TiO2 NPs Exposure Research Articles

Labeo rohita fingerlings exposed to titanium dioxide (TiO2 NPs): A concentration-dependent bi-modal effect on growth

Titanium dioxide nanoparticles (TiO2-NPs) are widely manufactured and can be released into the environment, where they have the potential to severely affect fish and human health. This study was conducted to evaluate the effect of TiO2-NPs on the growth of fingerlings of Labeo rohita. TiO2-NPs were used in different concentrations (1 mg/kg, 10 mg/kg, 100 mg/kg and 1000 mg/kg) mixed in fish basal feed for a period of 12 weeks. The mortality rate was recorded once the fish were acclimatized, after TiO2-NPs exposure. The growth in length (cm) and weight (g) of the fish was measured to evaluate the time and concentration dependent growth of the fingerlings. A high mortality rate was observed for the fish exposed to high concentrations of TiO2-NPs from week 10 onwards. A gradual increase in the body weight and length of the fish was observed for all treatments until the 8th week, which thereafter changed differently for different treatments. It could be shown that TiO2-NPs exert concentration dependent bi-modal effects on fish growth with a longer exposure to high concentrations of TiO2-NPs having an adverse effect on the growth. Therefore, TiO2-NPs in natural water bodies may affect the aquaculture industry as well as inland fisheries.

Effect of UV-activated TiO2 Nanoparticles on the Properties and Performance of PAni-TiO2 Nanocomposite Films for Solar Cell Applications

To improve the performance of organic solar cells by enhancing the properties of the photoactivated nanocomposite layer, the UV irradiation process was used to activate titanium dioxide nanoparticles (TiO2 NPs). Herein, polymer solar cells were fabricated with FTO/(PAni-TiO2)/Ag system. A series of mixed polyaniline (PAni) with 20% of activated TiO2 NPs at different processing times was used to form PAni-TiO2 nanocomposite films. The structural evolution, surface characteristics, optical and electrical properties of PAni-TiO2 films have been investigated. XRD patterns showed that the UV treatment of TiO2 NPs increased the crystallite from 18.35 to 24.1 nm and the degree of crystallinity increased by 5.6%. The irradiated PAni-TiO2 films showed a rougher and more porous surface compared to the untreated one. Moreover, the adhesion force and electrical conductivity of the treated nanocomposite films at 8 h improved to be 137 mN/m and 6.62 S/m, respectively. Incorporation of activated TiO2 NPs exposure to UV for different times from 0 to 8 h with the PAni matrix enhanced the current density (Jsc) of PAni-TiO2 based nanocomposite solar cells from 3.11 to 4.83 (mA/cm2) and their efficiency from 0.33 to 0.85%. The increase in the solar cell efficiency is mostly ascribed to a structural change accompanied by a rapid increase in surface roughness, which led to a decrease in the reflected photons and thus an increase in the charge carriers produced. These results revealed the effect of surface UV irradiation of TiO2 NPs on their structural properties and the electronic contact between PAni and TiO2 NPs, which greatly influenced the amount of carrier transport within the PAni-TiO2 composites.

Genotoxicity Evaluation of Titanium Dioxide Nanoparticles In Vitro: a Systematic Review of the Literature and Meta-analysis.

With the wide use of titanium dioxide nanoparticles (TiO2-NPs), the genotoxicity of TiO2-NPs, which is a factor for safety assessment, has attracted people's attention. However, their genotoxic effects in vitro remain controversial due to inconsistent reports. Therefore, a systematic review was conducted followed by a meta-analysis to reveal whether TiO2-NPs cause genotoxicity in vitro. A total of 59 studies were identified in this review through exhaustive database retrieval and exclusion. Meta-analysis results were presented based on different evaluation methods. The results showed that TiO2-NP exposure considerably increased the percentage of DNA in tail and olive tail moment in comet assay. Gene mutation assay revealed that TiO2-NPs could also induce gene mutation. However, TiO2-NP exposure had no effect on micronucleus (MN) formation in the MN assay. Subgroup analysis showed that normal cells were more vulnerable to toxicity induced by TiO2-NPs. Moreover, mixed form and small particles of TiO2-NPs increased the percentage of DNA in tail. In addition, short-term exposure could detect more DNA damage. The size, coating, duration, and concentration of TiO2-NPs influenced MN formation. This study presented that TiO2-NP exposure could cause genotoxicity in vitro. The physicochemical properties of TiO2-NPs and experimental protocols influence the genotoxic effects in vitro. Comet and gene mutation assays may be more sensitive to the detection of TiO2-NP genotoxic effects.

