Can exposure to Gymnodinium catenatum toxic blooms influence the impacts induced by Neodymium in Mytilus galloprovincialis mussels? What doesn't kill can make them stronger?

The presence in marine shellfish of toxins and pollutants like rare earth elements (REEs) poses a major threat to human well-being, coastal ecosystems, and marine life. Among the REEs, neodymium (Nd) stands out as a widely utilized element and is projected to be among the top five critical elements by 2025. Gymnodinum catenatum is a phytoplankton species commonly associated with the contamination of bivalves with paralytic shellfish toxins. This study evaluated the biological effects of Nd on the mussel species Mytilus galloprovincialis when exposed to G. catenatum cells for fourteen days, followed by a recovery period in uncontaminated seawater for another fourteen days. After co-exposure, mussels showed similar toxin accumulation in the Nd and G. catenatum treatment in comparison with the G. catenatum treatment alone. Increased metabolism and enzymatic defenses were observed in organisms exposed to G. catenatum cells, while Nd inhibited enzyme activity and caused cellular damage. Overall, this study revealed that the combined presence of G. catenatum cells and Nd, produced positive synergistic effects on M. galloprovincialis biochemical responses compared to G. catenatum alone, indicating that organisms' performance may be significantly modulated by the presence of multiple co-occurring stressors, such those related to chemical pollution and harmful algal blooms. ENVIRONMENTAL IMPLICATIONS: Neodymium (Nd) is widely used in green technologies like wind turbines, and this element's potential threats to aquatic environments are almost unknown, especially when co-occurring with other environmental factors such as blooms of toxic algae. This study revealed the cellular impacts induced by Nd in the bioindicator species Mytilus galloprovincialis but further demonstrated that the combination of both stressors can generate a positive defense response in mussels. The present findings also demonstrated that the impacts caused by Nd lasted even after a recovery period while a previous exposure to the toxins generated a faster biochemical improvement by the mussels.

Extension of a biotic ligand model for predicting the toxicity of neodymium to wheat: The effects of pH, Ca2+ and Mg2.

The damage excessive neodymium (Nd) causes to animals and plants should not be underestimated. However, there is little research on the impact of pH and associated ions on the toxicity of Nd. Here, a biotic ligand model (BLM) was expanded to predict the effects of pH and chief anions on the toxic impact of Nd on wheat root elongation in a simulated soil solution. The results suggested that Nd3+ and NdOH2+ were the major ions causing phytotoxicity to wheat roots at pH values of 4.5-7.0. The Nd toxicity decreased as the activities of H+, Ca2+, and Mg2+ increased but not when the activities of K+ and Na+ increased. The results indicated that H+, Ca2+, and Mg2+ competed with Nd for binding sites. An extended BLM was developed to consider the effects of pH, H+, Ca2+, and Mg2+, and the following stability constants were obtained: logKNdBL = 2.51, logKNdOHBL = 3.90, logKHBL = 4.01, logKCaBL = 2.43, and logKMgBL = 2.70. The results demonstrated that the BLM could predict the Nd toxicity well while considering the competition of H+, Ca2+, Mg2+ and the toxic species Nd3+ and NdOH2+ for binding sites.

Neodymium affects the generation of reactive oxygen species via GSK-3ß/Nrf2 signaling in the gill of zebrafish.

Rare earth element neodymium (Nd) is widely used in industry and agriculture, which may result in the pollution of aquatic environment. In this study, we exposed zebrafish with 10, 50, and 100 µg/L Nd for four weeks. The results showed that Nd could be accumulated in fish gill and Nd accumulation affected the equilibrium of nutrient elements. Nd decreased the antioxidant enzymes' activity and gene expression level, but enhanced the generation of reactive oxygen species (ROS). Moreover, various concentration of Nd treatments inhibited Nrf2 signaling in gill. To examine the critical role of GSK-3ß/Nrf2 signaling on ROS generation under Nd stress, we further interfered gsk-3ß gene in zebrafish under 100 µg/L Nd exposure. The result showed that gsk-3ß gene interference induced Nrf2 signaling as well as the expression and activity of antioxidant enzymes in fish gill. In all, Nd could be accumulated in fish gill, and the signaling of GSK-3ß/Nrf2 was involved in regulating ROS generation under Nd treatments.

