Investigating the evolution of reactive species in the CuO-mediated peroxymonosulfate activation process.

The utilization of copper oxide (CuO) as a catalyst in the peroxymonosulfate (PMS) activation process holds great promise for effectively degrading aqueous organic pollutants, while the relevant mechanism remains inadequately understood. In this study, we delve into the evolution pathways of reactive species in the CuO/PMS system through a comprehensive series of experimental analyses. Our findings indicate that various reactive species are generated in the CuO/PMS system with the specific sequence, where the decomposition of surface Cu(II)-OOSO3- leads to the formation of surface Cu(III) species, which are responsible for the subsequent generation of HO•. The reactivity of these reactive species and the sequence of their generation explain the distinct oxidation behaviors of pollutants with different values of ionization potential (IP). In addition, singlet oxygen (1O2) may be produced during the PMS activation process, while its involvement in the oxidation of substrates is deemed negligible. This investigation presents a novel perspective, enhancing our comprehension of the mechanism underlying transition metal-mediated PMS activation processes. ENVIRONMENTAL IMPLICATION: The removal of refractory organic contaminations in water constitutes a fundamental concern within the realm of environmental pollution management. Peroxymonosulfate activation induced by transition metal oxides has garnered significant recognition as a promising technological approach for the degradation of aqueous organic contaminants, while the underlying mechanism remains enigmatic. In this study, we systematically investigate the evolution pathways of reactive species in the CuO/peroxymonosulfate system to reveal the mystery of the reaction mechanism between CuO and peroxymonosulfate. The outcomes of our study contribute to enhancing the practical applicability of transition metal-triggered PMS activation processes.

Exploration for cobalt/nitrogen-doped catalyst to creatinine degradation via peroxymonosulfate activation: toxicity evaluation, statistical modeling, and mechanisms study.

Developing multifunctional catalysts applied in diversiform modes via advanced oxidation processes (AOPs) is a promising and attractive approach for organic pollution degradation. Herein, a novel hollow bamboo-like structural cobalt/nitrogen-doped carbonized material (CoC/N) was employed as a catalyst for AOPs, in which CoC/N was prepared in situ through calcining a Co-based coordination polymer. When CoC/N was utilized as a peroxymonosulfate (PMS) activator, the catalyst stood out prominent activities for effective CA oxidation. Furthermore, a five-level central composite rotatable design (CCRD) model describing CA decay as a function of PMS concentration, CoC/N dosage, and solution pH value was successfully constructed and engaged to explore the optimal operating conditions. Finally, the possible degradation mechanism of CA in CoC/N-PMS system was proposed by quantum chemistry calculation and LC/MS analysis. This work shed light on the structural morphology of the catalyst and its PMS synergy degradation pathway, which promotes its applications in miscellaneous pollutant degradation. A new Co/N-doped material was used to degrade unconventionality organic pollutant creatinine (CA) for the first time, in which the scientific approaches of five-level central composite rotatable design (CCRD) model, response surface methodology (RSM) and density function theory (DFT) were employed to evaluate the material performance and CA degradation pathway. The toxicity evaluation, statistical modeling and mechanisms study have been investigated meticulously.

Wearable sensor platforms for real-time monitoring and early warning of metabolic disorders in humans.

Nowadays, the prevalence of metabolic syndromes (MSs) has attracted increasing concerns as it is closely related to overweight and obesity, physical inactivity and overconsumption of energy, making the diagnosis and real-time monitoring of the physiological range essential and necessary for avoiding illness due to defects in the human body such as higher risk of cardiovascular disease, diabetes, stroke and diseases related to artery walls. However, the current sensing techniques are inconvenient and do not continuously monitor the health status of humans. Alternatively, the use of recent wearable device technology is a preferable method for the prevention of these diseases. This can enable the monitoring of the health status of humans in different health domains, including environment and structure. The use wearable devices with the purpose of facilitating rapid treatment and real-time monitoring can decrease the prevalence of MS and long-time monitor the health status of patients. This review highlights the recent advances in wearable sensors toward continuous monitoring of blood pressure and blood glucose, and further details the monitoring of abnormal obesity, triglycerides and HDL. We also discuss the challenges and future prospective of monitoring MS in humans.

