AgNP Exposure Research Articles

Resistance and Resilience of Fish Gut Microbiota to Silver Nanoparticles.

ABSTRACTUnderstanding mechanisms governing the resistance and resilience of microbial communities is essential for predicting their ecological responses to environmental disturbances. Although we have a good understanding of such issues for soil and lake ecosystems, how ecological resistance and resilience regulate the microbiota in the fish gut ecosystem remains unclear. Using the zebrafish model, we clarified the potential mechanisms governing the gut microbiota after exposure to silver nanoparticles (AgNPs). Here, we explored the ecological resistance and resilience of gut microbiota in zebrafish exposed to different concentrations of AgNPs (i.e., 10, 33 and 100 μg/liter) for 15, 45, 75 days. The high-throughput sequencing analysis of the 16S rRNA gene showed that AgNP exposure significantly reduced the α-diversity of gut microbiota and resulted in obvious dynamics of community composition and structure. However, the rebound of zebrafish gut microbiota was pushed toward an alternative state after 15 days of AgNP exposure. We found that homogeneous selection was a more prevalent contributor in driving gut community recovery after AgNP exposure. The resilience and resistance of gut microbiota responses to AgNP disturbance might be mainly determined by the predominant keystone taxa such as Acinetobacter and Gemmata. This study not only expanded our understanding of fish gut microbiota’s responses to pollutants but also provided new insights into maintaining host-microbiome stability during environmental perturbations.IMPORTANCE Understanding the ecological mechanisms governing the resistance and resilience of microbial communities is a key issue to predict their responses to environmental disturbances. Using the zebrafish model, we wanted to clarify the potential mechanisms governing the resistance and resilience of gut microbiota after exposure to silver nanoparticles (AgNPs). We found that AgNP contamination significantly reduced the α-diversity of gut microbiota and resulted in obvious changes in community composition. The resilience and resistance of gut microbiota to AgNPs might be associated with the predominant keystone taxa (e.g., Acinetobacter and Gemmata). This study greatly expanded our understanding of how fish gut microbiota responds to environmental perturbations and maintains stability.

Importance of exposure route in determining nanosilver impacts on a stream detrital processing chain

The commercial use and spread of silver nanoparticles (AgNPs) in freshwaters have greatly increased over the last decade. Both AgNPs and ionic silver (Ag+) released from nanoparticles are toxic to organisms and compromise ecosystem processes such as leaf litter decomposition. Yet little is known about how AgNPs affect multitrophic systems of interacting species. Furthermore, past work has focused on waterborne exposure with scarce attention given to effects mediated by the consumption of contaminated food. We assessed the importance of direct (via water) and indirect (via diet) AgNP exposure to a processing chain comprising leaf litter, fungi, a shredder (Gammarus pulex) and a collector (Habroleptoides confusa) in microcosms. Direct exposure to contaminated water for 15 days impaired microbial leaf decomposition by ∼50% and leaf-associated fungal biomass by ∼10%. Leaf consumption was reduced by ∼20% but only when G. pulex was exposed to silver via contaminated leaves. There was no effect on FPOM production. Ag + could impose oxidative stress on the shredders and collectors independent of exposure route, as indicated by increased catalase and glutathione S-transferase activities and decreased superoxide dismutase activity. The activity of a neuronal enzyme (cholinesterase) in collectors, but not shredders, also decreased by almost 50% when the animals were indirectly exposed to AgNP. Our results show that AgNPs and Ag+ may disrupt detrital processing chains through direct and indirect exposure routes, even at low concentrations. This highlights the importance of AgNP exposure pathways to interconnected stream biota and ecosystem processes for realistic assessments of risks to freshwater ecosystems.

