the mobilization of iron in sediments from an arsenic-affected area, and the microbial diversity was analyzed. The results showed that the addition of 50, 100, and 500 mg/L humic acids enhanced ferrous iron (Fe(II)) release in a time-dependent and dose-dependent fashion under anaerobic conditions. A significant increase in the soluble Fe(II) concentrations occurred in the aqueous phases of the samples during the first 2 weeks, and aqueous Fe(II) reached its maximum concentrations after 8 weeks at the following Fe(II) concentrations: 28.95 ± 1.16 mg/L (original non-sterilized sediments), 32.50 ± 0.71 mg/L (50 mg/L humic acid-amended, non-sterilized sediments), 37.50 ± 1.85 mg/L (100 mg/L humic acid-amended, non-sterilized sediments), and 39.00 ± 0.43 mg/L (500 mg/L humic acid-amended, non-sterilized sediments). These results suggest that humic acids can further enhance the microbially mediated release of sedimentary iron under anaerobic conditions. By contrast, very insignificant amounts of iron release were observed from sterilized sediments (the abiotic controls), even with the supplementation of humic acids under anaerobic incubation. In addition, the As(III) release was increased from 50 ± 10 μg/L (original non-sterilized sediments) to 110 ± 45 μg/L (100 mg/L humic acid-amended, non-sterilized sediments) after 8 weeks of anaerobic incubation. Furthermore, a microbial community analysis indicated that the predominant class was changed from Alphaproteobacteria to Deltaproteobacteria, and clearly increased populations of Geobacter sp., Paludibacter sp., and Methylophaga sp. were found after adding humic acids along with the increased release of iron and arsenic. Our findings provide evidence that humic acids can enhance the microbially mediated release of sedimentary ferrous iron in an arsenic-affected area. It is thus suggested that the control of anthropogenic humic acid use and entry into the environment is important for preventing the subsequent iron contamination in groundwater.

There is a growing interest in the exploitation of the residues generated by plants. This study explored the potential beneficial health effects from the main biowaste, tea seed pomace, produced when tea seed is processed. DPPH radical scavenging and total phenolic content assays were performed to evaluate the in vitro activities of the extracts. Caenorhabditis elegans was used as in vivo model to evaluate the beneficial health effects, including antioxidant activity, delayed aging, and reduced amyloid-β toxicity. Among all soluble fractions obtained from the extracts of tea seed pomace from Camellia tenuifolia, the methanol (MeOH)-soluble fraction has the best in vivo antioxidant activities. The MeOH-soluble extraction was further divided into six fractions by chromatography with a Diaion HP-20 column eluted with water/MeOH, and fraction 3 showed the best in vitro and in vivo antioxidant activities. Further analysis in C. elegans showed that the MeOH extract (fraction 3) of tea seed pomace significantly decreased intracellular reactive oxygen species, prolonged C. elegans lifespan, and reduced amyloid-β (Aβ) toxicity in transgenic C. elegans expressing human Aβ. Moreover, bioactivity-guided fractionation yielded two potent constituents from fraction 3 of the MeOH extract, namely, kaempferol 3-O-(2″-glucopyranosyl)-rutinoside and kaempferol 3-O-(2″-xylopyranosyl)-rutinoside, and both compounds exhibited excellent in vivo antioxidant activity. Taken together, MeOH extracts of tea seed pomace from C. tenuifolia have multiple beneficial health effects, suggesting that biowaste might be valuable to be explored for further development as nutraceutical products. Furthermore, the reuse of agricultural byproduct tea seed pomace also fulfills the environmental perspective.

Background Parkinson's disease (PD) is a neurodegenerative disease that is associated with aging and is characterized as a movement disorder. Currently, there is still no complete therapy for PD. In recent years, the identification and characterization of medicinal plants to cure or treat PD has gained increasing scientific interest. Purpose In this study, we investigated a pentacyclic triterpenoid compound, β-amyrin, which is found in many medicinal plants for its anti-Parkinsonian effects, using Caenorhabditis elegans (C. elegans) disease models and their underlying mechanisms. Methods C. elegans treated or untreated with β-amyrin were investigated for oxidative stress resistance, neurodegeneration, and α-synuclein aggregation assays. The C. elegans ortholog of Atg8/LC3, LGG-1 that is involved in the autophagy pathway was also evaluated by quantitative RT-PCR and transgenic strain experiments. Results β-Amyrin exerted excellent antioxidant activity and reduced intracellular oxygen species in C. elegans. Using the transgenic strain BZ555, β-amyrin showed a protective effect on dopaminergic neurons reducing cell damage induced by 6-hydroxydopamine (6-OHDA). In addition, β-amyrin significantly reduced the α-synuclein aggregation in the transgenic strain NL5901. Moreover, β-amyrin up-regulated LGG-1 mRNA expression and increased the number of localized LGG-1 puncta in the transgenic strain DA2123. Conclusion The results from this study suggest that the anti-Parkinsonian effects of β-amyrin might be regulated via LGG-1 involved autophagy pathway in C. elegans. Therefore, β-amyrin may be useful for therapeutic applications or supplements to treat or slow the progression of PD.

