Assessment of pulmonary toxicity of gold nanorods following intra-tracheal instillation in rats

The present investigation was aimed to evaluate the pulmonary toxicity of 10 and 25 nm gold nanorods (GNRs) following intra-tracheal instillation in rats using bronchoalveolar lavage (BAL) fluid and lung histopathological analysis. The GNRs displayed that the dose-dependent toxicity via elevated lactate dehydrogenase leakage, alkaline phosphatase, lipid peroxidation and total microprotein levels in BAL fluids after 1 day, 1 week and 1 month post exposure periods. All the parameters were returned to normal values after 3 months post exposure period may be due to recovery. The rat lung histopathology displayed that accumulation of macrophages, inflammatory response and tissue thickening for both sizes of GNRs. 10 nm GNRs increased all BAL fluid parameters significantly following 1 day, 1 week and 1 month post exposure periods whereas 25 nm GNRs have shown similar effects but less extent. These investigations proposed that the dose and size dependent pulmonary toxicity of GNRs.     

Combustion-derived nanoparticles: mechanisms of pulmonary toxicity

1. The general term 'nanoparticle' (NP) is used to define any particle less than 100 nm in at least one dimension and NPs are generally classified as natural, anthropogenic or engineered in origin. Anthropogenic, also referred to as 'ultrafine' particles (UFPs), are predominately combustion derived and are characterized by having an equivalent spherical diameter less than 100 nm. 2. These particles, considered to be 'combustion-derived nanoparticles' (CDNPs), are of toxicological interest given their nanosized dimensions, with properties not displayed by their macroscopic counterparts. 3. The pulmonary deposition efficiency of inhaled UFPs, along with their large surface areas and bound transition metals, is considered important in driving the emerging health effects linked to respiratory toxicity. 4. The toxicology of CDNPs is currently used to predict the health outcomes in humans following exposure to manufactured NPs. Their similar physicochemistry would suggest similar adverse health effects (i.e. pulmonary (and perhaps cardiac) toxicity). As such, it is essential to fully understand CDNP nanotoxicology in order to minimize occupational and environmental exposure.     

Simple in vitro models can predict pulmonary toxicity of silver nanoparticles

To study the effects of nanomaterials after inhalation, a large number of in vitro lung models have been reported in literature. Although the in vitro models contribute to the reduction of animal studies, insufficient data exists to determine the predictive value of these in vitro models for the in vivo situation. The aim of this study was to determine the correlation between in vitro and in vivo data by comparing the dose metrics of silver nanoparticles in an in vitro lung model of increasing complexity to our previously published in vivo inhalation study. In vivo, the previously published study showed that the alveolar dose expressed as particle surface area is the most suitable dose metric to describe the toxicity of silver nanoparticles after inhalation. The results of the present study show that particle surface area is a suitable dose metric to describe the effects of silver nanoparticles when using a simple monolayer of lung epithelial cells. The dose metric shifted from particle surface area to particle mass when adding an increasing number of macrophages. In addition, a co-culture of endothelial cells, epithelial cells and macrophages on a Transwell® insert correlated less well to the in vivo results compared to the epithelial monolayer. We conclude that for studying the acute pulmonary toxicity of nanoparticles simple in vitro models using an epithelial monolayer better predict the in vivo response compared to complex co-culture models.     

Pulmonary toxicity assessment of multiwalled carbon nanotubes in rats following intratracheal instillation