Impact of aqueous exposure to silver nanoparticles on growth performance, redox status, non-specific immunity, and histopathological changes of Nile Tilapia, Oreochromis niloticus, challenged with Aeromonas hydrophila

Silver nanoparticles (AgNP) are one of the most synthesised nanomaterials due to their widespread applications, which in turn increases the potential of release and accumulation in nature. Moreover, they are known as antibacterial and recommended to be used in different commercial drugs. However, the evaluation of their effect on living organisms, especially fish, at low levels is still not completely understood. Therefore, the present study was conducted to investigate the effects of aqueous exposure of AgNPs on growth performance, oxidative status, non-specific immunity, and histopathological changes of epidermis, gills, liver, and intestine of Nile Tilapia, Oreochromis niloticus. The fish were exposed to four concentrations of AgNP (0, 10, 20, and 30 μg L-1) for 8 weeks. At the end of the experiment, fish were intraperitoneally injected with pathogenic bacteria Aeromonas hydrophila and fish mortalities were recorded up to 14 days post-challenge. The results revealed that growth performance and feed utilisation of fish exposed to the lower AgNPs concentration improved significantly compared to other treatments. The increasing AgNP exposure levels decreased different growth indicators in a dose-dependent manner. The highest catalase, superoxide dismutase, glutathione peroxidase, lysozyme, and respiratory burst activities were recorded with 10 μg AgNPs L−1 and the enzyme activities were retarded with increasing AgNP concentrations. The total bacteria count in the water decreased with increasing AgNP concentrations. Meanwhile, the relative percentage of survival improved with low AgNP concentration and decreased with increasing exposure levels. The histopathological investigation of different studied tissues (gills, skin, liver, and intestine) revealed an increase of histological lesions’ frequency and severity with increasing AgNP concentrations. It can be concluded that the exposure of Nile Tilapia to AgNP at levels exceeding 10 μg L−1 could interrupt growth performance, immunity, and antioxidant status and induced histopathological changes.

Integration of transcriptomics and metabolomics reveals damage and recovery mechanisms of fish gills in response to nanosilver exposure.

Toxic effects of silver nanoparticles (AgNPs) on fish gills have been widely reported but the recoverability of AgNPs-induced fish gill injuries is still unknown. In this study, combined multiomics and conventional toxicological analytical methods were used to investigate the changes in the gills of common carp responses to AgNPs (0.1mg/L) toxicity after 24h exposure and 7-day recovery. Conventional toxicological results showed that AgNPs exposure significantly increased silver content in gills and caused epithelial hyperplasia and lamellar fusion. After the recovery period, the silver content in fish gills significantly decreased; accompanied by the disappearance of histopathological characteristics in fish gills. Multiomics results revealed that AgNPs exposure resulted in the differential expression of 687 genes and 96 metabolites in fish gills. These differentially expressed genes (DEGs) and metabolites mainly participate in amino acid, carbohydrate, and lipid metabolisms, and are significantly enriched in the tricarboxylic acid (TCA) cycle. After the recovery period, the number of DEGs and metabolites in gills decreased to 33 and 90, respectively. Moreover, DEGs and metabolites in the TCA cycle recovered to control levels. In summary, the present study found that AgNPs-induced fish gill toxicity showed potential recoverability at molecular and phenotype levels.

Sex-related response in mice after sub-acute intraperitoneal exposure to silver nanoparticles

Silver nanoparticles (AgNPs) are among the most commercialized nanomaterials in biomedicine due to their antimicrobial and anti-inflammatory properties. Nevertheless, possible health hazards of exposure to AgNPs are yet to be understood and therefore raise public concern in regards of their safety.In this study, sex-related differences, role of steroidal hormones and influence of two different surface stabilizing agents (polymer vs. protein) on distribution and adverse effects of AgNPs were investigated in vivo. Intact and gonadectomised male and female mice were treated with seven AgNPs doses administered intraperitoneally during 21 days. After treatment, steroid hormone levels in serum, accumulation of Ag levels and oxidative stress biomarkers in liver, kidneys, brain and lungs were determined.Sex-related differences were observed in almost all tissues. Concentration of Ag was significantly higher in the liver of females compared to males. No significant difference was found for AgNP accumulation in lungs between females and males, while the lungs of intact males showed significantly higher Ag accumulation compared to gonadectomised group. Effect of surface coating was also observed, as Ag accumulation was significantly higher in kidneys and liver of intact females, as well as in kidneys and brain of intact males treated with protein-coated AgNPs compared to polymeric AgNPs. Oxidative stress response to AgNPs was the most pronounced in kidneys where protein-coated AgNPs induced stronger effects compared to polymeric AgNPs. Interestingly, protein-coated AgNPs reduced generation of reactive oxygen species in brains of females and gonadectomised males. Although there were no significant differences in levels of hormones in the AgNP-exposed animals compared to controls, sex-related differences in oxidative stress parameters were observed in all organs.Results of this study highlight the importance of including the sex-related differences and effects of protein corona in biosafety evaluation of AgNPs exposure.

