AgNP Exposure Research Articles

A new test system for unraveling the effects of soil components on the uptake and toxicity of silver nanoparticles (NM-300K) in simulated pore water

Fate, bioavailability and toxicity of silver nanoparticles (AgNP) are largely affected by soil properties. Here we focused on how these processes are connected in simulated soil pore water. OECD soil components (sand, kaolin clay, peat) were covered with NM-300K-, AgNO3- and NM-300K dispersant-contaminated water, and Folsomia candida were exposed on the water surface. After 14 days the majority of AgNP was in nano form in sand pore water where also silver uptake was highest. Multilayered cross sections from X-ray micrographs of Collembola exposed to AgNP showed that silver was located in animal areas of direct contact to the contaminated pore water and was ingested. In contrast, in simulated peat pore water only a small fraction of silver was bioavailable. AgNO3 was only bioavailable at the start of the test and not anymore at test end. AgNP and AgNO3 caused immobilization in sand and kaolin pore water while no toxicity was found with peat and OECD soil. A strong correlation (correlation coefficient = 0.901) existed between the concentration of nano silver and immobilization; for ionic silver this was not the case. The dispersant of AgNP was toxic on its own in sand and kaolin pore water. As there are analytical limitations of quantifying AgNP in complex matrices this test system enables a mechanistic view of exposure and uptake of AgNP (and other substances) by F. candida from soil pore water.

Effects of Silver Nanoparticle Exposure to the Testicular Antioxidant System during the Prepubertal Rat Stage.

Humans and environments are constantly exposed to a wide range of commercial products containing silver nanoparticles (AgNPs) in their composition. The hypothalamic-pituitary-testicular (HP-testicular) axis is sensitive to low doses of AgNPs with repercussions in sperm functionality. The oxidative stress may be related to the pathogenesis of sperm alterations because Ag+ ions are released from AgNPs in the corporal fluids. This study aimed to investigate the effects of AgNP exposure in the antioxidant defense system. For this, the transcript expression and the activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione reductase (GSR) enzymes were evaluated in the testis of rats exposed during the prepubertal period to increasing doses of AgNPs (1.875, 3.75, 7.5, or 15 μg of AgNPs/kg). The higher dose of AgNPs (15 μg/kg) investigated promoted increases in the activity of CAT, GPX, and GSR enzymes and in the expression of Gpx4 var1 transcript. The exposure to 7.5 μg/kg of AgNP increased the Gpx4 var1 mRNA expression. In the group that received 3.75 μg of AgNP/kg, the expression of Sod1, Gpx4 var2, and Gsr transcripts was decreased while the Gpx4 var1 mRNA expression was augmented. The lower dose of AgNPs tested (1.875 μg/kg) increased the expression of Cat and Gpx4 var1 transcripts. Thus, AgNP alters the expression and activity of the antioxidant enzymes in a nonmonotonic dose-response curve and directly or indirectly modulates the events related to spermatogenesis process.

Alteration in MAPK/ERK and Akt signaling following exposure to sublethal silver nanoparticles in cultured adult neural stem cells

Silver nanoparticles (AgNPs), an emerging environmental contaminant, have been developed as antimicrobials, biosensors, and for other applications in products ranging from medical devices to consumer goods including toothpaste, socks, and appliances. AgNPs, particularly in consumer goods, can be shed off during use and ingested or inhaled, leading to bioaccumulation in tissues including brain. While they are effectively used for their antimicrobial properties, they also have negative effects on mammalian cells, even at low concentrations of 1µg/mL. We previously found that low-level AgNPs disrupt cytoskeletal function, leading to formation of f-actin inclusions and disrupting neurite dynamics. These effects are partially mediated by interaction with the β-catenin intracellular signaling pathway. Here, we investigate interactions of AgNPs with two other intracellular signaling pathways, MAPK/ERK and Akt, both of which are involved in regulation of neuronal cell differentiation. Specific pharmacological inhibitors of these pathways, in combination with AgNPs, are applied to cultured adult neural stem cells that provide a model for brain cells. Fluorescent labeling and time-lapse microscopy are used to assess disruption of f-actin dynamics and changes in neurite extension. Preliminary data indicate that AgNPs may inhibit both the MAPK/ERK and the Akt intracellular signaling pathways, and thereby induce formation of f-actin inclusions and disrupt neurite dynamics during differentiation. This work will help us to understand chronic effects of low-level AgNP exposure from consumer goods on brain cell function. Our work in neural stem cells is especially applicable to children, whose brains are still developing and therefore depend on neural stem cell function. This material is based upon work supported by NSF Award# 1553667.