Can temperature influence the impacts induced in Mytilus galloprovincialis by neodymium? Comparison between exposure and recovery periods.

Climate change-associated factors and pollutants, such as rare earth elements (REEs), have been identified as contributors to environmental changes. However, the toxicity resulting from the combination of these stressors has received little attention. Neodymium (Nd) is a REE that has been widely used, and this study aimed to evaluate the responses of Mytilus galloprovincialis to Nd exposure (10 µg/L), under actual (17 °C) and predicted warming conditions (21 °C), after fourteen days of exposure followed by fourteen days of recovery (without Nd), analyzing Nd accumulation, histopathological and biochemical alterations. The results showed that increased temperature and Nd exposure caused histopathological injuries in the gills. Contaminated mussels at 17 °C showed cellular damage, while at 21 °C, mussels were able to avoid cellular damage. After the recovery period, no improvements in gill's status were found and cellular damage was still present, highlighting the impacts caused by previous exposure to Nd.

The toxicity of neodymium and genome-scale genetic screen of neodymium-sensitive gene deletion mutations in the yeast Saccharomyces cerevisiae.

The wide usage of neodymium (Nd) in industry, agriculture, and medicine has made it become an emerging pollutant in the environment. Increasing Nd pollution has potential hazards to plants, animals, and microorganisms. Thus, it is necessary to study the toxicity of Nd and the mechanism of Nd transportation and detoxification in microorganisms. Through genome-scale screening, we identified 70 yeast monogene deletion mutations sensitive to Nd ions. These genes are mainly involved in metabolism, transcription, protein synthesis, cell cycle, DNA processing, protein folding, modification, and cell transport processes. Furthermore, the regulatory networks of Nd toxicity were identified by using the protein interaction group analysis. These networks are associated with various signal pathways, including calcium ion transport, phosphate pathways, vesicular transport, and cell autophagy. In addition, the content of Nd ions in yeast was detected by an inductively coupled plasma mass spectrometry, and most of these Nd-sensitive mutants showed an increased intracellular Nd content. In all, our results provide the basis for understanding the molecular mechanisms of detoxifying Nd ions in yeast cells, which will be useful for future studies on Nd-related issues in the environment, agriculture, and human health.

Identification of the function and regulatory network of circ_009773 in DNA damage induced by nanoparticles of neodymium oxide.

The health hazards of nanoparticles of neodymium oxide (NPs-Nd2O3) have aroused public concern in recent years. Exposure to NPs-Nd2O3 can change the level of reactive oxygen species (ROS) that cause DNA damage and alter whole transcriptome expression profiles for micro (mi)RNA, circular (circ)RNA, long noncoding (lnc)RNA, and mRNA. However, there have been no reports to our knowledge about the role of circRNAs in DNA damage caused by NPs-Nd2O3. In our study, we analyzed the circRNA expression profile of human bronchial epithelial cells(16HBE)exposed to 40 µg/ml NPs-Nd2O3. Our results indicated that exposure produced 1025 up-regulated and 890 down-regulated circRNAs. Real-time quantitative polymerase chain reaction (qRT-PCR) was applied to verify some of the significantly changed circRNAs and demonstrated that circ_009773 was apparently down-regulated. Through exploration of its host gene function, we found that circ_009773 may be related to DNA damage. Functional experiments found that circ_009773 regulated NPs-Nd2O3-induced DNA damage in 16HBE cells. A circ_009773-associated competing endogenous (ce)RNA network was constructed based on one differentially expressed (DE) circRNA, 74 DE miRNAs and 208 DE mRNAs. Module analysis identified hub genes related to DNA damage and repair and a protein-protein interaction (PPI) network was created.