Impact of silver nanoparticles exposure on neuro-behavior, hematology, and oxidative stress biomarkers of African catfish (Clarias gariepinus)

Recently, silver nanoparticles (AgNPs) established a prospective value in aquaculture; however, extensive use afflicts fish and environment. Therefore, the current study represents a premier report to investigate the acute exposure of African catfish, Clarias gariepinus (B.) to AgNPs and the ethological alterations in a static renewal system. Additionally, AgNPs impact on blood profile, stress, brain activity, and branchial oxidative stress parameters were evaluated. Fish (50.71 ± 3.85 g) were exposed to different concentrations (0, 6.25, 12.5, 25, 50, and 100 mg L−1) of AgNPs for 96-h without water exchange. Finney's probit analysis was used to estimate the 96-h LC50 value of AgNPs which recorded 21.38 mg L−1. In comparison to the control, the AgNPs exposed fish exhibited different ethological responses such as surfacing for gasping air, restlessness, slow swimming movement, aggressiveness, and nervousness and the scores of these behaviors and mortalities reached the high values with increasing AgNPs concentrations. There were marked reductions in hematological indices (RBCs, Hb, Hct, and WBCs), acetylcholine esterase (AChE) activity, and oxidative stress indices (superoxide dismutase (SOD), catalase (CAT), and reduced glutathione content (GSH)) of exposed groups in an AgNPs dose-dependent manner relative to the control group. On the contrary, the levels of stress-mediated indices (glucose and cortisol) and 8 hydroxy 2 deoxyguanosine (8OH2dG) were markedly decreased in all AgNPs exposed groups as compared with the control group and the reduction increased with increasing the exposure concentration. We concluded that AgNPs exposure of C. gariepinus induced marked alterations in behavior, blood profile, neurological, and branchial antioxidant parameters, and the 96-h LC50 of AgNPs was 21.38 mg L−1 and this provides a basis for future applying AgNPs as a safe therapeutic agent after considering the acute toxicity.

Differential Action of Silver Nanoparticles on ABCB1 (MDR1) and ABCC1 (MRP1) Activity in Mammalian Cell Lines.

Silver nanoparticles (AgNPs), due to their unique properties have been receiving immense attention in recent years. In addition to their antibacterial and antifungal activities, AgNPs also cause apoptosis, mitochondria disfunction, nucleic acid damage and show potent anticancer properties in both multidrug resistance (MDR) and sensitive tumors. The MDR phenomenon, caused by the presence of ATP-binding cassette (ABC) proteins, is responsible for the failure of chemotherapy. Thus, investigating the influence of widely used AgNPs on ABC transporters is crucial. In the present study, we have examined the cytotoxicity of silver nanoparticles of a nominal size of 20 nm (Ag20) on the cell lines of different tissue origins. In addition, we have checked the ATP-binding cassette transporters’ activity and expression under AgNP exposure. The results indicate that Ag20 shows a toxic effect on tested cells, as well as modulating the expression and transport activity of ABC proteins.