Impact of silver nanoparticles (AgNP) on soil microbial community depending on functionalization, concentration, exposure time, and soil texture

BackgroundIncreasing exposure to engineered inorganic nanoparticles takes actually place in both terrestric and aquatic ecosystems worldwide. Although we already know harmful effects of AgNP on the soil bacterial community, information about the impact of the factors functionalization, concentration, exposure time, and soil texture on the AgNP effect expression are still rare. Hence, in this study, three soils of different grain size were exposed for up to 90 days to bare and functionalized AgNP in concentrations ranging from 0.01 to 1.00 mg/kg soil dry weight. Effects on soil microbial community were quantified by various biological parameters, including 16S rRNA gene, photometric, and fluorescence analyses.ResultsMultivariate data analysis revealed significant effects of AgNP exposure for all factors and factor combinations investigated. Analysis of individual factors (silver species, concentration, exposure time, soil texture) in the unifactorial ANOVA explained the largest part of the variance compared to the error variance. In depth analysis of factor combinations revealed even better explanation of variance. For the biological parameters assessed in this study, the matching of soil texture and silver species, and the matching of soil texture and exposure time were the two most relevant factor combinations. The factor AgNP concentration contributed to a lower extent to the effect expression compared to silver species, exposure time and physico–chemical composition of soil.ConclusionsThe factors functionalization, concentration, exposure time, and soil texture significantly impacted the effect expression of AgNP on the soil microbial community. Especially long-term exposure scenarios are strongly needed for the reliable environmental impact assessment of AgNP exposure in various soil types.

Changes in protein expression in mussels Mytilus galloprovincialis dietarily exposed to PVP/PEI coated silver nanoparticles at different seasons

Potential toxic effects of Ag NPs ingested through the food web and depending on the season have not been addressed in marine bivalves. This work aimed to assess differences in protein expression in the digestive gland of female mussels after dietary exposure to Ag NPs in autumn and spring. Mussels were fed daily with microalgae previously exposed for 24 h to 10 μg/L of PVP/PEI coated 5 nm Ag NPs. After 21 days, mussels significantly accumulated Ag in both seasons and Ag NPs were found within digestive gland cells and gills. Two-dimensional electrophoresis distinguished 104 differentially expressed protein spots in autumn and 142 in spring. Among them, chitinase like protein-3, partial and glyceraldehyde-3-phosphate dehydrogenase, that are involved in amino sugar and nucleotide sugar metabolism, carbon metabolism, glycolysis/gluconeogenesis and the biosynthesis of amino acids KEGG pathways, were overexpressed in autumn but underexpressed in spring. In autumn, pyruvate metabolism, citrate cycle, cysteine and methionine metabolism and glyoxylate and dicarboxylate metabolism were altered, while in spring, proteins related to the formation of phagosomes and hydrogen peroxide metabolism were differentially expressed. Overall, protein expression signatures depended on season and Ag NPs exposure, suggesting that season significantly influences responses of mussels to NP exposure.

Silver nanoparticles induce protective autophagy via Ca2+/CaMKKβ/AMPK/mTOR pathway in SH-SY5Y cells and rat brains