[Effects of Nd(2)O(3) exposure of rare earth particles on C57 BL/6J male mice sex hormone secretion and CYP11A1/PLZF/STRA8 protein expression].

Objective: To explore the effects of Nd(2)O(3) exposure to rare earth particles on the secretion of sex hormones, cytochrome P450 family member 11A1 (CYP11A1) , spermatogenesis markers promyelocytic leukemia zinc finger protein (PLZF) and retinoic acid stimulating gene 8 (STRA8) protein in C57 BL/6J male mice. Methods: In March 2021, Forty-eight male C57 BL/6J mice aged 6-8 weeks divided into control group and Nd(2)O(3) exposure low, medium and high dose groups (exposing doses of 62.5, 125.0, 250.0 mg/ml Nd(2)O(3)) , 12 per group. The mice in the Nd(2)O(3) groups were perfused with different doses of Nd(2)O(3) suspension by a one-time non-exposing tracheal instillation method, and the control group was perfused with an equal volume of normal saline, with a volume of 0.1 ml, to establish a mouse reproductive function injury model. After 28 days of exposure, the mice's body weight, testes and epididymis were weighed, and the organ coefficients were calculated; the two epididymis were taken to make a sperm suspension to determine the sperm count, survival rate, and deformity rate; inductively coupled plasma mass spectrometry (ICP-MS) method was used to detect the content of Nd in mouse testis tissue; HE staining was used to detect testicular tissue pathological changes and quantitative analysis; enzyme-linked immunosorbent assay (ELISA) method was used to detect serum luteinizing hormone (LH) and follicle stimulating hormone (FSH) and testosterone (T) content; western blot was used to detect the protein levels of CYP11A1, PLZF and STRA8 in testicular tissues. Results: Compared with the control group, with the increase of the exposure dose, the Nd content in the testis of the mice showed an increasing trend, the sperm survival rate and LH showed a decreasing trend, and the sperm deformity rate showed an increasing trend (P<0.05) ; Pathological showed that the number of sperm in the seminiferous tubules of the testicular tissue in the Nd(2)O(3) medium and high dose groups was significantly reduced, and the germinal epithelial disintegration, intraepithelial vacuolization, and exfoliation of spermatogenic cells and supporting cells occurred; The height of germinal epithelium was significantly reduced, and the percentage of damaged seminiferous tubules showed an increasing trend (P<0.05) ; FSH and T levels in serum in the middle and high dose groups of Nd(2)O(3), and CYP11A1, PLZF and STRA8 proteins in testicular tissues showed a downward trend with increasing dose (P<0.05) . Conclusion: The rare earth particulate Nd(2)O(3) may interfere with the expression of CYP11A1, PLZF and STRA8 protein, thereby causing the disorder of sex hormone secretion in the body, the maintenance of spermatogonia and the obstruction of the process of meiosis, causing reproductive function damage.

Effect of the dose on the toxicokinetics of a quaternary mixture of rare earth elements administered to rats.

Large human biomonitoring studies are starting to assess exposure to rare earth elements (REEs). Yet, there is a paucity of data on the toxicokinetics of these substances to help interpret biomonitoring data. The objective of the study was to document the effect of the administered dose on the toxicokinetics of REEs. Male Sprague-Dawley rats were injected intravenously with 0.3, 1 or 10 mg/kg body weight (bw) of praseodynium chloride (PrCl3), cerium chloride (CeCl3), neodymium chloride (NdCl3) and yttrium chloride (YCl3) administered together as a mixture. Serial blood samples were withdrawn up to 72 h following injection, and urine and feces were collected at predefined time intervals up to 7 days post-dosing. The REEs were measured by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). For a given REE dose, the time courses in blood, urine and feces were similar for all four REEs. However, the REE dose administered significantly impacted their kinetics, as lower cumulative excretion in urine and feces was associated with higher REE doses. The fraction of REE remaining in rat tissues at the terminal necropsy on post-dosing day 7 also increased with the dose administered, most notably in the lungs and spleen at the 10 mg/kg bw dose. The toxicokinetic parameters calculated from the blood concentration-time profiles further showed significant increases in the mean residence time (MRTIV) for all four REEs at the 10 mg/kg bw dose. The shift in the REE kinetics at high dose may be explained by a higher retention in lysosomes, the main organelle responsible for accumulation of these REEs in different tissues.