Titanium dioxide nanoparticles exaggerate respiratory syncytial virus-induced airway epithelial barrier dysfunction.

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in children worldwide. While most develop a mild, self-limiting illness, some develop severe acute lower respiratory infection and persistent airway disease. Exposure to ambient particulate matter has been linked to asthma, bronchitis, and viral infection in multiple epidemiological studies. We hypothesized that coexposure to nanoparticles worsens RSV-induced airway epithelial barrier dysfunction. Bronchial epithelial cells were incubated with titanium dioxide nanoparticles (TiO2-NP) or a combination of TiO2-NP and RSV. Structure and function of epithelial cell barrier were analyzed. Viral titer and the role of reactive oxygen species (ROS) generation were evaluated. In vivo, mice were intranasally incubated with TiO2-NP, RSV, or a combination. Lungs and bronchoalveolar lavage (BAL) fluid were harvested for analysis of airway inflammation and apical junctional complex (AJC) disruption. RSV-induced AJC disruption was amplified by TiO2-NP. Nanoparticle exposure increased viral infection in epithelial cells. TiO2-NP induced generation of ROS, and pretreatment with antioxidant, N-acetylcysteine, reversed said barrier dysfunction. In vivo, RSV-induced injury and AJC disruption were augmented in the lungs of mice given TiO2-NP. Airway inflammation was exacerbated, as evidenced by increased white blood cell infiltration into the BAL, along with exaggeration of peribronchial inflammation and AJC disruption. These data demonstrate that TiO2-NP exposure exacerbates RSV-induced AJC dysfunction and increases inflammation by mechanisms involving generation of ROS. Further studies are required to determine whether NP exposure plays a role in the health disparities of asthma and other lung diseases, and why some children experience more severe airway disease with RSV infection.

High-dose intranasal application of titanium dioxide nanoparticles induces the systemic uptakes and allergic airway inflammation in asthmatic mice

BackgroundTitanium dioxide nanoparticles (TiO2 NPs) have a wide range of applications in several industrial and biomedical domains. Based on the evidence, the workers exposed to inhaled nanosized TiO2 powder are more susceptible to the risks of developing respiratory diseases. Accordingly, this issue has increasingly attracted the researchers’ interest in understanding the consequences of TiO2 NPs exposure. Regarding this, the present study was conducted to analyze the local effects of TiO2 NPs on allergic airway inflammation and their uptake in a mouse model of ovalbumin (OVA)-induced allergic airway inflammation.MethodsFor the purpose of the study, female BALB/c mice with or without asthma were intranasally administered with TiO2 NPs. The mice were subjected to histological assessment, lung function testing, scanning electron microscopy (SEM), inductively coupled plasma mass spectrometry (ICP-MS), and NP uptake measurement. In addition, T helper (Th) 1/Th2 cytokines were evaluated in the lung homogenate using the enzyme-linked immunosorbent assay.ResultsAccording to the results, the mice receiving OVA alone or OVA plus TiO2 NPs showed eosinophilic infiltrates and mucus overproduction in the lung tissues, compared to the controls. Furthermore, a significant elevation was observed in the circulating Th2 cytokines, including interleukin (IL)-4, IL-5, and IL-13 after NP exposure. The TiO2 NPs were taken up by alveolar macrophages at different time points. As the results of the SEM and ICP-MS indicated, TiO2 NPs were present in most of the organs in both asthmatic and non-asthmatic mice.ConclusionBased on the findings of the current study, intranasally or inhalation exposure to high-dose nanosized TiO2 particles appears to exacerbate the allergic airway inflammation and lead to systemic uptake in extrapulmonary organs. These results indicate the very important need to investigate the upper limit of intranasally or inhalation exposure to nanosized TiO2 particles in occupational and environmental health policy.