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.

The antioxidant activity and delayed aging effects of hot water extracts from leaves of Chamaecyparis obtusa var. formosana were investigated. Free radical, superoxide radical scavenging, and total phenolic content assays were employed to evaluate the in vitro activities of the extracts. In addition, in vivo assays using the nematode Caenorhabditis elegans were also performed in this study. The results showed that among all soluble fractions obtained from the extracts, the ethyl acetate-soluble fraction has the best in vitro and in vivo antioxidant activities. Moreover, it decreased significantly the deposition of lipofuscin (aging pigment) and extended the lifespan of C. elegans. Bioactivity-guided fractionation yielded six potent antioxidant constituents from the ethyl acetate-soluble fraction, namely, catechin, quercetin, quercetin-3-O-α-rhamnoyranoside, myricetin-3-O-α-rhamnoyranoside, vanillic acid, and 4-hydroxybenzoic acid. Quercetin-3-O-α-rhamnoyranoside pretreatment showed the highest survival of C. elegans upon juglone exposure. Taken together, the results revealed that hot water extracts from C. obtusa var. formosana leaves have the potential to be used as a source for antioxidant or delayed aging health food.

Scope Selenium is an essential micronutrient. In the present study, trace amount of selenite (0.01 μM) was evaluated for oxidative stress resistance and potential associated factors in Caenorhabditis elegans. Methods and results Selenite-treated C. elegans showed an increased survival under oxidative stress and thermal stress compared to untreated controls. Further studies demonstrated that the significant stress resistance of selenite on C. elegans could be attributed to its in vivo free radical-scavenging ability. We also found that the oxidative and thermal stress resistance phenotypes by selenite were absent from the forkhead transcription factor daf-16 mutant worms. Moreover, selenite influenced the subcellular distribution of DAF-16 in C. elegans. Furthermore, selenite increased mRNA levels of stress-resistance-related proteins, including superoxide dismutase-3 and heat shock protein-16.2. Additionally, selenite (0.01 μM) upregulated expressions of transgenic C. elegans carrying sod-3::green fluorescent protein (GFP) and hsp-16.2::GFP, whereas this effect was abolished by feeding daf-16 RNA interference in C. elegans. Finally, unlike the wild-type N2 worms, the oxidative stress resistance phenotypes by selenite were both absent from the C. elegans selenoprotein trxr-1 mutant worms and trxr-1 mutants feeding with daf-16 RNA interference. Conclusion These findings suggest that the antioxidant effects of selenite in C. elegans are mediated via DAF-16 and TRXR-1.

Scope Selenium is an important nutrient for human health. The influence of dietary selenium on lipid metabolism remains largely unknown. N-γ-(l-glutamyl)-l-selenomethionine (Glu-SeMet) on inhibition of fat accumulation and its underlying mechanisms in the nematode Caenorhabditis elegans are investigated. Methods and results Triacylglyceride quantification and post-fixed Nile red staining methods are conducted to evaluate fat accumulation in wild-type N2 worms in normal or high-glucose diet. Glu-SeMet (0.01 µm) treatment effectively reduces fat storage in wild-type N2 C. elegans in both a normal and high-glucose diet. Further evidence shows that Glu-SeMet (0.01 µm) decreases the ratio of oleic acid/stearic acid (C18:1Δ9/C18:0) using gas chromatography-mass spectrometry analysis. The mRNA levels of fatty acid stearoyl-CoA desaturases, FAT-6 and FAT-7, and the mediator-15 (MDT-15) are downregulated while the wild-type N2 worms are co-treated with high glucose and Glu-SeMet (0.01 µm). The effect of reduced fat accumulation is absent in fat-6, fat-7, and trxr-1 mutant worms under high glucose and Glu-SeMet (0.01 µm) co-treatment. Conclusions This study demonstrates that Glu-SeMet inhibiting fat accumulation may be associated with FAT-6 and FAT-7 and the selenoprotein TRXR-1 in C. elegans. This study implies a potential for Glu-SeMet as a new treatment for obesity or its complications.