The key role of autophagy in silver nanoparticle-induced BV2 cells inflammation and polarization

As the release of silver nanoparticles (AgNPs) in the environment continues to increase, great concerns have been raised about their potential toxicity to humans. It is urgent to assess the possible toxicity of AgNPs to the immune cells of the central nervous system due to the continuous accumulation of AgNPs in the brain. This study aimed to evaluate the neurotoxicity of AgNPs and the regulatory mechanism of autophagy in AgNPs-induced inflammation by using mouse microglia BV2 cell lines. AgNPs decreased the microglia cell activity in a concentration and time-dependent manner. The exposure of BV2 cells to AgNPs at a non-cytotoxic level of 5 μg/mL resulted in increase of pro-inflammatory cytokines and decrease of mRNA expression of anti-inflammatory cytokines. AgNPs exposure increased M1 markers of iNOS expression and decreased the expression of M2 markers of CD206 in a time-dependent manner. Meanwhile, the expression of inflammatory proteins IL-1β and NF-κB increased significantly. Additionally, AgNPs induced an increase in autophagosome and upregulation of LC3II, Beclin1, and p62 expression levels. Pretreatment by an autophagy inhibitor, 3-Methyladenine, caused more AgNPs-treated microglia to polarized into pro-inflammatory phenotypes. Inhibition of autophagy also increased the expression of inflammation-associated mRNA and proteins in BV2 cells. These results indicated that AgNPs could induce pro-inflammatory phenotypic polarization of microglia and the autophagy could play a key regulatory role in the pro-inflammatory phenotypic polarization of microglia induced by AgNPs.

Microplastic fibers influence Ag toxicity and bioaccumulation in Eisenia andrei but not in Enchytraeus crypticus.

Microplastic fibers (MF) are released from synthetic textiles during washing and end up in the wastewater. Similarly, silver nanoparticles (AgNP), incorporated in textiles as antimicrobial agents, are released in washing machines, also reaching the wastewater treatment plants. Therefore, both MF and AgNP co-exist in the environment and enter the soil compartment mainly via the application of biosolids. Yet, the combined effect of MF and AgNP has not been studied. Here, we assessed the effects of polyester MF on the toxicity of AgNP and AgNO3 to the earthworm Eisenia andrei and the enchytraeid Enchytraeus crypticus. The organisms were exposed to a range of concentration of AgNP (32, 100, 320, 1000, 3200 mg Ag/kg) and AgNO3 (12.8, 32, 80, 200, 500 mg Ag/kg) in LUFA 2.2 soil in the absence or presence of MF (0.01% DW). Reproduction tests were conducted and the toxicity outcomes compared between soils with and without MF. The exposure to MF caused a decrease in the number of juveniles and changed the biochemical composition of earthworms. Moreover, the presence of MF increased the toxicity of AgNP to earthworm reproduction (EC50 = 165 mg Ag/kg) when compared to AgNP exposure alone (EC50 = 450 mg Ag/kg), but did not alter the toxicity of AgNO3 (EC50 = 40 mg Ag/kg). For enchytraeids, no significant difference in Ag toxicity could be detected when MF was added to the soil for both AgNP and AgNO3. Overall, Ag bioaccumulation was not affected by MF, except for a decrease in earthworm body concentration at the highest Ag soil concentration (3200 mg Ag/kg). Our results suggest that the presence of MF in the soil compartment may be a cause of concern, and that the joint exposure to Ag may be deleterious depending on the Ag form, organism, and endpoint. The present work provides the first evidence that a realistic MF concentration in soil lowers AgNP concentration necessary to provoke reproductive impairment in earthworms. The influence of MF on the risk assessment of AgNP should be considered.

Neurobehavior and neuron damage following prolonged exposure of silver nanoparticles with/without polyvinylpyrrolidone coating in Caenorhabditis elegans.