Toxicity of polyelectrolyte-functionalized titania nanoparticles in zebrafish (Danio rerio) embryos

We investigated the effects of short-term exposure of bare TiO2NPs and polyelectrolyte-coated TiO2NPs in the 5–25 nm size range, at relatively high concentrations (of 500 and 1000 mg/L) under light or dark conditions, in D. rerio embryos. The biological endpoints investigated included embryo viability and mRNA transcript levels of antioxidant and membrane transport genes relative to control embryos. The presence of nanoparticles on the surface of embryos was assessed using TEM. The results confirm an accumulation of TiO2NPs on the outer surface (chorion) of the embryo, but not within the embryo. No significant difference in embryo viability was detected following each exposure regime. The expression of antioxidant biomarker, SOD2, was significantly impacted by the type of TiO2NP, with TiO2NPs/PSS/PAH coating exposure showing down regulation; the concentration of the nanoparticles, with down regulation at 500 mg/L; and dark/light condition with down regulation in the light. The expression levels of the hypoxia and membrane markers, HIF1 and Pxmp2, were not significantly impacted by any factor. The study indicates that SOD2 mRNA expression levels may be useful in the detection of apparent oxidative stress induced by the titania nanoparticle build up on the embryo chorion surface.

Duration-dependent effects induced by titanium dioxide nanoparticles on pancreas of adult male albino rats (histological and biochemical study)

ABSTRACT Titanium dioxide nanoparticles (TiO2NPs) have been widely used in numerous applications and enter the human body through different routes. This study aimed to investigate the effect of intraperitoneal TiO2NPs on the histological and biochemical structure of rat pancreas. Fifty adult male albino rats were divided into four groups. Group I (control) was equally divided into two subgroups. Groups II, III, and IV: rats received intraperitoneal TiO2NPs for 7, 14, and 45 days, respectively. Blood samples were taken for the estimation of blood glucose, serum insulin, serum α-amylase, and lipase activity levels. Sections of the pancreas were processed for light, electron microscope examination, and immunohistochemical detection of insulin protein. Other parts were exposed to Real-Time Polymerase Chain Reaction for Bax, Bcl-2, SOD, and GST mRNA gene expression. Results showed pancreatic tissue damage, including acinar and islet cells, which became worse with increased duration of exposure to TiO2NPs. Decreased immune expression of the insulin protein together with decreased serum insulin and increased blood glucose levels indicated the alteration of β cells. Decreased serum α-amylase and lipase activities indicated alteration of acinar cells. Increased Bax and decreased Bcl-2 mRNA expression levels showed the apoptotic effect of TiO2NPs caused by oxidative stress and evidenced by a significant reduction in the mRNA expression of SOD and GST in a duration-dependent manner. In conclusion: the present study stated that TiO2NPs exposure for long durations had toxic effects on both exocrine and endocrine pancreas mediated by apoptotic and oxidative stress pathways.

Oral exposure of titanium oxide nanoparticles induce ileum physical barrier dysfunction via Th1/Th2 imbalance.

In this work, we aimed to evaluate the adverse effects and the mechanism of intestinal barrier caused by titanium dioxide nanoparticles (TiO2 NPs). Here, the effects of two different dosages (300 and 1200 mg/kg) of TiO2 NPs on female mice (n = 5) were investigated. After 28-day oral exposure, the results of Ti content were significantly increased in the ileum in comparison with the control. The histopathological structure index of the ileum was significantly changed after TiO2 NPs exposure; villi height and crypt depth were decreased and increased, respectively. Meanwhile, TiO2 NPs treatment also significantly altered the transcription levels of genes. First, the GATA-3 and STAT-4 were upregulation and downregulation, respectively. Second, gene expressions of the Zonula Occludens-1, claudin (CLDN)-12, occludin, and myosin light chain kinase were significantly upregulated, while the CLDN-3 was decreased. Finally, the caspase-3, caspase-9, and caspase-12 were upregulated. The results of TUNEL staining indicated apoptosis in the ileum. In general, TiO2 NPs treatment significantly changed the intestine physical barrier in a dose-dependent manner. The toxicity of TiO2 NPs could be through the imbalance in the Th1/Th2.