Silver nanoparticles (AgNPs) are widely used for manufacturing products containing antibacterial agents, as well as food technologies such as edible films and food packaging. Routes of AgNPs exposure are principally derived by contacting with certain medical sprays, food, toothpaste, and purification products. Previously, we showed that AgNPs induce endoplasmic reticulum (ER) stress and promote apoptosis progression in SH-SY5Y cells; however, whether AgNP-induced ER stress is able to trigger autophagy in vivo and in vitro, and the role of autophagy in AgNP-induced cytotoxicity remain unclear. In the present study, we found that increased intracellular calcium (Ca2+) levels arising from AgNP-induced-ER stress resulted in activation of calmodulin-dependent protein kinase kinase β (CaMKKβ) and adenosine 5′-monophosphate-activated protein kinase (AMPK), which downregulated the level of mammalian target of rapamycin (mTOR) and upregulated Beclin-1 to activate autophagy in SH-SY5Y cells. Specifically, inhibition of autophagy by the addition of chloroquine (CQ) or silencing of Beclin-1 significantly enhanced the cytotoxicity of AgNPs, suggesting that autophagy plays a protective role in AgNP-induced cell apoptosis. Furthermore, we showed that oral administration of AgNPs for 28 continuous days induced ER stress-mediated apoptosis and autophagy in rats via activation of CaMKKβ and AMPK. In summary, this study is the first to report that AgNPs induce protective autophagy via a Ca2+/CaMKKβ/AMPK/mTOR pathway in vivo and in vitro. Therefore, public exposure to AgNPs should arouse concerns regarding environmental safety and human health.HighlightSilver nanoparticle-induced ER stress elicits protective autophagy via a Ca2+-dependent mechanism in SH-SY5Y cells.The Ca2+/CaMKKβ/AMPK/mTOR pathway is involved in autophagy.Orally administered silver nanoparticles induce ER stress-mediated autophagy and apoptosis in rats.

Discovery of CRR1-targeted copper deficiency response in Chlamydomonas reinhardtii exposed to silver nanoparticles

The molecular mechanisms behind the adaptive responses for interactions between organisms and nanoparticles, such as silver nanoparticles (AgNPs), are of great concern. In this study, the transcriptome of freshwater alga Chlamydomonas reinhardtii was characterized via RNA sequencing (RNA-seq) after exposure to a nontoxic concentration of AgNPs (0.5 mg/L). The cytochrome c6 (CYC6) and ferredoxin-5 (FDX5) genes were identified with the greatest increase in expression level, which were indications of the copper deficiency in the algae. Gene set enrichment analysis also showed significant enrichment of copper deficiency responsive genes in the transcriptome of algae exposed to AgNPs. These results indicated that AgNPs induced a copper deficiency response in algae, and the excessive intracellular copper content suggested this was due to functional copper deficiency. This deficiency response was further validated to be regulated by transcription factor CRR1 (copper response regulator 1) according to the assays on the mutant strain with defect of CRR1. To the best of our knowledge, this is the first corroboration of a CRR1-targeted copper deficiency response in algae following AgNP exposure. Given the function of copper in fundamental metabolic pathways, such as photosynthesis and respiration, we propose a potential role of CRR1-targeted copper deficiency as an adaptation of algae after exposure to AgNPs.

Effect of silver nanoparticle contaminated biosolids on the soil microbial community

This study investigated the effects of AgNPs on soil microbial communities when biosolids, containing AgNPs, were amended into soil. A field-collected sandy loam soil was amended with biosolids containing aged, PVP-coated AgNPs at measured concentrations of 3, 48, 123, 290 and 706 mg Ag kg−1 of soil (dry weight). The control treatment consisted of soil without AgNPs (Con-0) but amended with biosolids. An additional treatment of Ag+ (AgNO3) at 138 mg Ag kg−1 was included as appropriate. The AgNPs were aged in biosolids for 72 h before being spiked into soil. The impact of aged-AgNPs on the in-situ soil microbial community was assessed using a suite of microbial tests that assessed the effects on microbial growth, biomass, activity and diversity. The extractable Ag+ in AgNPs spiked soils increased with increasing AgNP concentrations and ranged from <0.1 to 3.38 mg Ag+ kg−1 soil. The extractable Ag+ in the AgNO3 treatment (i.e., 138 mg Ag kg−1) was 5 times lower than the comparable AgNP treatment (i.e., 123 mg Ag kg−1). A significant impact of AgNPs on the soil microbial community was observed with median inhibitory concentrations (IC50) ranging from 11 to >706 mg Ag kg−1. AgNP treatments showed a 10–64% reduction in microbial activities than the AgNO3 treatment at a similar total Ag concentration. The toxicity of AgNPs were more pronounced overtime, suggesting that Ag+ continued to be released from biosolid-aged AgNPs in the soil environment and likely contributed to the observed toxicity. Emergence of a silver tolerant bacterium (Rhodanobacter sp.) was observed in soils with low to moderately high AgNP concentrations (48 to 290 mg Ag kg−1). Our results suggest that AgNP exposure in soil amended with biosolids may have significant inhibitory effects on the soil microbial community despite their potential sulfidation in biosolid-amended soils.