Silver nanoparticles (AgNPs) have become widespread in the environment with increasing industrial applications. But the studies about their potential health risks are far from enough, especially in neurotoxic effects. This study aimed to investigate the neurotoxic effects of longer-term exposure (prolonged exposure for 48 h and chronic exposure for 6 days) of 20nm AgNPs with/without polyvinylpyrrolidone (PVP) coating at low concentrations (0.01-10 mg·L-1 ) to Caenorhabditis elegans. The results suggested that exposure to AgNPs induced damage to nematode survival, with the longest and relative average life span reduced. Exposure to AgNPs caused neurotoxicity on locomotion behaviors (head thrashes, body bends, pharyngeal pumping frequency, and defecation interval) and sensory perception behaviors (chemotaxis assay and thermotaxis assay), as well as impaired dopaminergic, GABAergic, and cholinergic neurons, except for glutamatergic, based on the alters fluorescence intensity, in a dose- and time-dependent manner. Further investigations suggested that the low-dose AgNPs (0.01-0.1 mg·L-1 ) exposure raises receptors of GABAergic and dopamine in C.elegans at the genetic level, whereas opposite results were observed at higher doses (1-10 mg·L-1 ), which implied that AgNPs could cause neurotoxicity by impairing neurotransmitter delivery. The PVP-AgNPs could cause a higher fatality rate and neurotoxicity at the same dose. Notably, AgNPs did not cause any deleterious effect on nematodes at the lowest dose of 0.01 mg·L-1 . In general, these results suggested that AgNPs possess the neurotoxic potential in C.elegans and provided useful information to understand the neurotoxicity of AgNPs, which would offer an inspiring perspective on the safe application.

Toxicity, inflammatory and antioxidant genes expression, and physiological changes of green synthesis silver nanoparticles on Nile tilapia (Oreochromis niloticus) fingerlings

The rapid increase of incorporating silver nanoparticles (Ag-NPs) in different anthropogenic and industrial activities increased the discharge of these particles in the aquatic ecosystem. The environmental impact of Ag-NPs, especially the green synthesized is still not completely understood on fish. Therefore, this study aimed to investigate the effects of exposure to graded series of starch-mediated Ag-NPs at levels of 0, 3.31, 6.63, 13.25, and 26.50 mg L−1 representing 0, 6.25, 12.5, 25, and 50% of LC50 on Nile tilapia (O. niloticus), respectively. Fish with initial weight 37.63 ± 0.41 g were maintained in 70 L glass aquaria and exposed to starch-mediated Ag-NPs (average particle size 40 nm) for 28 days. The results revealed that starch-mediated Ag-NPs induced severe changes in the mRNA levels of toxicity (CYP1A and Hsp70) and inflammatory (TNF-α and TGF-β) genes. The expression of antioxidant genes (SOD and CAT) was significantly suppressed, and the activities of their enzymes were inhibited significantly upon exposure. Simultaneously, the malondialdehyde level increased significantly with increasing the exposure levels of starch-mediated Ag-NPs. The red blood cells, hemoglobin, hematocrit and white blood cell values were decreased significantly with doses over 3.31 mg L−1 of Ag-NPs. In addition, the total protein and globulin decreased significantly with increasing Ag-NPs in a dose-dependent manner. The liver function enzymes and kidney function indicators revealed severe toxicity with Ag-NPs exposure. In conclusion, the effect of starch-mediated Ag-NPs in doses over 3.31 mg L−1 induced obvious toxicity in the molecular and proteomic levels in Nile tilapia fingerlings.

Perinatal exposure to silver nanoparticles reprograms immunometabolism and promotes pancreatic beta-cell death and kidney damage in mice

Silver nanoparticles (AgNPs) are extensively utilized in food, cosmetics, and healthcare products. Though the effects of AgNPs exposure on adults are well documented, the long-term effects of gestational/perinatal exposure upon the health of offspring have not been addressed. Herein, we show that only perinatal exposure to AgNPs through the mother could lead to chronic inflammation in offspring which persists till adulthood. Further, AgNPs exposure altered offspring’s immune responses against environmental stresses. AgNPs exposed offspring showed an altered response in splenocyte proliferation assay when challenged to lipopolysaccharide, concanavalin-A, AgNPs, or silver ions. Perinatal AgNPs exposure affected metabolic parameters (resistin, glucagon-like peptide-1, leptin, insulin) and upregulated JNK/P38/ERK signaling in the pancreas. We observed pancreatic damage, reduced insulin level, and increased blood glucose levels. Further, we observed renal damage, particularly to tubular and glomerular regions as indicated by histopathology and electron microscopy. Our study thus shows that only perinatal exposure to AgNPs could induce persistent inflammation, alter immune responses against foreign antigens and metabolism which may contribute to pancreatic and renal damage later in life.