Irreversible disruption of the cytoskeleton as induced by non-cytotoxic exposure to titanium dioxide nanoparticles in lung epithelial cells

Exposure to TiO2 NPs induces several cellular alterations after NPs uptake including disruption of cytoskeleton that is crucial for lung physiology but is not considered as a footprint of cell damage. We aimed to investigate cytoskeleton disturbances and the impact on cell migration induced by an acute TiO2 NPs exposure (24 h) and the recovery capability after 6 days of NPs-free treatment, which allowed investigating if cytoskeleton damage was reversible. Exposure to TiO2 NPs (10 μg/cm2) for 24 h induced a decrease 20.2% and 25.1% in tubulin and actin polymerization. Exposure to TiO2 NPs (10 μg/cm2) for 24 h followed by 6 days of NPs-free had a decrease of 26.6% and 21.3% in tubulin and actin polymerization, respectively. The sustained exposure for 7 days to 1 μg/cm2 and 10 μg/cm2 induced a decrease of 22.4% and 30.7% of tubulin polymerization respectively, and 28.7% and 46.2% in actin polymerization. In addition, 24 h followed 6 days of NPs-free exposure of TiO2 NPs (1 μg/cm2 and 10 μg/cm2) decreased cell migration 40.7% and 59.2%, respectively. Cells exposed (10 μg/cm2) for 7 days had a decrease of 65.5% in cell migration. Ki67, protein surfactant B (SFTPB) and matrix metalloprotease 2 (MMP2) were analyzed as genes related to lung epithelial function. The results showed a 20% of Ki67 upregulation in cells exposed for 24 h to 10 μg/cm2 TiO2 NPs while a downregulation of 20% and 25.8% in cells exposed to 1 μg/cm2 and 10 μg/cm2 for 24 h followed by 6 days of NPs-free exposure. Exposure to 1 μg/cm2 and 10 μg/cm2 for 24 h and 7 days upregulates SFTPB expression in 53% and 59% respectively, MMP2 expression remain unchanged. In conclusion, exposure of TiO2 NPs affected cytoskeleton of lung epithelial cells irreversibly but this damage was not cumulative.

Impact of co-exposure to titanium dioxide nanoparticles (TiO2 NPs) and lead (Pb) on African catfish Clarias gariepinus (Burchell, 1922) fed contaminated copepods (Eucyclop sp.).

The fast-growing discharge of effluents of engineered nanomaterials (ENM) and heavy metals in freshwater ecosystems raises concern in recent times. This study investigated the effects of the co-exposure between nanoparticles (TiO2 NPs) and lead (Pb) in a simplified freshwater food web model, including zooplankton (copepods sp.) and Clarias gariepinus on bioaccumulation and antioxidant activity. We carried out a chronic (28days) semi-static bioassay by feeding individually fish with zooplankton exposed to TiO2 NPs (0.09 and 0.20μM), Pb (0.01 and 0.04μM), and their binary mixtures. The binary mixtures caused a significant (p < 0.05) decrease in malondialdehyde (1.64-2.01-fold), catalase (3.18-3.89-fold), glutathione reductase (1.37-1.46-fold), and glutathione peroxidase (1.19-1.89-fold) levels. Lead accumulated in the tissues had bioaccumulation factor between 0.40 and 1.42 in binary mixture. These results indicate that chronic exposure of TiO2 NPs could influence the BAF of Pb, neurotoxicity, changes of antioxidant enzymes, and retardation of food uptake. These findings raise concerns regarding the fate of higher trophic levels in polluted freshwater ecosystems with a binary mixture of engineer nanomaterials and heavy metals.