Contribution of differential alteration in oxidative stress and anti-oxidation related molecular signals to toxicity difference between atrazine and its main metabolites in nematodes.

As a widely used herbicide, atrazine and its two main metabolites of deethylatrazine (DEA) and deisopropylatrazine (DIA) pose an exposure risk for both human beings and animals in the environment. In this study, Caenorhabditis elegans was selected as an in vivo model to compare the toxicity between atrazine and its main metabolites. Upon exposure from the larval stage L1 to adult day 3, both DEA and DIA showed less toxicity on locomotion and reproduction compared with atrazine at concentration of 0.001, 0.01 0.1 and 1 mg/L for parental generation. In addition, exposure to DEA and DIA at concentration of 0.1 mg/L also induced less transgenerational toxicity on locomotion than exposure to atrazine for both parental generation and offspring of F1-F4. Accordingly, exposure to DEA and DIA caused less ROS production and alteration in the expression of some genes (mev-1, gas-1, and clk-1) governing oxidative stress compared to atrazine. Meanwhile, DEA and DIA lead to less increase in expression of superoxide dismutase genes (sod-2 and sod-3) and SOD-3::GFP than atrazine. Moreover, atrazine and its two main metabolites differentially activated the daf-16 encoding FOXO transcriptional factor in insulin signaling pathway during the control of downstream target of SOD-3. Overall, our results highlighted the important role of oxidative stress and anti-oxidation related molecular signals in mediating toxicity of atrazine, DEA and DIA, which provided a novel explanation for the different toxicity between atrazine and its main metabolites.

Remediation technologies for neonicotinoids in contaminated environments: Current state and future prospects.

Neonicotinoids (NEOs) are synthetic insecticides with broad-spectrum insecticidal activity and outstanding efficacy. However, their extensive use and persistence in the environment have resulted in the accumulation and biomagnification of NEOs, posing significant risks to non-target organisms and humans. This review provides a summary of research history, advancements, and highlighted topics in NEOs remediation technologies and mechanisms. Various remediation approaches have been developed, including physiochemical, microbial, and phytoremediation, with microbial and physicochemical remediation being the most extensively studied. Recent advances in physiochemical remediation have led to the development of innovative adsorbents, photocatalysts, and optimized treatment processes. High-efficiency degrading strains with well-characterized metabolic pathways have been successfully isolated and cultured for microbial remediation, while many plant species have shown great potential for phytoremediation. However, significant challenges and gaps remain in this field. Future research should prioritize isolating, domesticating or engineering high efficiency, broad-spectrum microbial strains for NEO degradation, as well as developing synergistic remediation techniques to enhance removal efficiency on multiple NEOs with varying concentrations in different environmental media. Furthermore, a shift from pipe-end treatment to pollution prevention strategies is needed, including the development of green and economically efficient alternatives such as biological insecticides. Integrated remediation technologies and case-specific strategies that can be applied to practical remediation projects need to be developed, along with clarifying NEO degradation mechanisms to improve remediation efficiency. The successful implementation of these strategies will help reduce the negative impact of NEOs on the environment and human health.

Combinational exposure to hydroxyatrazine increases neurotoxicity of polystyrene nanoparticles on Caenorhabditis elegans.