Dietary pomegranate (Punica granatum) peel mitigated the adverse effects of silver nanoparticles on the performance, haemato-biochemical, antioxidant, and immune responses of Nile tilapia fingerlings

The present study investigated the adverse effects of silver nanoparticles (AgNPs) on haemato-biochemical, oxidant/antioxidant, and immunological responses of Nile tilapia (Oreochromis niloticus) as well as the beneficial roles of pomegranate (Punica granatum) peel (PP) powder to mitigate these effects. Fish (29.6–31.5 g) were fed on diets supplemented with PP at levels of 0.0% (control), 3%, and 5% and exposed to sub-lethal levels of AgNPs (0.0 and 2.0 mg/L) for six weeks. The results showed that AgNPs exposure alone significantly suppressed the fish growth and elevated stress biomarkers (blood glucose and cortisol), induced liver damage (alanine and aspartate aminotransferases), and renal failure (creatinine and uric acid). Additionally, AgNPs exposure significantly decreased serum immune parameters (lysozyme activity, respiratory burst activity, and total immunoglobulin) and affected hepatic and renal oxidant/antioxidant biomarkers (superoxide dismutase, catalase, malondialdehyde, and reduced glutathione). Dietary supplementation of PP powder alone reduced the fish performance but markedly enhanced antioxidant and immunological activities. Additionally, dietary PP powder significantly mitigated AgNPs-induced effects, attenuating hepato-renal damage, oxidative stress, and immunity biomarkers. In conclusion, AgNPs adversely affected the performance of Nile tilapia; however, dietary supplementation of 5% PP powder effectively mitigated the oxidative stress and immune suppression resulted from AgNPs exposure.

Impact of multigenerational exposure to AgNO3 or NM300K Ag NPs on antioxidant defense and oxidative stress in Caenorhabditis elegans

Adaptation of the nematode Caenorhabditis elegans towards NM300K silver nanoparticles (Ag NPs) has previously been demonstrated. In the current study, the sensitivity to a range of secondary stressors (CeO2 NP, Ce3+, Cu2+, Cd2+, and Paraquat) following the multigenerational exposure to silver nanoparticles (Ag NPs NM300K) or AgNO3 was investigated. This revealed improved tolerance to the ROS inducer Paraquat with higher fecundity after pre-exposure to Ag NP, indicating an involvement of reactive oxygen species (ROS) metabolism in the adaptive response to NM300K. The potential contribution of the antioxidant defenses related to adaptive responses was investigated across six generations of exposure using the sod-1::GFP reporter (GA508), and the Grx1-roGFP2 (GRX) biosensor strains. Results showed an increase in sod-1 expression by the F3 generation, accompanied by a reduction of GSSG/GSH ratios, from both AgNO3 and Ag NP exposures. Continuous exposure to AgNO3 and Ag NP until the F6 generation resulted in a decreased sod-1 expression, with a concomitant increase in GSSG/GSH ratios. The results thus show that despite an initial enhancement, the continuous exposure to Ag caused a severe impairment of the antioxidant defense capacity in C. elegans.

The effects of gene × environment interactions on silver nanoparticle toxicity in the respiratory system: An adverse outcome pathway.