In this study, we have evaluated the pulmonary toxicity of intratracheally (i.t.) instilled two multi walled carbon nanotubes (MWCNT) in rats. The lungs of rats were instilled with phosphate buffered saline + 1% of Tween 80 or MWCNT or carbonyl iron or quartz particles at a dose of 0.2, 1, and 5 mg/kg b.w. Following exposure, bronchoalveolar lavage (BAL) fluid was collected from the lungs to analyze lactate dehydrogenase (LDH), alkaline phosphatase (ALP), lipid peroxidation products (MDA; malondialdehyde), and total microprotein (MTP) levels at 24 h, one week, one month, and three months post instillation periods. The lungs of particle exposed rats were also collected at the same intervals to evaluate for histopathology. Exposures of MWCNT and quartz particles to rats produced transient dose dependant increase in BAL fluid LDH, ALP, MDA, and MTP values than control at all post exposure periods. Results of lung histopathology revealed that exposure of MWCNT produced a dose dependant focal peribronchiolar lymphoid aggregates, foamy alveolar macrophage accumulation, lymphoplasmocytic infiltration, fibrosis and diffuse alveolar damage. In conclusion, instillation of MWCNT produced a greater pulmonary toxicity in rats and was comparable with that of quartz. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2012.     

Assessment of cellular toxicity of TiO2 nanoparticles for cardiac tissue engineering applications

Abstract

Because of the increased use of titanium dioxide (TiO₂) nanoparticles (NPs) in tissue engineering (TE), and in new constructs for cardiac TE, their effect was studied on three relevant cell types: Adult rat ventricular cardiomyocytes, human embryonic stem cell-derived cardiomyocytes (hESC-CM) and fibroblasts. For adult rat myocytes, 10 μg/mL TiO₂ NPs showed no significant effect on myocyte survival over 24 h or acute myocyte contractility. Increasing the concentration to 100 μg/mL was seen to reduce contraction amplitude (p < 0.05). For hESC-CM, 10 μg/mL TiO₂ reduced the beating rate significantly by 24 h. No arrhythmias or cessation of beating were observed in either cell type. Culturing fibroblasts in 5–150 μg/mL TiO₂ significantly reduced cell proliferation at day 4 and increased cell death. We conclude that there may be modest but potentially adverse effects of TiO₂ NPs if used in fast degrading polymers for myocardial tissue engineering (MTE) applications.     

Assessment of the toxicity of silver nanoparticles in vitro: A mitochondrial perspective

The major toxicological concern associated with nanomaterials is the fact that some manufactured nanomaterials are redox active, and some particles transport across cell membranes, especially into mitochondria. Thus, evaluation of their toxicity upon acute exposure is essential. In this work, we evaluated the toxicity of silver nanoparticles (40 and 80 nm) and their effects in rat liver mitochondria bioenergetics.Wistar rat liver mitochondria demonstrate alterations in respiration and membrane potential capacities in the presence of either 40 or 80 nm silver nanoparticles. Our data demonstrated a statistically significant decrease in mitochondrial membrane potential, ADP-induced depolarization, and respiratory control ratio (RCR) upon exposure to silver nanoparticles.Our results show that silver nanoparticles cause impairment of mitochondrial function, due mainly to alterations of mitochondrial membrane permeability. This results in an uncoupling effect on the oxidative phosphorylation system. Thus, mitochondrial toxicity may have a central role in the toxicity resulting from exposure to silver nanoparticles.     

钙纳米粒子急性毒性及长期毒性试验

近年来纳米粒子的研制及应用已成为一个研究热点[1].该文观察了钙纳米粒子对小鼠的急性毒性和对大鼠的长期毒性,以评价钙纳米粒子的用药安全性.     

Assessing toxicity of fine and nanoparticles: comparing in vitro measurements to in vivo pulmonary toxicity profiles.