Using Caenorhabditis elegans as an animal model, we investigated combinational effect between 2-hydroxyatrazine (HA) and polystyrene nanoparticle (PS-NP) on function and development of D-type motor neurons. Exposure to HA (10 and 100 µg/L) alone caused decreases in body bend, head thrash, and forward turn and increase in backward turn. Exposure to 100 µg/L HA also caused neurodegeneration of D-type motor neurons. Moreover, combinational exposure to HA (0.1 and 1 µg/L) induced enhancement in PS-NP (10 µg/L) toxicity in inhibiting body bend, head thrash, and forward turn, and in increasing backward turn. In addition, combinational exposure to HA (1 µg/L) could result in neurodegeneration of D-type motor neurons in PS-NP (10 µg/L) exposed nematodes. Combinational exposure to HA (1 µg/L) and PS-NP (10 µg/L) increased expressions of crt-1, itr-1, mec-4, asp-3, and asp-4, which govern the induction of neurodegeneration. Moreover, combinational exposure to HA (0.1 and 1 µg/L) strengthened PS-NP (10 µg/L)-induced decreases in glb-10, mpk-1, jnk-1, and daf-7 expressions, which encode neuronal signals regulating response to PS-NP. Therefore, our results demonstrated the effect of combinational exposure to HA and nanoplastics at environmentally relevant concentrations in causing toxic effect on nervous system in organisms.

Occurrence, spatial distributions, and temporal trends of bisphenol analogues in an E-waste dismantling area: Implications for risk assessment.

The environmental occurrences of bisphenol analogues (BPs) have been extensively reported, whereas their concentration profile, spatial distribution, and temporal trend in e-waste dismantling area are still poorly understood. Herein, typical BPs (BPA, BPS, TBBPA, TBBPA-DHEE, and TBBPA-MHEE) were investigated in water, soil, and biological samples from three representative regions (FJT, JJP, and RIB) in e-waste recycling area in Taizhou, Zhejiang Province. Overall, the detection frequency of BPs in all samples was 100 %, confirming widespread presence of BPs in e-waste recycling area. Wherein, BPA was the predominant BPs in water (33.3 %) and soil samples (34.9 %), but TBBPA accounted for the largest proportion (41.3 %) in biological samples. In addition, the concentration of BPs in FJT was lower than that in JJP and RIB owing to the renovations on FJT by the local government in recent years, whereas the higher BPs level in RIB implied that elevated BPs contents was related to massive e-waste dismantling activities. From 2017 to 2021, a decreased trend of BPs concentration was observed in FJT, but aggravation of BPs levels in RIB was caused by the ongoing e-waste dismantling. The risk assessment revealed that the BPs in e-waste recycling area posed a low ecological and human health risk. Our finding could provide a valuable reference for the development of strict legislation systems related to e-waste management in China.

Effects of perfluorobutane sulfonate and perfluorooctane sulfonate on lipid homeostasis in mouse liver.

Perfluorobutane sulfonate (PFBS), an alternative to perfluorooctane sulfonate (PFOS), has been increasingly used in recent years. However, emerging evidence has raised concerns about the potential health risks of PFBS. Here, the toxicityof low-dose PFBS on livers was explored and compared with that of PFOS. Adult C57BL/6 mice were exposed to 10 µg/L, 500 µg/L PFBS, or 500 µg/L PFOS for 28 days through drinking water. At the phenotypic level, no liver damage was observed in the 10 µg/L PFBS group. The cell apoptosis and decrease of CAT activities were observed in the 500 µg/L PFBS group, while accumulation of lipid droplets, increase of CAT activities and TAG levels were found in the 500 µg/L PFOS group. Lipidomics analysis revealed that 138, 238, and 310 lipids were significantly changed in the 10 µg/L, 500 µg/L PFBS and 500 µg/L PFOS groups, respectively. The two PFBS-treated groups induced similar global lipid changes in a dose-dependent manner, which were distinct from PFOS. Overall, PFBS exposure induced an increase in phosphatidylcholines and sphingomyelins, but a decrease in phosphatidylinositol. PFOS exposure caused an increase in triacylglycerols. This study provides more evidence on the health hazards caused by exposure to low-dose PFBS.

Preinoculation with Endophytic fungus Phomopsis liquidambaris reduced rice bakanae disease caused by Fusarium proliferatum via enhanced plant resistance.