The Adverse Outcome Pathway (AOP) framework is serving as a basis to integrate new data streams in order to enhance the power of predictive toxicology. AOP development for engineered nanomaterials (ENM), including silver nanoparticles (AgNP), is currently lagging behind other chemicals of regulatory interest due to our limited understanding of the mechanism by which underlying genetics or diseases directly modify host response to AgNP exposures. This also highlights the importance of considering the Aggregate Exposure Pathway (AEP) framework, which precedes the AOP framework and outlines source to target site exposure. The AEP and AOP frameworks interface at the target site, where a molecular initiating event (MIE) occurs and is followed by key events (KE) for adverse cellular and organ responses along a biological pathway and ends with the adverse organism response. The primary goal of this study is to use AgNP to interrogate the AEP-AOP framework by organizing and integrating in vitro dose-response data and in vivo exposure-response data from previous studies to evaluate the effects of interactions between host genetic and acquired factors, or gene × environment interactions (G × E), on AgNP toxicity in the respiratory system. Using this framework will help us to identify plausible key event relationships (KER) between MIE and adverse organism responses when KE are not measured using the same assay in order to derive future predictive models, guide research, and support development of tools for making risk-based, regulatory decisions on ENM. This article is categorized under: Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials Toxicology and Regulatory Issues in Nanomedicine > Regulatory and Policy Issues in Nanomedicine.

Developmental exposure to silver nanoparticles leads to long term gut dysbiosis and neurobehavioral alterations

Due to their antimicrobial properties, silver nanoparticles (AgNPs) are used in a wide range of consumer products that includes topical wound dressings, coatings for biomedical devices, and food-packaging to extend the shelf-life. Despite their beneficial antimicrobial effects, developmental exposure to such AgNPs may lead to gut dysbiosis and long-term health consequences in exposed offspring. AgNPs can cross the placenta and blood–brain-barrier to translocate in the brain of offspring. The underlying hypothesis tested in the current study was that developmental exposure of male and female mice to AgNPs disrupts the microbiome–gut–brain axis. To examine for such effects, C57BL6 female mice were exposed orally to AgNPs at a dose of 3 mg/kg BW or vehicle control 2 weeks prior to breeding and throughout gestation. Male and female offspring were tested in various mazes that measure different behavioral domains, and the gut microbial profiles were surveyed from 30 through 120 days of age. Our study results suggest that developmental exposure results in increased likelihood of engaging in repetitive behaviors and reductions in resident microglial cells. Echo-MRI results indicate increased body fat in offspring exposed to AgNPs exhibit. Coprobacillus spp., Mucispirillum spp., and Bifidobacterium spp. were reduced, while Prevotella spp., Bacillus spp., Planococcaceae, Staphylococcus spp., Enterococcus spp., and Ruminococcus spp. were increased in those developmentally exposed to NPs. These bacterial changes were linked to behavioral and metabolic alterations. In conclusion, developmental exposure of AgNPs results in long term gut dysbiosis, body fat increase and neurobehavioral alterations in offspring.

Akt and MAPK/ERK signaling regulate neurite extension in adult neural progenitor cells but do not directly mediate disruption of cytoskeletal structure and neurite dynamics by low-level silver nanoparticles

Silver nanoparticles (AgNPs) are an environmental contaminant of emerging concern. Ionic and colloidal silver has long been used for its antimicrobial properties, but with the development of engineered AgNPs, these are increasingly incorporated in the manufacture of nano-enhanced products. AgNPs are released into the environment from manufacturing plants and they can be shed from products during use and after disposal. This can lead to chronic low-level environmental exposure in animals. Unlike traditional forms of silver, the unique physical properties of AgNPs allow them to bypass biological barriers and enter tissues, like the brain, where they can bioaccumulate. Thus, it is important to understand if low-level AgNPs induce physiological changes in brain cells. Previously we found that 1.0 μg/mL AgNP exposure resulted in disruption of f-actin organization and neurite collapse in cultured differentiating adult neural stem cells, and that interaction with β-catenin signaling was involved. Here, we report that AgNP exposure may interact with pAkt signaling irreversibly or indirectly to disrupt cytoskeleton and inhibit neurite extension. Furthermore, the MAPK/ERK signaling pathway is not a target for AgNP-mediated dysregulation. Environmental exposure to low-level AgNPs therefore appears to target specific cellular mechanisms to alter brain cell physiology. Understanding these underlying mechanisms is important for decisions regulating the use and disposal of manufactured AgNPs.