Previous studies have reported little correlation between the relative toxicity of particle types when comparing lung toxicity rankings following in vivo instillation versus in vitro cell culture exposures. This study was designed to assess the capacity of in vitro screening studies to predict in vivo pulmonary toxicity of several fine or nanoscale particle types in rats. In the in vivo component of the study, rats were exposed by intratracheal instillation to 1 or 5 mg/kg of the following particle types: (1) carbonyl iron (CI), (2) crystalline silica (CS) (Min-U-Sil 5, alpha-quartz), (3) precipitated amorphous silica (AS), (4) nano-sized zinc oxide (NZO), or (5) fine-sized zinc oxide (FZO). Depending on particle type and solution state, these particles range in size from 90 to 500 nm in size. Following exposures, the lungs of exposed rats were lavaged and inflammation (neutrophil recruitment) and cytotoxicity end points (bronchoalveolar lavage [BAL] fluid lactate dehydrogenase [LDH] values) were measured at 24 h, 1 week, 1 and 3 months postexposure. For the in vitro component of the study, three different culture conditions were utilized. Cultures of (1) rat L2 lung epithelial cells, (2) primary alveolar macrophages (AMs) (collected via BAL from unexposed rats), as well as (3) AM-L2 lung epithelial cell cocultures were incubated with the particle types listed above, and the culture fluids were evaluated for cytotoxicity end points (LDH, 1-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan [MTT]) as well as inflammatory cytokines (macrophage inflammatory 2 protein [MIP-2], tumor necrosis factor alpha [TNF-alpha], and interleukin-6 [IL-6]) at one (i.e., cytokines) or several (cytotoxicity) time periods. Results of in vivo pulmonary toxicity studies demonstrated that instilled CI particles produced little toxicity. CS particles produced sustained inflammation and cytotoxicity. AS particles produced reversible and transient inflammatory responses. NZO or FZO particles produced potent but reversible inflammation which was resolved by 1 month postinstillation exposure. Results of in vitro pulmonary cytotoxicity studies demonstrated a variety of responses to the different particle types, primarily at high doses. With respect to the LDH results, L2 cells were the most sensitive and exposures to nano- or fine-sized ZnO for 4 or 24 h were more cytotoxic than exposures to CS or AS particles. Macrophages essentially were resistant and epithelial macrophage cocultures generally reflected the epithelial results at 4 and 24 h incubation, but not at 48 h incubation. MTT results were also interesting but, except for nano- and fine-sized ZnO, did not correlate well with LDH results. Results of in vitro pulmonary inflammation studies demonstrated that L2 cells did not produce MIP-2 cytokines, but CS- or AS-exposed AMs and, to a lesser degree, cocultures secreted these chemotactic factors into the culture media. Measurements of TNF-alpha in the culture media by particle-exposed cells demonstrated little activity. In addition, IL-6 secretion was measured in CS, AS, and nano-sized ZnO-exposed cocultures. When considering the range of toxicity end points to five different particle types, the comparisons of in vivo and in vitro measurements demonstrated little correlation, particularly when considering many of the variables assessed in this study-such as cell types to be utilized, culture conditions and time course of exposure, as well as measured end points. It seems clear that in vitro cellular systems will need to be further developed, standardized, and validated (relative to in vivo effects) in order to provide useful screening data on the relative toxicity of inhaled particle types.     

Silver nanoparticles testicular toxicity in rat

To evaluate the potential testicular toxicity induced by silver nanoparticles (AgNPs) in Sprague Dawley rate. The protocol study was designed as follows: G1: 30 adult male rats were kept as control. G2: 30 adult male rats were administered 5.36 mg/kg of AgNPs orally, twice weekly for six months. G3: 30 adult male rats were administered 13.4 mg/kg of AgNPs orally, twice weekly for six months. The results of hormonal assay revealed that a significant decrease in testosterone level while a significant increase in LH level was obtained. The testicular homogenate showed a significant decrease in SOD activity accompanied by a significant increase in MDA level in both G2 and G3 in comparison with the control in a dose-response relationship. Sperm viability indicates a significant decrease in rats in G2 and G3 groups. A significant decrease in DNA chromatin integrity % was obtained in rats of G3 in comparison with G2 and control. The semithin and TEM sections of the testis of G2 and G3 groups showed Sertoli cells have vacuolations with a disturbance in the arrangement and the staining affinity of spermatogenic cells. The spermatogonia appeared with a moderate electron density of the nucleus and cytoplasm. The acrosome and its cap become oval and light electron dens of spermatid cells.     