LncRNA loc105377478 promotes NPs-Nd2O3-induced inflammation in human bronchial epithelial cells through the ADIPOR1/NF-κB axis.

With the wide application of neodymium oxide nanoparticles (NPs-Nd2O3) in various fields, their health hazards have aroused public concern in recent years. However, data regarding the cytotoxicity of NPs-Nd2O3 is limited. In this study, we investigated the function and mechanism of long-chain non-coding RNAs (lncRNAs) in NPs-Nd2O3-induced airway inflammation. Treatment with NPs-Nd2O3 induced an inflammatory response in human bronchial epithelial cells (16HBE) by upregulating the expression of interleukin-6 (IL-6) and interleukin-8 (IL-8). The levels of LDH and intracellular ROS in the cells treated by various doses of NPs-Nd2O3 also increased significantly. After treatment with 10 µg/ml NPs-Nd2O3, RNA microarray and real-time quantitative polymerase chain reaction (qRT-PCR) showed a significant upregulation of lncRNA loc105377478. Functional experiments suggested lncRNA loc105377478 enhanced the expression of IL-6, IL-8 and ROS in NPs-Nd2O3-treated 16HBE cells, and it was further demonstrated that lncRNA loc105377478 promoted the activation of NF-κB by negatively regulating ADIPOR1 expression. Moreover, the expression of IL-6 and IL-8 in NPs-Nd2O3-treated 16HBE cells was regulated by lncRNA loc105377478, which was mediated by the NF-κB signaling pathway. In conclusion, lncRNA loc105377478 promotes NF-κB activation by negatively regulating ADIPOR1 expression, thereby upregulating the expression of IL-6 and IL-8 in 16HBE cells treated with NPs-Nd2O3.

Nd2O3 Nanoparticles Induce Toxicity and Cardiac/Cerebrovascular Abnormality in Zebrafish Embryos via the Apoptosis Pathway.

INTRODUCTION: Rare-earth nanoparticles in the environment and human body pose a potential threat to human health. Although toxic effects of rare-earth nanoparticles have been extensively studied, the effects on the early development are not well understood. In this study, we attempted to explain the toxic effects of neodymium oxide (Nd2O3) nanoparticles on early development. METHODS: We added the Nd2O3 nanoparticles at different concentrations and recorded the mortality and malformation rate per 24 hrs under a microscope. The live embryos treated with Nd2O3 nanoparticles were imaged as movies and Z step lapses with a confocal microscope, and heart rates were counted for 30 s to measure the cardiac function. The live Tg (Flk1:EGFP) transgenic embryos exposed to Nd2O3 nanoparticles were observed under confocal microscope to measure the cerebrovascular development. Subsequently, we extracted the total protein for Western blot at 5 days post-fertilisation (dpf). Embryos were collected to undergo TUNEL staining for apoptosis detection. RESULTS: Nd2O3 nanoparticles disturbed embryo development at high concentrations (>200 µg/mL). The mortality and malformation rate gradually increased in a dose-dependent manner by morphological observation, while the Nd2O3 median lethal concentration (LD50) was 203.4 µg/mL at 120 hrs post-fertilisation (hpf). Furthermore, the Nd2O3-treated embryos showed severe arrhythmia and reduced heart rate. We also observed the markedly cerebrovascular disappearance at middle concentration (100 and 200 µg/mL). The downregulated autophagy flux in brain blood vessels and increased apoptosis level in neurons might affect vessels sprouting and contribute to the vanished cerebrovascular. CONCLUSION: The results suggested that the embryos exposed to Nd2O3 activated the apoptosis pathway and induced toxicity and abnormal cardiac/cerebrovascular development.