Summary Arsenic (As) is an odorless semi-metal that occurs naturally in rock and soil, and As contamination in groundwater resources has become a serious threat to human health. Thus, assessing the spatial and temporal variability of As concentration is highly desirable, particularly in heavily As-contaminated areas. However, various difficulties may be encountered in the regional estimation of As concentration such as cost-intensive field monitoring, scarcity of field data, identification of important factors affecting As, over-fitting or poor estimation accuracy. This study develops a novel systematical dynamic-neural modeling (SDM) for effectively estimating regional As-contaminated water quality by using easily-measured water quality variables. To tackle the difficulties commonly encountered in regional estimation, the SDM comprises of a neural network and four statistical techniques: the Nonlinear Autoregressive with eXogenous input (NARX) network, Gamma test, cross-validation, Bayesian regularization method and indicator kriging (IK). For practical application, this study investigated a heavily As-contaminated area in Taiwan. The backpropagation neural network (BPNN) is adopted for comparison purpose. The results demonstrate that the NARX network (Root mean square error (RMSE): 95.11 μg l−1 for training; 106.13 μg l−1 for validation) outperforms the BPNN (RMSE: 121.54 μg l−1 for training; 143.37 μg l−1 for validation). The constructed SDM can provide reliable estimation (R2 > 0.89) of As concentration at ungauged sites based merely on three easily-measured water quality variables (Alk, Ca2+ and pH). In addition, risk maps under the threshold of the WHO drinking water standard (10 μg l−1) are derived by the IK to visually display the spatial and temporal variation of the As concentration in the whole study area at different time spans. The proposed SDM can be practically applied with satisfaction to the regional estimation in study areas of interest and the estimation of missing, hazardous or costly data to facilitate water resources management.

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.

Amyloid-β (Aβ)-induced oxidative stress and toxicity are leading risk factors for Alzheimer's disease (AD). Monascin (MS) is a novel compound proposed for antioxidative stress applications and is derived from an edible fungus secondary metabolite. This study assessed the effects of MS on oxidative stress, paralysis, Aβ accumulation, and lifespan in the nematode Caenorhabditis elegans and investigated its underlying mechanisms of action. The results showed that MS increased the survival of C. elegans under juglone-induced oxidative stress and attenuated endogenous levels of reactive oxygen species. Furthermore, MS induced a decline in Aβ-induced paralysis phenotype and Aβ deposits in the transgenic strains CL4176 and CL2006 of C. elegans, which expresses human muscle-specific Aβ1-42 in the cytoplasm of body wall muscle cells. In addition, mRNA levels of strain CL4176 of several antioxidant genes (sod-1, sod-2, sod-3, hsp16.2) and daf-16 were up-regulated by MS treatment when compared to the nontreated controls. Further evidence showed that MS treatment in C. elegans strains lacking DAF-16/FOXO did not affect paralysis or lifespan phenotypes. The findings indicate that MS reduces oxidative stress and Aβ toxicity via DAF-16 in C. elegans, suggesting that MS can be used for the prevention of AD-associated oxidative stress complications.

ZnO nanoparticles (ZnO-NPs) are emerging contaminants that raise the concerns of potential risk in the aquatic environment. It has been estimated that the environmental ZnO-NPs concentration is 76 μg/l in the aquatic environment. Our aim was to determine the aquatic toxicity of ZnO-NPs with chronic exposure at environmentally relevant concentrations using the nematode Caenorhabditis elegans. Two simulated environmentally relevant mediums—moderately hard reconstituted water (EPA water) and simulated soil pore water (SSPW)—were used to represent surface water and pore water in sediment, respectively. The results showed that the ZnO-NPs in EPA water has a much smaller hydrodynamic diameter than that in SSPW. Although the ionic release of Zn ions increased time-dependently in both mediums, the Zn ions concentrations in EPA water increased two-fold more than that in SSPW at 48 h and 72 h. The ZnO-NPs did not induce growth defects or decrease head thrashes in C. elegans in either media. However, chronic exposure to ZnO-NPs caused a significant reduction in C. elegans body bends in EPA water even with a relatively low concentration (0.05 μg/l); similar results were not observed in SSPW. Moreover, at the same concentrations (50 and 500 μg/l), body bends in C. elegans were reduced more severely in ZnO-NPs than in ZnCl2 in EPA water. The ATP levels were consistently and significantly decreased, and ROS was induced after ZnO-NPs exposure (50 and 500 μg/l) in EPA water. Our results provide evidences that chronic exposure to ZnO-NPs under environmentally relevant concentrations causes metabolic and locomotive toxicities implicating the potential ecotoxicity of ZnO-NPs at low concentrations in aquatic environments.