AIMS: This study evaluated the control effect of the endophytic fungus Phomopsis liquidambaris B3 against rice bakanae disease (RBD) caused by Fusarium proliferatum and the disease control result of different inoculation times of beneficial micro-organisms. METHODS AND RESULTS: Rice seedlings preinoculated, coinoculated and noninoculated with B3 were exposed to F. proliferatum stress and grown under controlled conditions. Greenhouse experimental results showed that rice preinoculation with B3 significantly reduced rice bakanae disease by 21.45%, inhibited the colonization of F. proliferatum, increased defence-related enzyme activities, upregulated the expression of defence genes and promoted plant photosynthesis. However, bakanae disease in rice coinoculation with B3 increased by 11.45%, resulted in excessive reactive oxygen species (ROS) bursts and plant cell death. CONCLUSIONS: Preinoculation with the endophytic fungus P. liquidambaris B3 significantly reduced rice bakanae disease by triggering the SA-dependent defence pathways of plants, and promoted plant growth. However, coinoculatiton with P. liquidambaris B3 activated excessive defence responses, resulting in plants cell death and aggravation of bakanae disease. SIGNIFICANCE AND IMPACT OF THE STUDY: This study indicated that P. liquidambaris B3 was an effective method for agricultural control against rice bakanae disease caused by F. proliferatum, and provides an experimental basis for the development of sustainable endophytic fungal resources to effectively control plant diseases caused by pathogenic fungi, and suggests that precise application of beneficial micro-organisms may be become a key factor in farmland crop disease management.

Long-term exposure to polystyrene nanoparticles causes transgenerational toxicity by affecting the function and expression of MEV-1 and DAF-2 signals in Caenorhabditis elegans.

In this study, we determined the roles of oxidative stress and related signals in mediating transgenerational toxicity of 30 nm polystyrene nanoparticles (PS-NPs) in Caenorhabditis elegans. Using brood size and locomotion behavior as endpoints, exposure to 1-100 µg/L PS-NPs caused transgenerational toxicity. Meanwhile, the activation of reactive oxygen species (ROS) was also observed transgenerationally after exposure to 1-100 µg/L PS-NPs. After exposure to 1 µg/L PS-NPs, the transgenerational toxicity was monitored until F2 generation (F2-G) and recovered at F3-G. At the F1-G of 1 µg/L PS-NPs-exposed nematodes, RNAi knockdown of daf-2 with function to inhibit oxidative stress suppressed the transgenerational toxicity and increased the mitochondrial SOD-3 expression. In contrast, at F3-G of 1 µg/L PS-NPs-exposed nematodes, RNAi knockdown of mev-1 with function to induce oxidative stress promoted locomotion and brood size, and suppressed the SOD-3 expression. Moreover, we observed the dynamic expressions of mev-1, daf-2, and sod-2 transgenerationally after exposure to 1 µg/L PS-NPs at P0-G, which further suggested the involvement of MEV-1, DAF-2, and SOD-3 in affecting induction of transgenerational PS-NP toxicity. Therefore, we provided the evidence to suggest the roles of oxidative stress activation and related molecular signals in mediating induction of transgenerational PS-NP toxicity. Our data highlights the crucial function of oxidative stress-related signals during induction of transgenerational PS-NP toxicity.

[Occurrence Characteristics and Risk Assessment of Antibiotics in the Surface Water of Luoma Lake and Its Main Inflow Rivers].

The concentration levels of 39 antibiotics, including sulfonamides (SAs), quinolones (QUs), tetracyclines (TCs), macrolides (MLs), and penicillins (PLs), in the surface water of Luoma Lake, and its main inflow rivers were analyzed using SPE-UPLC-MS/MS. The contribution rates of pollution of major rivers entering the lake were analyzed, and the potential ecological and health risks of antibiotics were assessed. The results showed that ρ(antibiotics)in 42 sampling sites was between 30.10 ng·L-1 and 582.37 ng·L-1, and a total of four classes of 23 antibiotics were detected. Among them, the average detection concentration of enrofloxacin (ERX) was the highest (88.05 ng·L-1), and the detection rate of lincomycin (LIN) was the highest (100%). The average concentration of antibiotics in the northern region of Luoma Lake was higher than that in the south, and among the two main rivers entering the lake, Yihe River was the main river contributing to the pollution of antibiotics in Luoma Lake, with a contribution rate of 53.91%. The results of risk assessment showed that ERX had the largest risk quotient. For the cumulative risk quotient (RQcum), RQcum of L6, R30, R31, R32, R33, and R42 was between 0.1 and 1, which is considered medium risk, and RQcum of other points was>1, which is considered high risk. The health risk assessment of 11 antibiotics showed that the health risk quotient (RQH) of adults and children ranged from 4.16×10-6 to 2.46×10-3, and there was no health risk to the human body.