Evaluation of neuroglobin and cytoglobin expression in adult rats exposed to silver nanoparticles during prepubescence.

Silver nanoparticles (AgNPs) are clusters of silver atoms with diameters that range from 1 to 100nm. Due to the various shapes and large surface areas, AgNPs have been employed in the food and textile industries and medical fields. Therefore, because of the widespread use of these compounds, the aim of this study was to evaluate the effect of AgNP exposure on the gene and protein expression levels of Neuroglobin (Ngb) and Cytoglobin (Cygb), in the rat cortex, hippocampus and cerebellum. Post-natal day (PND) 21 male Wistar rats were randomly divided into three groups. One group received 15μg/kg body weight of AgNP by gavage another group received 30μg/kg and the control group that received saline, from PND23 to PND58. On PND102 the animals were euthanized and the cortex, hippocampus and cerebellum were isolated and evaluated for gene and protein expression levels of Nbg and Cygb. The results demonstrated that the 30μg/kg AgNP group displayed increased gene and protein expression of Cygb in the cortex. In the Hippocampus, AgNP exposure did not modulate gene or protein expression levels of Ngb and Cygb. In cerebellum the Ngb gene and protein expression was increased with both doses of AgNP. AgNP exposure during prepubescence can modulate the gene and protein expression levels of Ngb and Cygb in adulthood. Furthermore, the observed modulation was specific to the cerebellum, and cortex, and was dose dependent.

Histopathological changes in zebrafish exposed to sublethal concentrations of 89 nm silver nanoparticles for application in environmental diagnostics

The use of biomarkers as indicators of environmental contamination has been shown to be an excellent indicator of changes in biota. Histopathological lesions are commonly used in biomonitoring studies as they provide information regarding both acute and chronic exposure. The use of nanoparticle materials has been widespread in recent years. However, not much is known about their ecological effects on the natural environment. Thus, the aim of this study was to assess the sublethal effects of silver nanoparticles (AgNP) with mean diameters of 89 nm in the zebrafish Danio rerio by the determination of the LC50; 48 h and histopathological assays in gills. The obtained LC50; 48 h was 8.18 µgL−1. The histopathological gill assessment showed primary responses indicative of acute damage as aneurysms (32.76%), hyperplasia (20.69%) and partial (30.17%) and total lamellar fusion (6.9%) of secondary lamellae. No deposition of AgNP was observed in any tested sample gills, suggesting other organs target to absorption and detoxification. In fact, the AgNP causes sublethal damage in the gills of zebrafish but is not able to accumulate in this tissue. Finally, the data shown in this study contribute to the construction of a database on the AgNP exposure in aquatic organisms.

Silver nanoparticles inhibit beige fat function and promote adiposity

ObjectiveObesity is a complex chronic disease of high prevalence worldwide. Multiple factors play integral roles in obesity development, with rising interest focusing on the contribution of environmental pollutants frequent in modern society. Silver nanoparticles (AgNPs) are widely used for bactericidal purpose in various applications in daily life. However, their potential toxicity and contribution to the obesity epidemic are not clear. MethodsBeige adipocytes are newly discovered adipocytes characterized by high thermogenic and energy dissipating capacity upon activation and the “browning” process. In the present study, we assess the impact of AgNPs exposure on beige adipocytes differentiation and functionality both in vitro and in vivo. We also systematically investigate the influence of AgNPs on adiposity and metabolic performance in mice, as well as the possible underlying molecular mechanism. ResultsThe results showed that, independent of particle size, AgNPs inhibit the adipogenic, mitochondrial, and thermogenic gene programs of beige adipocytes, thus suppressing their differentiation ability, mitochondrial activity, and thermogenic response. Importantly, exposure to AgNPs in mice suppresses browning gene programs in subcutaneous fat, leading to decreased energy expenditure and increased adiposity in mice. Mechanistically, we found that AgNPs increase reactive oxidative species (ROS) levels and specifically activate MAPK-ERK signaling in beige adipocytes. The negative impacts of AgNPs on beige adipocytes can be ameliorated by antioxidant or ERK inhibitor FR180204 treatment. ConclusionsTaken together, these results revealed an unexpected role of AgNPs in promoting adiposity through the inhibition of beige adipocyte differentiation and functionality, possibly by disrupting ROS homeostasis and ERK phosphorylation. Future assessments on the health risk of AgNPs applications and their safe dosages are warranted.