Effects of oral administration of titanium dioxide particles on sperm parameters and in vitro fertilization potential in mice: A comparison between nano- and fine-sized particles.

Titanium dioxide particles (TiO2) as the second most widely used materials in consumer products are composed of nano-sized (<100 nm) particles (NPs) and fine-sized (>100 nm) particles (FPs). Toxicological studies on animals have shown that TiO2 NPs exposure can cross the blood-testis barrier and accumulate in the testis resulting in testicular tissue damage and reduction of sperm count and motility. However, there is no information on the toxic effects of TiO2 FPs on male reproductive fertility. Twenty-four adult male mice were randomly divided into three groups including control, TiO2 NPs, and TiO2 FPs (150 mg kg-1 per day). After intragastric administration for 35 days, testicular tissue alterations (seminiferous tubule diameter and germinal epithelial height), sperm parameters (count, motility, viability, morphology, and DNA quality), in vitro fertilization potential, oxidative stress assays such as malondialdehyde (MDA) content, level of glutathione (GSH) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in testicular tissue were investigated. The results showed that both sizes of TiO2 caused pathologic changes in the testis and significantly increased MDA level and decreased GSH levels and activities of SOD and GPx in testicular tissue. Moreover, the administration of both sizes of TiO2 significantly decreased all of the sperm parameters and in vitro fertility (fertilization rate and pre-implantation embryos development) compared to control. Administration of TiO2 FPs similar to TiO2 NPs through inducing damages to testis led to a marked reduction in sperm quality, in vitro fertilization, and embryos development in male mice.

The mTOR/GCLc/GSH Pathway Mediates the Dose-Dependent Bidirectional Regulation of ROS Induced by TiO2NPs in Neurogenic Cells

Objective. The effect of TiO2NP exposure on the nervous system and the underlying mechanism remain unclear. The antioxidant effect of TiO2NPs at a low dose was newly found in our study, which was different from the effect at high dose. This study is aimed at exploring the mechanism underlying the antioxidant effects of TiO2NPs at low dose and the induction of ROS accumulation by TiO2NPs at high dose in neurogenic cell lines.Methods. We measured the changes in key molecules in the ROS regulation pathway by western blotting, flow cytometry, and commercial assay kits, and these key molecules were further evaluated to verify their interactions and roles using SH-SY5Y, U251, and SK-N-SH cell lines treated with TiO2NPs.Results. Our results showed that the weak antioxidant effect at low dose was caused by mTOR/GCLc-induced GSH overproduction and GSH-Px activity impairment. ROS accumulation at high dose was caused by a mTOR/GCLc-mediated decrease in GSH production, GSH-Px activity impairment, and dramatic ROS production. Furthermore, we found that the ROS species were mainly O2-⋅, and that SOD played a crucial role in reducing O2-⋅levels before the mTOR protein was activated.Conclusion. We revealed the mechanism underlying the bidirectional regulation of ROS induced by TiO2NPs at different doses in neurogenic cell lines. Our study emphasized the potential neurotoxic effects of NPs at low dose, which should arouse concern about their safety.

Hepatotoxicity and the role of the gut-liver axis in rats after oral administration of titanium dioxide nanoparticles