Reproductive toxicity and underlying mechanisms of di(2-ethylhexyl) phthalate in nematode Caenorhabditis elegans.

DEHP (di(2-ethylhexyl) phthalate) is an endocrine disruptor commonly found in plastic products that has been associated with reproduction alterations, but the effect of DEHP on toxicity is still widely unknown. Using DEHP concentrations of 10, 1, and 0.1 mg/L, we showed that DEHP reduced the reproductive capacity of Caenorhabditis elegans after 72 hr. of exposure. DEHP exposure reduced the reproductive capacity in terms of decreased brood sizes, egg hatchability (0.1, 1 and 10 mg/L), and egg-laying rate (1 and 10 mg/L), and increased numbers of fertilized eggs in the uterus (1 and 10 mg/L). DEHP also caused damage to gonad development. DEHP decreased the total number of germline cells, and decreased the relative area of the gonad arm of all exposure groups, with worms in the 1 mg/L DEHP exposure group having the minimum gonad arm area. Additionally, DEHP caused a significant concentration-dependent increase in the expression of unc-86. Autophagy and ROS contributed to the enhancement of DEHP toxicity in reducing reproductive capacity, and glutathione peroxidase and superoxide dismutase were activated as the antioxidant defense in this study. Hence, we found that DEHP has a dual effect on nematodes. Higher concentration (10 mg/L) DEHP can inhibit the expression of autophagy genes (atg-18, atg-7, bec-1, lgg-1 and unc-51), and lower concentrations (0.1 and 1 mg/L) can promote the expression of autophagy genes. Our data highlight the potential environmental risk of DEHP in inducing reproductive toxicity toward the gonad development and reproductive capacity of environmental organisms.

Indirect competitive-structured electrochemical immunosensor for tetrabromobisphenol A sensing using CTAB-MnO2 nanosheet hybrid as a label for signal amplification.

Tetrabromobisphenol A (TBBPA) is a kind of brominated flame retardant that is usually added to products to reduce their flame retardancy. However, its extensive use has resulted in their residues being found in the environment, which is very harmful. Herein, an indirect competitive immunosensor has been established for TBBPA detection based on the signal amplification system. Pd nanospheres in situ reduced on the surface of MnO2 nanosheet hybrid (MnO2/Pd) was used as the label for the secondary antibody through the Pd-N bond, and gold-toluidine blue composite was loaded onto MWCNTs (MWCNTs/Au-TB), which functioned as the platform for the immunosensor. The spherical structure of Pd had abundant catalytic active sites, which enhanced the catalytic activity of MnO2/Pd as the label, hence amplifying the signal response. Besides, MWCNTs/Au-TB improved electron transfer and produced a strong signaling pathway for immobilizing antigens through the Au-NH2 bond, which can specifically recognize primary antibodies to improve sensitivity. The immunosensor had a linear concentration range of 0-81 ng/mL, a low detection limit of 0.17 ng/mL (S/N = 3), with good stability, selectivity, and reproducibility based on the above advantages. Additionally, the acceptable accuracy and recoveries (recoveries, 92-124%; CV, 3.3-8.8%) in the real water sample analysis indicated that this strategy is promising for emerging pollutant analysis.

The use of different sublethal endpoints to monitor atrazine toxicity in nematode Caenorhabditis elegans.