Toxicological effects of the rare earth element neodymium in Mytilus galloprovincialis.

The wide range of applications of rare earth elements (REE) is leading to their occurrence in worldwide aquatic environments. Among the most popular REE is Neodymium (Nd), being widely used in permanent magnets, lasers, and glass additives. Neodymium-iron-boron (NdFeB) magnets is the main application of Nd since they are used in electric motors, hard disk drives, speakers and generators for wind turbines. Recent studies have already evaluated the toxic potential of different REE, but no information is available on the effects of Nd towards marine bivalves. Thus, the present study evaluated the biochemical alterations caused by Nd in the mussel Mytilus galloprovincialis exposed to this element for 28 days. The results obtained clearly demonstrated that Nd was accumulated by mussels, leading to mussel's metabolic capacity increase and GLY expenditure, in an attempt to fuel up defense mechanisms. Antioxidant and biotransformation defenses were insufficient in the elimination of ROS excess, resulting from the presence of Nd and increased electron transport system activity, which caused cellular damages (measured by lipid peroxidation) and loss of redox balance (assessed by the ratio between reduced and oxidized glutathione). The results obtained clearly highlight the potential toxicity of REEs and, in particular of Nd, with impacts at cellular level, which may have consequences in mussel's survival, growth and reproduction, affecting mussel's population.

The bioeffects of degradable products derived from a biodegradable Mg-based alloy in macrophages via heterophagy.

Biodegradable magnesium alloys are promising candidates for use in biomedical applications. However, degradable particles (DPs) derived from Mg-based alloys have been observed in tissue in proximity to sites of implantation, which might result in unexpected effects. Although previous in vitro studies have found that macrophages can take up DPs, little is known about the potential phagocytic pathway and the mechanism that processes DPs in cells. Additionally, it is necessary to estimate the potential bioeffects of DPs on macrophages. Thus, in this study, DPs were generated from a Mg-2.1Nd-0.2Zn-0.5Zr alloy (JDBM) by an electrochemical method, and then macrophages were incubated with the DPs to reveal the potential impact. The results showed that the cell viability of macrophages decreased in a concentration-dependent manner in the presence of DPs due to effects of an apoptotic pathway. However, the DPs were phagocytosed into the cytoplasm of macrophages and further degraded in phagolysosomes, which comprised lysosomes and phagosomes, by heterophagy instead of autophagy. Furthermore, several pro-inflammatory cytokines in macrophages were upregulated by DPs through the induction of reactive oxygen species (ROS) production. To the best of our knowledge, this is the first study to show that DPs derived from a Mg-based alloy are consistently degraded in phagolysosomes after phagocytosis by macrophages via heterophagy, which results in an inflammatory response owing to ROS overproduction. Thus, our research has increased the knowledge of the metabolism of biodegradable Mg metal, which will contribute to an understanding of the health effects of biodegradable magnesium metal implants used for tissue repair. STATEMENT OF SIGNIFICANCE: Biomedical degradable Mg-based alloys have great promise in applied medicine. Although previous studies have found that macrophages can uptake degradable particles (DPs) in vitro and observed in the sites of implantation in vivoin vivo, few studies have been carried out on the potential bioeffects relationship between DPs and macrophages. In this study, we analyzed the bioeffects of DPs derived from a Mg-based alloy on the macrophages. We illustrated that the DPs were size-dependently engulfed by macrophages via heterophagy and further degraded in the phagolysosome rather than autophagosome. Furthermore, DPs were able to induce a slight inflammatory response in macrophages by inducing ROS production. Thus, our research enhances the knowledge of the interaction between DPs of Mg-based alloy and cells, and offers a new perspective regarding the use of biodegradable alloys.