Silver Nanoparticles Compromise Female Embryonic Stem Cell Differentiation through Disturbing X Chromosome Inactivation.

The widespread use of silver nanoparticles (AgNPs) has raised substantial health risks to human beings. Despite a wealth of progress on toxicity studies, the understanding of the adverse effects on fetuses, embryos, and early stage cells is still rather limited, particularly under low-dose exposure settings. Moreover, nearly all previous studies ascribed AgNP-induced toxic effects to oxidative stress. Differently, we here unearthed a mechanism, namely, interruption of X chromosome inactivation (XCI) in female mouse embryonic stem cells (mESCs). Albeit with no observable cytotoxicity, significant differentiation retardation was found in female mESCs upon low-dose AgNP exposure. Mechanistic investigations uncovered expedited inactivation for the inactive X chromosome (Xi) and attenuated maintenance of the active X chromosome (Xa) state during mESC differentiation upon the challenge of low-dose AgNPs, indicative of disordered XCI. Thereby, a few X-linked genes (which are closely involved in orchestrating ESC differentiation) were found to be repressed, partially attributable to reinforced enrichment of histone modification ( e. g., histone 3 lysine 27 trimethylation, H3K27me3) on their promoter regions, as the result of disordered XCI. In stark contrast to female mESCs, no impairment of differentiation was observed in male mESCs under low-dose AgNP exposure. All considered, our data unearthed that AgNPs at low concentrations compromised the differentiation program of female mESCs through disturbing XCI. Thus, this work would provide a model for the type of studies necessary to advance the understandings on AgNP-induced developmental toxicity.

Silver nanoparticle-induced expression of proteins related to oxidative stress and neurodegeneration in an in vitro human blood-brain barrier model

Silver nanoparticles (AgNPs) have been reported to penetrate the central nervous system (CNS) and induce neurotoxicity. However, there is a paucity of understanding of the toxicity of AgNPs and their effect on the blood-brain barrier (BBB) including the underlying molecular mechanism(s) of action. Such information is important for the formulation of new strategies for delivery of biological therapeutics to central nervous system (CNS) targets. Using an in vitro BBB model and mass spectrometry-based proteomics, we investigated alterations in the proteomes of brain endothelial cells and astrocytes at different time points after AgNPs exposure (24 and 48 h). Our data showed that several proteins involved in neurodisorders and neurodegeneration were significantly upregulated in endothelial cells (e.g. 7-dehydrocholesterol reductase, zinc transporters 1 and 6), while proteins responsible for maintaining brain homeostasis were significantly downregulated (e.g anti-oxidative proteins glutathione peroxidase 1 and glutathione peroxidase 4). Many inflammatory pathways were significantly upregulated at 24 h post-AgNPs exposure (C9 pathway), while at 48 h proteins involved in BBB damage and anti-inflammatory responses were upregulated (quinoneoxidoreductase1 and glutamate cysteine ligase catalytic subunit) suggesting that by the later time point, cellular protection pathways had been activated to rescue the cells from AgNPs-induced toxicity. Our study suggests that in the initial stage of exposure, AgNPs exerted direct cellular stress on the endothelial cells by triggering a pro-inflammatory cascade. This study provides detailed insight into the toxic potency of AgNPs on in vitro BBB model and adds to the understanding of the adaptive role of BBB with regards to AgNPs-mediated toxicity.

Mechanisms of silver nanoparticles-induced cytotoxicity and apoptosis in rat tracheal epithelial cells.