Biodistribution and toxicity of spherical aluminum oxide nanoparticles

With the rapid development of the nano‐industry, concerns about their potential adverse health effects have been raised. Thus, ranking accurately their toxicity and prioritizing for in vivo testing through in vitro toxicity test is needed. In this study, we used three types of synthesized aluminum oxide nanoparticles (AlONPs): γ‐aluminum oxide hydroxide nanoparticles (γ‐AlOHNPs), γ‐ and α‐AlONPs. All three AlONPs were spherical, and the surface area was the greatest for γ‐AlONPs, followed by the α‐AlONPs and γ‐AlOHNPs. In mice, γ‐AlOHNPs accumulated the most 24 h after a single oral dose. Additionally, the decreased number of white blood cells (WBC), the increased ratio of neutrophils and the enhanced secretion of interleukin (IL)‐8 were observed in the blood of mice dosed with γ‐AlOHNPs (10 mg kg^?1). We also compared their toxicity using four different in vitro test methods using six cell lines, which were derived from their potential target organs, BEAS‐2B (lung), Chang (liver), HACAT (skin), H9C2 (heart), T98G (brain) and HEK‐293 (kidney). The results showed γ‐AlOHNPs induced the greatest toxicity. Moreover, separation of particles was observed in a transmission electron microscope (TEM) image of cells treated with γ‐AlOHNPs, but not γ‐AlONPs or α‐AlONPs. In conclusion, our results suggest that the accumulation and toxicity of AlONPs are stronger in γ‐AlOHNPs compared with γ‐AlONPs and α‐AlONPs owing their low stability within biological system, and the presence of hydroxyl group may be an important factor in determining the distribution and toxicity of spherical AlONPs. Copyright © 2015 John Wiley & Sons, Ltd.     

Oral administration of amphotericin B nanoparticles: antifungal activity,bioavailability and toxicity in rats

Amphotericin B (AMB) is used most commonly in severe systemic life-threatening fungal infections. There is currently an unmet need for an efficacious (AMB) formulation amenable to oral administration with better bioavailability and lower nephrotoxicity. Novel PEGylated polylactic-polyglycolic acid copolymer (PLGA-PEG) nanoparticles (NPs) formulations of AMB were therefore studied for their ability to kill Candida albicans (C. albicans). The antifungal activity of AMB formulations was assessed in C. albicans. Its bioavalability was investigated in nine groups of rats (n?=?6). Toxicity was examined by an in vitro blood hemolysis assay, and in vivo nephrotoxicity after single and multiple dosing for a week by blood urea nitrogen (BUN) and plasma creatinine (PCr) measurements. The MIC of AMB loaded to PLGA-PEG NPs against C. albicans was reduced two to threefold compared with free AMB. Novel oral AMB delivery loaded to PLGA-PEG NPs was markedly systemically available compared to Fungizone® in rats. The addition of 2% of GA to the AMB formulation significantly (p??790% that of Fungizone®. The novel AMB formulations showed minimal toxicity and better efficacy compared to Fungizone®. No nephrotoxicity in rats was detected after a week of multiple dosing of AMB NPs based on BUN and PCr, which remained at normal levels. An oral delivery system of AMB-loaded to PLGA-PEG NPs with better efficacy and minimal toxicity was formulated. The addition of glycyrrhizic acid (GA) to AMB NPs formulation resulted in a significant oral absorption and improved bioavailability in rats.     

Acute oral toxicity study of magnesium oxide nanoparticles and microparticles in female albino Wistar rats

Advancements in nanotechnology have led to the development of the nanomedicine, which involves nanodevices for diagnostic and therapeutic purposes. A key requirement for the successful use of the nanoparticles (NPs) in biomedical applications is their good dispensability, colloidal stability in biological media, internalization efficiency, and low toxicity. Therefore, toxicological profiling is necessary to understand the mechanism of NPs and microparticles (MPs). MgO NPs have attracted wide scientific interest due to ease of synthesis, chemical stability and unique properties. However, their toxic effects on humans should also be of concern with the increased applications of nano MgO. The present study was aimed to assess the toxicological potential of MgO NPs in comparison to their micron counterparts in female Wistar rats. Toxicity was evaluated using genotoxicity, histological, biochemical, antioxidant and biodistribution parameters post administration of MgO particles to rats through oral route. The results obtained from the investigation revealed that the acute exposure to the high doses of MgO NPs produced significant (p < 0.01) DNA damage and biochemical alterations. Antioxidant assays revealed prominent oxidative stress at the high dose level for both the particles. Toxicokinetic analysis showed significant levels of Mg accumulation in the liver and kidney tissues apart from urine and feces. Further, mechanistic investigational reports are warranted to document safe exposure levels and health implications post exposure to high levels of NPs.     