Synthesis and characterization of newly synthesized neodymium zirconate zinc sulfide nanocomposite and its effect on selected aspects of albino mice behavior.

Present study was conducted to report the effect of variable doses of neodymium zirconate zinc sulfide nanocomposite on behavior of albino mice of both sexes. Five-week-old albino mice (C57BL/6 strain) of both sexes were orally treated either with 10 mg (low dose) or 20 mg/ml saline/kg body weight (high dose) of neodymium zirconate zinc sulfide nanocomposite for 11 days. An untreated control group was maintained in parallel for same duration that received saline solution orally. A series of neurological (rotarod, light and dark box, open field, and novel object recognition) tests were conducted in all treatments. Oral supplementation of both low and high dose of nanocomposite significantly reduced the rotarod test performance as well as stretch attend reflex in male mice during light dark box test. Male mice treated with high dose of neodymium zirconate zinc sulfide nanocomposite had significantly increased time mobile and decreased time immobile than control group during open field test. Female mice treated with 10 mg/ml saline/kg body weight of neodymium zirconate zinc sulfide nanocomposite had significantly more line crossing during trial 1, and they spend more time with object A during trial 2 of novel object recognition test than their saline-treated control group. Change in body weight remained unaffected when compared between nanocomposite treated and untreated albino mice. In conclusion, we are reporting that both the applied doses of neodymium zirconate zinc sulfide nanocomposite are drastically affecting the muscular activity and exploratory behavior in male albino mice, while the studied behavioral tests, in general, remained unaffected in female albino mice.

Circular RNA 0039411 Is Involved in Neodymium Oxide-induced Inflammation and Antiproliferation in a Human Bronchial Epithelial Cell Line via Sponging miR-93-5p.

Adverse health effects induced by neodymium oxide (Nd2O3) particles have raised concern as a result of their increasing applications in various arenas. However, information on their potential cytotoxicity is currently limited. In the present study, we investigated the underlying cytotoxicity of Nd2O3 in human bronchial epithelial cells (16HBE) and the potential mechanisms mediated by circular RNAs (circRNAs). Nd2O3 exposure initiated an inflammatory response in 16HBE cells via the release of the proinflammatory cytokines interleukin (IL)-6 and IL-8. The 5-ethynyl-2'-deoxyuridine assays showed that Nd2O3 treatment inhibited 16HBE cell proliferation and caused cell cycle arrest at G0/G1 phase and cell apoptosis. Microarray analyses demonstrated that Nd2O3 treatment altered circRNA expression profiles and significantly upregulated circRNA 0039411 (circ_0039411) in 16HBE cells. Further functional studies showed that silencing circ_0039411 prevented Nd2O3-induced inflammation and reversed its antiproliferative effect by moderating the G0/G1 phase cell cycle arrest, whereas overexpression of circ_0039411 had the opposite effects. Luciferase reporter assays showed that circ_0039411 bound to miR-93-5p, whereas fluorescence in situ hybridization showed that circ_0039411 and miR-93-5p colocalized in the cytoplasm. Moreover, transfection of 16HBE cells with a miR-93-5p mimic decreased the phosphorylation of signal transducer and activator of transcription 3 (STAT3). The levels of phospho-STAT3 were decreased by circ_0039411 silencing and elevated after circ_0039411 overexpression. These results suggested that upregulation of circ_0039411 mediated Nd2O3-induced inflammation and dysfunction by sponging miR-93-5p.

Time course of cytochrome oxidase blob plasticity in the primary visual cortex of adult monkeys after retinal laser lesions.