In this work, Caenorhabditis elegans was employed as an in vivo model to determine the toxic effects of atrazine at different concentrations. After the exposure period from the larval stage L1 to adulthood day 1, atrazine (10 mg/L) significantly decreased the body length and lifespan of nematodes. In addition, exposure to ≥0.01 mg/L atrazine remarkably increased the intestinal reactive oxygen species (ROS) levels and reduced locomotion behavior of nematodes, while exposure to ≥ 1 mg/L atrazine decreased the brood size of nematodes. Moreover, atrazine (0.001-0.1 mg/L) upregulated the expression levels of hsp-6::GFP and hsp-6/60 in nematodes, indicating the activation of mitochondrial unfolded protein response (mtUPR). On the contrary, atrazine (1-10 mg/L) downregulated the expression levels of hsp-6::GFP and hsp-6/60 in nematodes. Furthermore, mtUPR induction governed by the RNAi knockdown of atfs-1 could increase the vulnerability of nematodes against atrazine toxicity. Overall, our findings highlighted the dynamic responses of nematodes toward different concentrations of atrazine, which could be monitored using different sublethal endpoints as bioindicators.

The effect of combined exposure of zinc and nickel on the development of zebrafish.

Excessive accumulation of Zn2+ or Ni2+ can cause various problems to aquatic animals. In this study, the developmental toxicity induced by individual or combined exposure of Zn2+ and Ni2+ to zebrafish embryos and larvae were evaluated to better understand the interaction between Zn2+ and Ni2+ . Both of individual and combined exposure of Zn2+ and Ni2+ could cause obvious developmental toxicity, which mainly occurred after hatching, at a concentration-dependent manner. The calculated 168-h LC50 were 2.79 mg/L for Zn2+ and 7.44 mg/L for Ni2+ . The interaction of Zn2+ and Ni2+ based on mortality was found to be an antagonism. Various malformations, including tail curving, spinal curvature, pericardial edema, and yolk sac edema, were observed with significant effects on body length and heartbeat rates after exposure of Zn2+ and Ni2+ . Meanwhile, some genes related to cardiovascular development and bone formation were mainly down-regulated by the individual and combined exposure of Zn2+ and Ni2+ . The individual exposure was more toxic than combined exposure because the interaction of Zn2+ and Ni2+ was determined to be an antagonism. The down-regulation of genes related to cardiovascular development and bone formation may contribute to the observed malformation and decreases of body length and heartbeat rates.

Male reproductive toxicity involved in spermatogenesis induced by perfluorooctane sulfonate and perfluorooctanoic acid in Caenorhabditis elegans.

As a persistent organic pollutant, perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) have gained increasing research attention over recent years because of their potential risk to humans and the environment. In this paper, we investigated the reproductive toxicity of these pollutants using a C. elegans model to evaluate spermatogenesis throughout the entire developmental cycle of him-5 mutant by exposing to 0.001, 0.01, and 0.1 mmol/L PFOS or PFOA for 48 h. Experimental results suggested that PFOS and PFOA exposure led to reductions in brood size, germ cell number, spermatid size, and motility, and increases in rate of malformation spermatids. Analysis of variance (ANOVA) showed that exposure to PFOS resulted in higher levels of damage than PFOA in germ cells only in 0.001 mmol/L exposure group. RT-qPCR was used to further investigate the expression of genes associated with different stages of spermatogenesis, such as mitosis and meiosis, fibrous body-membranous organelles (FB-MOs), and sperm activation. The expression levels of wee-1.3, spe-4, spe-6, and spe-17 genes were increased, while those of puf-8, spe-10, fer-1, swm-1, try-5, and spe-15 genes were decreased. Our results suggesting that PFOS or PFOA may cause spermatogenesis damage by disrupting the mitotic proliferation, meiotic entry, formation of the MOs, fusion of the MOs and plasma membrane (PM), and pseudopods. Loss-of-function studies using puf-8 and spe-10 mutants revealed spe-10 gene was specifically involved in PFOS- or PFOA-induced reproductive toxicity via regulating one or more critical palmitoylation events, while puf-8 gene was not direct target of PFOS and PFOA, and PFOS and PFOA may act on the upstream gene of puf-8, thus affecting reproductive ability. Taken together, these results demonstrate the potential adverse impact of PFOS and PFOA exposure on spermatogenesis and provide valuable data for PFC risk assessment. Grapical abstract.