BackgroundDue to its excellent physicochemical properties and wide applications in consumer goods, titanium dioxide nanoparticles (TiO2 NPs) have been increasingly exposed to the environment and the public. However, the health effects of oral exposure of TiO2 NPs are still controversial. This study aimed to illustrate the hepatotoxicity induced by TiO2 NPs and the underlying mechanisms. Rats were administered with TiO2 NPs (29 nm) orally at exposure doses of 0, 2, 10, 50 mg/kg daily for 90 days. Changes in the gut microbiota and hepatic metabolomics were analyzed to explore the role of the gut-liver axis in the hepatotoxicity induced by TiO2 NPs.ResultsTiO2 NPs caused slight hepatotoxicity, including clear mitochondrial swelling, after subchronic oral exposure at 50 mg/kg. Liver metabolomics analysis showed that 29 metabolites and two metabolic pathways changed significantly in exposed rats. Glutamate, glutamine, and glutathione were the key metabolites leading the generation of energy-related metabolic disorders and imbalance of oxidation/antioxidation. 16S rDNA sequencing analysis showed that the diversity of gut microbiota in rats increased in a dose-dependent manner. The abundance of Lactobacillus_reuteri increased and the abundance of Romboutsia decreased significantly in feces of TiO2 NPs-exposed rats, leading to changes of metabolic function of gut microbiota. Lipopolysaccharides (LPS) produced by gut microbiota increased significantly, which may be a key factor in the subsequent liver effects.ConclusionsTiO2 NPs could induce slight hepatotoxicity at dose of 50 mg/kg after long-term oral exposure. The indirect pathway of the gut-liver axis, linking liver metabolism and gut microbiota, played an important role in the underlying mechanisms.

The protective effects of vitamin C on common carp (Cyprinus carpio) exposed to titanium oxide nanoparticles (TiO2-NPs)

The aim of this study was to investigate the hematological, biochemical, immunological, oxidative and mucosal changes in common carp (Cyprinus carpio) (15.18 ± 0.22 g) exposed to titanium oxide nanoparticles (TiO2-NPs), as well as the possible role of vitamin C in counteracting undesirable effects. Six experimental groups were examined for 21 days. T1: Control- basal diet; T2: TiO2-NPs (0.125 mg L−1) + basal diet; T3: basal diet + vitamin C (500 mg kg−1 of food); T4: basal diet + vitamin C (1000 mg kg−1 of food); T5: basal diet + vitamin C (500 mg kg−1 of food) + TiO2-NPs (0.125 mg L−1); T6: basal diet + vitamin C (1000 mg kg−1 of food) + TiO2-NPs (0.125 mg L−1). The results showed that TiO2-NPs alone significantly elevated the level of biomarkers for stress (glucose, cortisol) and liver damage (ALT, AST, ALP) and significantly declined immune parameters of serum (TP, Ig, ACH50, LYZ) and mucus (Ig, LYZ) due to increased oxidative stress and lower activity of antioxidant enzymes compared to the control group. In addition, TiO2 caused some histological damages to liver, however the severity of these damages was lower in fish supplemented with 1000 mg kg−1 vitamin C compared to other TiO2 exposed groups. Vitamin C supplementation considerably prevented TiO2-NPs-induced changes and attenuated the intensity of liver damages. In conclusion, although TiO2-NPs produced toxicity in Cyprinus carpio, supplementation of diet with vitamin C at a level of 500 to 1000 mg kg−1 of feed could effectively prevent oxidative stress and undesirable effects of TiO2-NPs exposure.

TiO2 nanoparticles and multi-walled carbon nanotubes monitoring and bioremediation potential using ciliates Pseudocohnilembus persalinus

In recent years, the release of nanomaterials pollutants to water bodies, to a great extent, attributed to anthropogenic activities. Their impacts on aquatic organisms as well as nanomaterial monitoring and bioremediation using organism have drawn much attentions. However, studies on relationship of nano-contaminants and aquatic organisms are very scarce. Our results showed that titanium dioxide nanoparticles (TiO2-NPs) and Multi-walled carbon nanotubes (MWCNTs) caused an obvious cell decreases on the whole, but a significant increase at 48 h TiO2-NPs exposure, indicating a resistant mechanism in ciliates for nano-toxic. Besides, MWCNTs was more toxic to Pseudocohnilembus persalinus than that of TiO2-NPs in terms of EC50 value. It is firstly found that P. persalinus ingested and released TiO2-NPs through cytostome and cytoproct, which might be the reason that TiO2-NPs less toxic than MWCNTs. The significantly increased superoxide dismutase (SOD) and glutathione S-transferase (GST) enzyme activities and expression levels were evaluated by reactive oxygen species ROS generation, which demonstrated that P. persalinus antioxidant defense enzyme played roles on nano-toxic resistant in ciliates. Moreover, the integrated biomarker response (IBR) was also determined, which demonstrated that MWCNTs had comparatively higher values than those of TiO2-NPs after higher concentration exposure to ciliates. In addition, it was confirmed by the present work that sod, gst and cat played different roles on immunity, and the sensitivity of cat gene expression to these two nanomaterials exposure was dissimilar. Damages of shrunk as well as losses of cilia on the cell surface caused by TiO2-NPs and MWCNTs exposure in P. persalinus using SEM revealed possible physical hazards of aggregated nanomaterials. Our findings will be helpful to understand the effect mechanisms of NPs on ciliates, and also demonstrated the possibility of P. persalinus as bio-indicator of nanomaterials in aquatic and potentials on bioremediation.