Potential cytotoxicity of silver nanoparticles: Stimulation of autophagy and mitochondrial dysfunction in cardiac cells.

In the present study, we elucidated the potential cytotoxicity of AgNPs in H9c2 rat cardiomyoblasts and assessed the underlying toxicological manifestations responsible for their toxicity thereof. The results indicated that the exposure of AgNPs to H9c2 cardiac cells decreased cell viability in a dose-dependent manner and caused cell cycle arrest followed by induction of apoptosis. The AgNPs treated cardiac cells showed a generation of reactive oxygen species (ROS) and mitochondrial dysfunction where mitochondrial ATP was reduced and the expression of AMPK1α increased. AgNPs also induced ROS-mediated autophagy in H9c2 cells. There was a significant time-dependent increase in intracellular levels of Atg5, Beclin1, and LC3BII after exposure to AgNPs, signifying the autophagic response in H9c2 cells. More importantly, the addition of N-acetyl-L-cysteine (NAC) inhibited autophagy and significantly reduced the cytotoxicity of AgNPs in H9c2 cells. The study highlights the prospective toxicity of AgNPs on cardiac cells, collectively signifying a potential health risk.

Does the adsorbent capacity of orange and banana peels toward silver nanoparticles improve the biochemical status of Oreochromis niloticus?

Silver nanoparticles (Ag NPs) have wide medical and industrial applications; therefore, their release into aquatic environments is a problematic issue. The present study aims to evaluate the removal efficiency of Ag NPs from water using orange peel (OP) and banana peel (BP) to moderate their toxicity on Oreochromis niloticus. Fish were divided into 4 groups: control group (dechlorinated tap water), Ag NPs (4 mg/L) exposed group, Ag NPs (4 mg/L) + OP (40 mg/L) group, and Ag NPs (4 mg/L) + BP (40 mg/L) group for 24 h, 48 h, and 96 h. The adsorptive ability of both peels was confirmed by scanning electron microscope and energy-dispersive X-ray spectroscopy after the exposure processes. The biochemical results revealed a gradual elevation in plasma glucose, total proteins, globulin, liver enzymes (AST, ALT, and ALP), creatinine, and uric acid after Ag NPs exposure, while albumin and total lipid concentrations were significantly decreased. The recorded antioxidant biomarkers in gills, and liver tissues after Ag NPs exposure showed severe oxidative damages (maximally after 96 h) as indicated by marked elevations in thiobarbituric acid reactive substances, glutathione peroxidase, catalase, and superoxide dismutase values, and decreased glutathione reduced content. All studied parameters restored more or less to that of control groups after OP and BP water treatment. The adsorbent abilities of both peels could reduce Ag NPs bioavailability and moderate their toxicological impacts.

On the developmental toxicity of silver nanoparticles

With the increasing production and applications, silver nanoparticles (AgNPs) can be released into the air, water and soil environment, leading to direct exposure to human beings. Embryos and fetuses are more sensitive to environmental pollutants than adults. Thus, the developmental toxicity of AgNPs should be of great concern. However, the targets and molecular mechanisms how prenatal AgNP exposure affects fetal development in mammals are largely unknown. In the current review, the translocation and developmental toxicities of AgNPs upon maternal exposure in mammals are summarized. AgNPs are able to translocate to the fetus, resulting in resorption, growth retardation and histological and functional abnormalities in the fetal central nervous system (CNS), reproductive system, immune system and other systems and organs. A few likely mechanisms, including direct and indirect mechanisms, and knowledge gaps are elucidated. The fundamental physiochemical properties that determine their behaviors are discussed in order to develop safe-by-design nanomaterials for personal care and medical applications. This review aims to advance the understanding of the developmental toxicities of AgNPs for the design of nanomaterials that harbor better biocompatibility.