We studied the time course of changes of cytochrome oxidase (CytOx) blob spatial density and blob cross-sectional area of deprived (D) and nondeprived (ND) portions of V1 in four capuchin monkeys after massive and restricted retinal laser lesions. Laser shots at the border of the optic disc produced massive retinal lesions, while low power laser shots in the retina produced restricted retinal lesions. These massive and restricted retinal lesions were intended to simulate glaucoma and diabetic retinopathy, respectively. We used a Neodymium-YAG dual frequency laser to make the lesions. We measured Layer III blobs in CytOx-reacted tangential sections of flat-mounted preparations of V1. The plasticity of the blob system and that of the ocular dominance columns (ODC) varied with the degree of retinal lesions. We found that changes in the blob system were different from that of the ODC. Blob sizes changed drastically in the region corresponding to the retinal lesion. Blobs were larger and subjectively darker above and below the non deprived ODC than in the deprived columns. With restricted lesions, blobs corresponding to the ND columns had sizes similar to those from non-lesioned areas. In contrast, blobs corresponding to the deprived columns were smaller than those from nonlesioned areas. With massive lesions, ND blobs were larger than the deprived blobs. Plastic changes in blobs described here occur much earlier than previously described.

Behavioral deficits and neural damage of Caenorhabditis elegans induced by three rare earth elements.

Rare earth elements (REEs) are widely used in industry, agriculture, medicine and daily life in recent years. However, environmental and health risks of REEs are still poorly understood. In this study, neurotoxicity of trichloride neodymium, praseodymium and scandium were evaluated using nematode Caenorhabditis elegans as the assay system. Median lethal concentrations (48 h) were 99.9, 157.2 and 106.4 mg/L for NdCl3, PrCl3 and ScCl3, respectively. Sublethal dose (10-30 mg/L) of these trichloride salts significantly inhibited body length of nematodes. Three REEs resulted in significant declines in locomotor frequency of body bending, head thrashing and pharyngeal pumping. In addition, mean speed and wavelength of crawling movement were significantly reduced after chronic exposure. Using transgenic nematodes, we found NdCl3, PrCl3 and ScCl3 resulted in loss of dendrite and soma of neurons, and induced down-expression of dat-1::GFP and unc-47::GFP. It indicates that REEs can lead to damage of dopaminergic and GABAergic neurons. Our data suggest that exposure to REEs may cause neurotoxicity of inducing behavioral deficits and neural damage. These findings provide useful information for understanding health risk of REE materials.

Neodymium Oxide Induces Cytotoxicity and Activates NF-κB and Caspase-3 in NR8383 Cells.

We investigated whether Nd2O3 treatment results in cytotoxicity and other underlying effects in rat NR8383 alveolar macrophages. Cell viability assessed by the MTT assay revealed that Nd2O3 was toxic in a dose-dependent manner, but not in a time-dependent manner. An ELISA analysis indicated that exposure to Nd2O3 caused cell damage and enhanced synthesis and release of inflammatory chemokines. A Western blot analysis showed that protein expression levels of caspase-3, nuclear factor-κB (NF-κB) and its inhibitor IκB increased significantly in response to Nd2O3 treatment. Both NF-κB and caspase-3 signaling were activated, suggesting that both pathways are involved in Nd2O3 cytotoxicity.

Tannic acid alleviates bulk and nanoparticle Nd2O3 toxicity in pumpkin: a physiological and molecular response.