NPs-TiO2 and Lincomycin Coexposure Induces DNA Damage in Cultured Human Amniotic Cells.

Titanium dioxide nanoparticles (NPs-TiO2 or TiO2-NPs) have been employed in many commercial products such as medicines, foods and cosmetics. TiO2-NPs are able to carry antibiotics to target cells enhancing the antimicrobial efficiency; so that these nanoparticles are generally used in antibiotic capsules, like lincomycin, added as a dye. Lincomycin is usually used to treat pregnancy bacterial vaginosis and its combination with TiO2-NPs arises questions on the potential effects on fetus health. This study investigated the potential impact of TiO2-NPs and lincomycin co-exposure on human amniocytes in vitro. Cytotoxicity was evaluated with trypan blue vitality test, while genotoxic damage was performed by Comet Test, Diffusion Assay and RAPD-PCR for 48 and 72 exposure hours. Lincomycin exposure produced no genotoxic effects on amniotic cells, instead, the TiO2-NPs exposure induced genotoxicity. TiO2-NPs and lincomycin co-exposure caused significant increase of DNA fragmentation, apoptosis and DNA damage in amniocytes starting from 48 exposure hours. These results contribute to monitor the use of TiO2-NPs combined with drugs in medical application. The potential impact of antibiotics with TiO2-NPs during pregnancy could be associated with adverse effects on embryo DNA. The use of nanomaterials in drugs formulation should be strictly controlled in order to minimize risks.

Differential responses of encoding-amoA nitrifiers and nir denitrifiers in activated sludge to anatase and rutile TiO2 nanoparticles: What is active functional guild in rate limiting step of nitrogen cycle?

The long-terms effects of different crystal-composition TiO2 nanoparticles (NPs) on nitrogen-cycle-related functional guilds in activated sludge remain unclear, especially under natural light irradiation. Accordingly, activated sludge was exposed to anatase TiO2-NPs (TiO2-A) and rutile TiO2-NPs (TiO2-R) for up to 45 days. With markedly (p < 0.05) reducing nitrification-/denitrification-enzymatic-activities and abundances of ammonia-oxidizing-microorganisms (AOMs) and nitrite-reducing-bacteria (NRB), TiO2-NPs triggered bacteria and archaea UPGMA clustering and a deep modification of N-cycling functional diversity guided by crystal structure. in situ13C-DNA-SIP confirmed ammonia-oxidizing-bacteria (AOB) (Nitrosomonas and Nitrosospira) in original sludge as main active AOMs with 75.4 times more abundance than ammonia-oxidizing-archaea (AOA), while AOA within Nitrosopumilus and Nitrososphaera genera were the main active AOMs and tended to aggregate inside sludge after 10-mg/L TiO2-NPs exposure. Encoding-nirK NRB were more sensitive, while encoding-nirS Zoogloea with a total share of 4.97% to 14.93%, etc. were the main active NRB. AOB was more sensitive to TiO2-A, while TiO2-R showed the stronger toxicity to AOA and NRB resulting from differences in water environmental behaviors and crystal characteristics of two TiO2-NPs. This work expands understanding of the ecological risks of titanium-dioxide-crystal-NPs in aquatic environment and may help devise better methods to alleviate environmental stress caused by NPs at wastewater treatment plants.