Silver nanoparticles (AgNPs) are increasingly utilized in a number of applications. This study was designed to investigate AgNPs induced cytotoxicity, oxidative stress and apoptosis in rat tracheal epithelial cells (RTE). The RTE cells were treated with 0, 100 μg/L and 10,000 μg/L of the AgNPs with diameters of 10 nm and 100 nm for 12 hr. The cell inhibition level, apoptosis ratio, reactive oxygen species (ROS), malondialdehyde (MDA) and metallothionein (MT) content were determined. The mRNA expression of cytoc, caspase 3, and caspase 9 was measured by quantitative real-time polymerase chain reaction (qRT-PCR). In addition, we also analyzed the cytoc, caspase 3, pro-caspase 3, caspase 9, and pro-caspase 9 protein expression by western blotting. Electric cell-substrate impedance sensing (ECIS) analysis showed that the growth and proliferation of RTE cells were significantly inhibited in a dose-dependent manner under AgNPs exposure. The cell dynamic changes induced by 10 nm AgNPs were more severe than that of the 100 nm AgNPs exposure group. The intracellular MT, ROS, and MDA content increased when the exposure concentration increased and size reduced, whereas Ca2+-ATPase activity and Na+/K+-ATPase activity changed inversely. The relative expression of protein of cytoc, caspase 3, and caspase 9 were upregulated significantly, which indicated that AgNPs induced apoptosis of RTE cells through the caspase-dependent mitochondrial pathway. Our results demonstrate that AgNPs caused obvious cytotoxicity, oxidative stress, and apoptosis in RTE cells, which promoted the releasing of cytochrome C and pro-apoptotic proteins into the cytoplasm to activate the caspase cascade and finally led to apoptosis.

Dietary exposure to silver nitrate compared to two forms of silver nanoparticles in rainbow trout: bioaccumulation potential with minimal physiological effects

Overall, fish showed more Ag accumulation from AgNO3 and Ag NP exposures compared to the Ag2S NP treatment.

Proteomics and antioxidant enzymes reveal different mechanisms of toxicity induced by ionic and nanoparticulate silver in bacteria

Ag+had stronger effects than AgNPs on the growth ofPseudomonassp. M1. Responses of metabolic, energetic and stress pathways to Ag+and AgNP exposure suggested distinct mechanisms of toxicity.

Toxicity of silver nanoparticles in mouse bone marrow-derived dendritic cells: Implications for phenotype

Silver nanoparticles (AgNP) are one of the most studied nanoparticles due to their anti-bacterial, -fungal, -viral, -parasitic, and -inflammatory properties. This raises the need to evaluate the toxicity and biological effects of AgNP in the immune system in order to develop new safer biomedical products. In this study, an AgNP formulation currently approved for veterinary applications was applied to mouse bone marrow-derived dendritic cells (BMDC), considered important antigen-presenting cells of the immune system, to evaluate cytotoxicity, genotoxicity, and any significant influence on expression of cellular markers associated with BMDC phenotype and maturation status. The results showed that after 12 h of AgNP exposure, a significant decrease in BMDC viability occurred at the highest concentration tested (1.0 µg AgNP/ml) and at lower doses, the cells maintained membrane integrity and metabolic activity. DNA damage was not significant with any AgNP level aside from the 1.0 µg AgNP/ml level. Regarding phenotype, no differences in expression of CD40 (co-stimulatory molecule highly present in mature BMDC) or in CD273 (a marker for inhibitory T-cell response) were observed. The current results showed that the toxicity of this AgNP formulation was dose-related. The findings also suggest BMDC could maintain structural conservation of co-stimulatory/co-inhibitory surface molecules after 12 h of exposure to this AgNP. This work represents the first step in identifying the toxic effects of this AgNP formulation on dendritic cells.