Distribution, abundance, and risk assessment of selected antibiotics in a shallow freshwater body used for drinking water, China.

With rapid improvements in industrialization and urbanization, antibiotics are now extensively used to prevent and treat human and animal diseases and husbandry and aquaculture. Some research has been conducted to assess the environmental distribution and risk level of antibiotics, but their distribution remains largely uncharacterized. Thus, this study investigated the distribution and abundance of 39 antibiotics belonging to five groups, and their associated risks in surface water around Luoma Lake in the north of Jiangsu province, China. Nineteen antibiotics were detected, at a detection frequency (DF) ranging from 2.27% to 100%. The total antibiotics (ΣABs) concentrations ranged from 34.91 to 825.93 ng/L, with a median concentration of 195.45 ng/L. Among these antibiotics, chlortetracycline (DF: 100%; median: 172.02 ng/L) was the dominant antibiotic, accounting for a median percentage of 91.0% of ΣABs concentrations. Spearman rank correlation method found a significant correlation between clindamycin (DF: 72.7%; median: 2.01 ng/L) and lincomycin (DF: 79.5%; median: 4.58 ng/L). The ecological risk quotient (RQ) values for two out of 44 sampling sites were higher than 1, indicating a high risk; 11.4% of the RQ values fell between 0.1 and 1, indicating a medium risk. Moreover, roxithromycin was found to be the dominant contributor to the ecological risk, accounting for a median of 79.7% of ΣABs. However, the total non-carcinogenic (<6.54 × 10-4) and carcinogenic risks (<1.64 × 10-7) of ΣABs were negligible at the detected concentrations.

Developmental neurotoxicity of low concentrations of bisphenol A and S exposure in zebrafish.

The vulnerability to environmental insults is heightened at early stages of development. However, the neurotoxic potential of bisphenol A (BPA) and bisphenol S (BPS) at developmental windows remains unclear. To investigate the mechanisms mediating the developmental neurotoxicity, zebrafish embryos were treated with 0.01, 0.03, 0.01, 0.3, 1 µM BPA/BPS. Also, we used Tg(HuC:GFP) zebrafish to investigate whether BPA/BPS could induce neuron development. The reduction in body length, and increased heart rate were significant in 0.3 and 1 µM BPA/BPS groups. The green fluorescence protein (GFP) intensity increased at 72 hpf and 120 hpf in Tg(HuC:GFP) larvae which was consistent with the increased mRNA expression of elval3 following BPS treatments, an indication of the plausible effect of BPS on embryonic neuron development. Additionally, BPA/BPS treatments elicited hyperactivity and reduced static time in zebrafish larvae, suggesting behavioral alterations. Moreover, qRT-PCR results showed that BPA and BPS could interfere with the normal expression of development-related genes vegfa, wnt8a, and mstn1 at the developmental stages. The expression of neurodevelopment-related genes (ngn1, elavl3, gfap, α1-tubulin, mbp, and gap43) were significantly upregulated in BPA and BPS treatments, except for the remarkable downregulation of mbp and gfap elicited by BPA at 48 (0.03 µM) and 120 hpf (0.3 µM) respectively; ngn1 at 48 hpf for 0.1 µM BPS. Overall, our results highlighted that embryonic exposure to low concentrations of BPA/BPS could be deleterious to the central nervous system development and elicit behavioral abnormalities in zebrafish at developmental stages.

Serum Trace Elements in Patients With Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis.