Novel luminescence assay offers new possibilities for the risk assessment of silica nanoparticles

Recent opinions of the Scientific Committee on Consumer Products (SCCP) of the European Commission emphasize the missing validation of in vitro methodologies for nanomaterials and suggest that a review of the safety of insoluble nanomaterials presently used is required. Therefore the influence of Fluospheres® and silica nanoparticles, representing the class of organic and inorganic nanoparticles, respectively, on the lactate dehydrogenase (LDH) assay and the novel luminescence based Vialight® assay was tested. While LDH assay showed strong interactions with the tested silica particles, these problems may be overcome by novel methods like luminescence based assays. These findings suggest that even well characterized assay systems need a careful evaluation of the particle assay interactions when working with nanoparticles. Furthermore, particles based on the same material exhibit different biological properties depending on whether the material is used in micro- or nanometer range.     

Reproductive toxicity induced by nickel nanoparticles in Caenorhabditis elegans

To investigate the reproductive toxicity and underlying mechanism of nickel nanoparticles (Ni NPs), Caenorhabditis elegans (C. elegans ) were treated with/without 1.0, 2.5, and 5.0 μg cm^?2 of Ni NPs or nickel microparticles (Ni MPs). Generation time, fertilized egg numbers, spermatide activation and motility were detected. Results indicated, under the same treatment doses, that Ni NPs induced higher reproductive toxicity to C. elegans than Ni MPs. Reproductive toxicities observed in C. elegans included a decrease in brood size, fertilized egg and spermatide activation, but an increase in generation time and out‐of‐round spermatids. The reproductive toxicity of Ni NPs on C. elegans may be induced by oxidative stress. The reproductive toxicity in C. elegans induced by Ni NPs is consistent with our previous results in the rats. Therefore, C. elegans can be used as an alternative model to detect the early reproductive toxicity of Ni NPs exposure. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1530–1538, 2017.     

Acute inhalation toxicity of cerium oxide nanoparticles in rats

The aim of the present study was to assess the acute toxic potential of cerium oxide nanoparticles (CeO₂ NPs) in rats when exposed through the head and nose inhalation route. The rats were exposed to CeO₂ NPs and the resultant effects if any, to cause cytotoxicity, oxidative stress and inflammation in the lungs were evaluated on a 24 h, 48 h and 14 day post exposure period. Our results showed a significant decrease in the cell viability, with the increase of lactate dehydogenase, total protein and alkaline phosphatase levels in the bronchoalveolar lavage fluid (BALF) of the exposed rats. Total leukocyte count and the percentage of neutrophils in BALF were elevated within 24 h of post exposure. The concentrations of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) were significantly increased in the BALF and in the blood throughout the observation period. The level of malondialdehyde was elevated with the decreased levels of intracellular reduced glutathione (GSH) in the lung after exposure. The alveolar macrophages (AMs) and neutrophils overloaded with phagocytosed CeO₂ NPs were observed along with non-phagocytosed free CeO₂ NPs that were deposited over the epithelial surfaces of the bronchi, bronchiole and alveolar regions of lungs within 24 h of post exposure and were consistent throughout the observation period. A well distributed, multifocal pulmonary microgranulomas due to impairment of clearance mechanism leading to biopersistence of CeO₂ NPs for an extended period of time were observed at the end of the 14 day post exposure period. These results suggest that acute exposure of CeO₂ NPs through inhalation route may induce cytotoxicity via oxidative stress and may lead to a chronic inflammatory response.     