The effect of dissolved organic matter (DOM) on nanoparticle toxicity to plants is poorly understood. In this study, tannic acid (TA) was selected as a DOM surrogate to explore the mechanisms of neodymium oxide NPs (Nd2O3 NPs) phytotoxicity to pumpkin (Cucurbita maxima). The results from the tested concentrations showed that 100 mg L(-1) Nd2O3 NPs were significantly toxic to pumpkin in term of fresh biomass, and the similar results from the bulk particles and the ionic treatments were also evident. Exposure to 100 mg L(-1) of Nd2O3 NPs and BPs in 1/5 strength Hoagland's solution not only significantly inhibited pumpkin growth, but also decreased the S, Ca, K and Mg levels in plant tissues. However, 60 mg L(-1) TA significantly moderated the observed phytotoxicity, decreased Nd accumulation in the roots, and notably restored S, Ca, K and Mg levels in NPs and BPs treated pumpkin. TA at 60 mg L(-1) increased superoxide dismutase (SOD) activity in both roots (17.5%) and leaves (42.9%), and catalase (CAT) activity (243.1%) in the roots exposed to Nd2O3 NPs. This finding was confirmed by the observed up-regulation of transcript levels of SOD and CAT in Nd2O3 NPs treated pumpkin analyzed by quantitative reverse transcription polymerase chain reaction. These results suggest that TA alleviates Nd2O3 BPs/NPs toxicity through alteration of the particle surface charge, thus reducing the contact and uptake of NPs by pumpkin. In addition, TA promotes antioxidant enzymatic activity by elevating the transcript levels of genes involved in ROS scavenging. Our results shed light on the mechanisms underlying the influence of DOM on the bioavailability and toxicity of NPs to terrestrial plants.

Properties of nanoparticles prepared from NdFeB-based compound for magnetic hyperthermia application.

Nanoparticles were prepared from a NdFeB-based alloy using the hydrogen decrepitation process together with high-energy ball milling and tested as heating agent for magnetic hyperthermia. In the milling time range evaluated (up to 10 h), the magnetic moment per mass at H = 1.59 MA m(-1) is superior than 70 A m(2) kg(-1); however, the intrinsic coercivity might be inferior than 20 kA m(-1). The material presents both ferromagnetic and superparamagnetic particles constituted by a mixture of phases due to the incomplete disproportionation reaction of Nd(2)Fe(14)BH(x) during milling. Solutions prepared with deionized water and magnetic particles exposed to an AC magnetic field (H(max) ~ 3.7 kA m(-1) and f = 228 kHz) exhibited 26 K ≤ ΔT(max) ≤ 44 K with a maximum estimated specific absorption rate (SAR) of 225 W kg(-1). For the pure magnetic material milled for the longest period of time (10 h), the SAR was estimated as ~2500 W kg(-1). In vitro tests indicated that the powders have acceptable cytotoxicity over a wide range of concentration (0.1-100 µg ml(-1)) due to the coating applied during milling.

Effects of lanthanum, cerium, and neodymium on the nuclei and mitochondria of hepatocytes: accumulation and oxidative damage.

The aim of this study was to investigate the contents of lanthanum (La), cerium (Ce), and neodymium (Nd) that accumulate in nuclei and mitochondria isolated from the liver and their corresponding potential oxidative damage effects on nuclei and mitochondria. Five-week-old male imprinting control region (ICR) mice were exposed to chlorides of La, Ce, or Nd by oral gavage with one of three doses: 10, 20, or 40 mg/kgBW/day for 6 weeks. The concentrations of administered elements in hepatocyte nuclei and mitochondria were determined with inductively coupled plasma-mass (ICP-MS) spectrometry. The accumulation of La, Ce, and Nd in hepatocyte nuclei and mitochondria gradually increased in a dose-dependent manner with exposure to the elements, although the concentrations of La, Ce, and Nd in hepatocyte mitochondria were lower than those in their counterpart nuclei. In hepatocyte nuclei, superoxide dismutase (SOD) and catalase (CAT) activities decreased, whereas glutathione peroxidase (GPx) activity, glutathione (GSH) and malondialdehyde (MDA) levels increased. In hepatocyte mitochondria, SOD, CAT, and GPx activities and GSH levels were significantly decreased, and MDA levels were significantly increased. These results suggest that La, Ce, and Nd presumably enter hepatocytes and mainly accumulate in the nuclei and induce oxidative damage in hepatic nuclei and mitochondria.