Molecular mechanisms underlying titanium dioxide nanoparticles (TiO2NP) induced autophagy in mesenchymal stem cells (MSC)

ABSTRACTThe bone marrow is one of the target tissues for titanium dioxide nanoparticles (TiO2NP) following environmental exposure. At present, the consequences of TiO2NP exposure in bone are not well known. The aim of this study was to investigate the effects of TiO2NP on mesenchymal stem cells (MSCs) and potential underlying mechanisms. Mesenchymal bone marrow-derived cells were cultured and treated with various concentrations of TiO2NP. Results showed that TiO2NP incubation produced cytotoxicity as evidenced by reduced cell viability. Using Western blotting TiO2NP was found to increase autophagy as determined by elevation in ratio of LC3-II from LC3-I without evidence of necrotic cell death as estimated by lactic dehydrogenase (LDH) level. TiO2NP produced a rise in intracellular reactive oxygen species (ROS) levels. The observed alterations in autophagy and oxidant stress were associated with upregulation of protein expression of p38, JNK, and ERK. Data indicate that TiO2NP-mediated decrease in MSC survival involves a complex series of events associated stimulation of mitogen-activated protein kinase (MAPK) pathway and consequent autophagy and oxidative damage.

Foliar spray of TiO2 nanoparticles prevails over root application in reducing Cd accumulation and mitigating Cd-induced phytotoxicity in maize (Zea mays L.)

Cadmium (Cd) pollution is considered one of the global environmental issues due to its adverse effects on plant and human health. With the rapid development of nanotechnology and the practical application of engineered nanoparticles (ENPs) in agriculture, the mechanisms underlying the interactions between NPs and heavy metal on their uptake, accumulation, and phytotoxicity in crops are still not fully understood. Therefore, the impact of TiO2 NPs (0, 100, 250 mg/L) and Cd (0, 50 μM) co-exposure on hydroponic maize (Zea mays L.) was determined under two exposure modes. Results showed that root co-exposure to TiO2 NPs and 100 mg/L Cd significantly enhanced Cd uptake and produced greater phytotoxicity in maize than foliar exposure to TiO2 NPs. Meanwhile, plant dry weight and chlorophyll content showed a reduction of 45.3% and 50.5%, respectively, when compared with single Cd treatment. In addition, the accumulation of Ti in shoots and roots increased by 1.61 and 4.29 times, respectively when root exposure to 250 mg/L TiO2 NPs. By contrast, foliar exposure of TiO2 NPs could markedly decrease shoot Cd contents from 15.2% to 17.8% and had a stronger influence on alleviating Cd-induced toxicity via increasing superoxide dismutase (SOD) and glutathione S-transferase (GST) activities and upregulating several metabolic pathways, including galactose metabolism and citrate cycle, alanine, aspartate and glutamate metabolism, as well as glycine, serine and threonine metabolism. This study provides a new strategy for the application of TiO2 NPs in crop safety production in Cd contaminated soils.

Effect of Long-Term Intake of Dietary Titanium Dioxide Nanoparticles on Intestine Inflammation in Mice.

Early stage exposure of foodborne substances, such as brightening agent titanium dioxide nanoparticles (TiO2 NPs), can cause long-term effects in adulthood. We aimed to explore the potential adverse effect of long-term dietary intake of TiO2 NPs. After feeding for 2-3 months from weaning, TiO2 NPs-exposed mice showed lower body weight and induced intestinal inflammation. However, this phenomenon was not observed in gut microbiota-removed mice. TiO2 NPs exposure rarely affected the diversity of microbial communities, but significantly decreased the abundance of several probiotic taxa including Bifidobacterium and Lactobacillus. Additionally, TiO2 NPs aggravated DSS-induced chronic colitis and immune response in vivo, and reduced the population of CD4+T cells, regulatory T cells, and macrophages in mesenteric lymph nodes. Therefore, dietary TiO2 NPs could interfere with the balance of immune system and dynamic of gut microbiome, which may result in low-grade intestinal inflammation and aggravated immunological response to external stimulus, thus introducing potential health risk.