Polycystic ovary syndrome (PCOS) is reported to be associated with certain trace elements. However, previous data are inconsistent and potentially biased due to small sample sizes. The potential utility of trace element levels for screening of PCOS remains to be established. The aim of this meta-analysis was to investigate the potential relationships between PCOS and serum levels of zinc (Zn), copper (Cu), magnesium (Mg), iron (Fe) and ferritin. We carried out a literature search of PubMed, EMBASE, and Web of Science for relevant cross-sectional/case-control studies published prior to October 2019. Random-effect models were used to estimate the overall standard mean differences (SMDs) between PCOS and healthy control subjects. The screening value of potential microelement biomarkers for PCOS was assessed using the receiver operating characteristic (ROC) curve. Twenty-one studies featuring 2,173 women with PCOS and 1,897 healthy women were selected for analysis. Our results showed that Cu and ferritin levels were significantly higher in women with PCOS than healthy controls, with SMDs of 0.52 [95% confidence interval (CI): 0.38-0.67, I2 = 47.6%] and 1.05 (95% CI: 0.25-1.86, I2 = 97.0%), respectively. The serum ferritin concentration was distinguished as a potential biomarker for PCOS based on the high area under ROC curve value of 0.71 (95% CI: 0.57-0.86). Although we did not identify a statistical association between serum Zn concentration and PCOS overall, the concentration of Zn in PCOS women with insulin resistance (IR) was lower than that in healthy women (SMD = -0.89, 95% CI: -1.73 to -0.06). Furthermore, the concentrations of Mg (SMD = 0.31, 95% CI: -0.32-0.94, I2 = 95.4%) and Fe (SMD = -0.59, 95% CI: -1.29-0.12, I2 = 97.2%) were not statistically significant between the PCOS and control groups. We generated hypothetical pathways for associations among serum Cu, ferritin and PCOS. The serum concentrations of both Cu and ferritin were significantly higher in women with PCOS, and ferritin was identified as a potential early indicator for PCOS screening. Further studies are essential to determine the specific underlying mechanisms.

Non-targeted metabolomic profiling of atrazine in Caenorhabditis elegans using UHPLC-QE Orbitrap/MS.

The widespread use of the herbicides Atrazine (ATR) has been raised attention due to its ubiquitous occurrence in the environment. As an endocrine disruptor, ATR causes reproductive, immune, nervous system toxicity in biota. In this study, we aimed to investigate metabolic profile characteristics and potential metabolic biomarker that reflects specific damage in toxic effect after ATR exposure. Hence, a metabolomics study was performed to determine the significantly affected metabolites and the reproduction and locomotion of C. elegans were investigated. Mediation analysis was used to evaluate the mediating effect of metabolites on association between ATR exposure and toxic effect. ATR (≥0.04 mg/L) caused the significant dose dependent reduction of brood size and locomotion behavior, however, the body length and width were significantly decreased only in 40 mg/L group. These results suggesting that brood size, head thrashes and body bends are more sensitive indictor to assessment ATR toxicity in C. elegans. Meanwhile, metabolomics analysis revealed that ATR exposure can induce metabolic profiles significant alterations in C. elegans. We found that 9 metabolites significantly increased and 18 metabolites significantly decreased, such as phosphatidylcholine, GMP, CDP-choline, neopterin etc. Those alteration of metabolites were mainly involved in the pathways: glycerophospholipid metabolism, glycolysis/gluconeogenesis, folate biosynthesis, glycine, serine and threoninemetabolism, pyrimidine and purine metabolism. Overall, these changes are signs of possible oxidative stress and ATP synthesis disruption modification. Mediation analysis showed a significant indirect effect of ATR exposure on brood size, via 7,8-dihydroneopterin 2',3'-cyclic-p, and phosphatidylcholine might mediate association between ATR exposure and body bends, suggesting that 7,8-dihydroneopterin 2',3'-cyclic-p and phosphatidylcholine might be potentially specificity marker for brood size and body bend respectively. This preliminary analysis investigates metabolic characteristics in C. elegans after ATR exposure, helping to understand the pathways involved in the response to ATR exposure and provide potential biomarkers for the safety evaluation of ATR.