Involvement of β-catenin in cytoskeleton disruption following adult neural stem cell exposure to low-level silver nanoparticles

Silver nanoparticles (AgNPs) are increasingly incorporated in consumer products to confer antibacterial properties. AgNPs are shed during everyday use of these products, resulting in ingestion or inhalation and bioaccumulation in tissues including the brain. While these low levels of AgNPs do not induce DNA fragmentation typical of apoptosis or necrosis, they do interfere with cytoskeletal structure and dynamics in cultured differentiating adult neural stem cells (NSCs). Moreover, these cells form f-actin inclusions in response to 1 μg/ml AgNPs. Here, we report that these cytoskeletal inclusions colocalize with aggregates of the signaling protein β-catenin, a modulator of cytoskeletal dynamics. Pharmacological alteration of β-catenin signaling reduced formation of f-actin inclusions. AgNP exposure also resulted in a reduction of neurite length in differentiating NSCs, which was mimicked by pharmacological activation of β-catenin signaling. Conversely, pharmacological inhibition of the Wnt/β-catenin signaling pathway resulted in increased neurite lengths in control cells, but did not reverse the neurite collapse induced by AgNP exposure. Substantial changes in neurite length, in response to low-level AgNP or pharmacological manipulation of β-catenin signaling, occurred within the first six hours of exposure and were most evident in cells differentiating towards neural-like morphologies. We conclude that low-level exposure to AgNP, such as that resulting from use of consumer products, may disrupt β-catenin signaling in neural cells in an indirect or non-additive manner. Exposure to AgNP shed from consumer products at levels currently considered safe, may therefore alter physiological function of neural cells. This is of concern particularly regarding children, whose brains contain many developing neurons, and who may face bioaccumulation of AgNP over decades of exposure.

A potential involvement of plant systemic response in initiating genotoxicity of Ag-nanoparticles in Arabidopsis thaliana

The extensive availability of engineered nanomaterials in global markets has led to the release of substantial amounts of nanoparticles (NP) into atmosphere, water body and soil, yielding both beneficial and harmful effects in plant systems. The NP are mainly aggregated onto the surface of plant roots and leaves exposed and only slightly transported into other tissues with a low rate of internalization. This raises a question of whether plant systemic response is involved in the induction of biological effects of NP. To address this, model plant Arabidopsis thaliana were root exposed to low concentrations of Ag-NP of two particle sizes (10-nm and 60-nm), and expressions of homologous recombination (HR)-related genes and the alleviation of transcriptional gene silencing (TGS) in aerial leafy tissues were examined as genotoxic endpoints. Results showed that exposure of roots to two sizes of Ag-NP up-regulated expressions of HR genes, and reactivated TGS-silenced repetitive elements in aerial tissues. These effects were blocked by the impairment in the salicylic acid signal pathway, indicating a potential involvement of plant systemic response in the induction of Ag-NP genotoxicity. This is further supported by ICP-MS analysis, in which the Ag content in aerial tissues was not significantly changed by root exposure to 10-nm Ag-NP. Although a significant increase in the Ag content in aerial tissues was observed after root exposure to 60-nm Ag-NP, its genotoxic effects had no obvious difference from that by 10-nm Ag-NP exposure, also suggesting that the genotoxicity might be mainly induced via plant systemic response, at least in the experiments of root exposure to Ag-NP.

Assessment of AgNPs exposure on physiological and biochemical changes and antioxidative defence system in wheat (Triticum aestivum L) under heat stress.

The present study was designed to check the role of silver nanoparticles (AgNPs) on physiological, biochemical parameters and antioxidants of wheat (Triticum aestivum L.) under heat stress. Plant extract of Moringa oleifera was used for AgNPs synthesis followed by characterization through UV-Vis spectroscopy, SEM, XRD and Zeta analyser. Heat stress was applied in range of 35-40°C for 3 hrs/ day for 3 days to wheat plants at trifoliate stage. Heat stress decreased the RWC (13.2%), MSI (16.3%), chl a (5.2%), chl b (4.1%) and TCCs (9.9%). Wheat plants treated with AgNPs showed significant increase in RWC (12.2%), MSI (26.5%), chl a (10%), chl b (16.4%), TCCs (19%), TPC (2.4%), TFC (2.5%), TASC (2.5%), SOD (1.3%), POX (1.5%), CAT (1.8%), APX (1.2%) and GPX (1.4%), under heat stress. Lower concentration of AgNPs (50 mg/l) decreased the sugar (5.8%) and proline contents (4%), while increase was observed in higher AgNPs concentrations. Overall, AgNPs treatment enhanced thermo-tolerance in wheat plants, but the mechanism of AgNPs action needs further investigation at genome and proteome level in wheat plants under heat stress.