Gender difference in hepatic toxicity of titanium dioxide nanoparticles after subchronic oral exposure in Sprague‐Dawley rats

Existing literature pointed out that the liver may be the target organ of toxicity induced by titanium dioxide nanoparticles (TiO₂ NPs) via oral exposure. Gender differences in health effects widely exist and relevant toxicological research is important for safety assessment. To explore the gender susceptibility of TiO₂ NP‐induced hepatic toxicity and the underlying mechanism, we examined female and male Sprague‐Dawley rats administrated with TiO₂ NPs orally at doses of 0, 2, 10 and 50 mg/kg body weight per day for 90 days. The serum biochemical indicators and liver pathological observation were used to assess hepatic toxicity. We found significant hepatic toxicity could be induced by subchronic oral exposure to TiO₂ NPs, which was more obvious and severe in female rats. No accumulation of TiO₂ NPs in the liver was observed, indicating that hepatic toxicity may not be caused through direct pathways. Oxidized glutathione, lipid peroxidation products increased significantly and reduced glutathione decreased significantly in the liver of rats in repeated TiO₂ NP‐exposed groups. Hematological parameters of white blood cells and inflammatory cytokines in serum including interleukin 1α, interleukin 4 and tumor necrosis factor also increased significantly. Indirect pathways through initiating oxidative stress and inflammatory responses were suggested as the possible mechanism of the hepatic toxicity in this experiment. The higher sensitivity to redox homeostasis imbalance and inflammation of female rats may be the main reason for gender differences. Our research suggested that gender should be a susceptible factor for identifying and monitoring long‐term oral toxicity of TiO₂ NPs.     

Effects of silver and gold nanoparticles of different sizes in human pulmonary fibroblasts

Abstract

Silver and gold nanoparticles (Ag–AuNPs) are currently some of the most manufactured nanomaterials. Accordingly, the hazards associated with human exposure to Ag–AuNPs should be investigated to facilitate the risk assessment process. In particular, because pulmonary exposure to Ag–AuNPs occurs during handling of these nanoparticles, it is necessary to evaluate the toxic response in pulmonary cells. The aim of this study was to evaluate the in vitro mechanisms of toxicity of different sizes of silver (4.7 and 42?nm) and gold nanoparticles (30, 50 and 90?nm) in human pulmonary fibroblasts (HPF). The toxicity was evaluated by observing cell viability and oxidative stress parameters. Data showed that AgNPs-induced cytotoxicity was size-dependent, whereas the AuNPs of the three sizes showed similar cytotoxicity. Silver nanoparticles of 4.7?nm were much more toxic than the large silver nanoparticles and the AuNPs. However, the pre-treatment with the antioxidant, N-acetyl-l-cysteine, protected HPF cells against treatment with Ag–AuNPs. The oxidative stress parameters revealed significant increase in reactive oxygen species levels, depletion of glutathione level and slight, but not statistically significant inactivation of superoxide dismutase, suggesting generation of oxidative stress. Hence, care has to be taken while processing and formulating the Ag–AuNPs till their final finished product.     

Oral subchronic exposure to silver nanoparticles in rats

Because of their extremely small size, silver nanoparticles (AgNPs) show unique physical and chemical properties, with specific biological effects, which make them particularly attractive for being used in a number of consumer applications. However, these properties also influence the potential toxicity of AgNPs. In this study, we assessed the potential toxic effects of an in vivo oral sub-chronic exposure to polyvinyl pyrrolidone coated AgNPs (PVP-AgNPs) in adult male rats. We also assessed if oral PVP-AgNPs exposure could alter the levels of various metals (Fe, Mg, Zn and Cu) in tissues. Rats were orally given 0, 50, 100 and 200 mg/kg/day of PVP-AgNPs. Silver (Ag) accumulation in tissues, Ag excretion, biochemical and hematological parameters, metal levels, as well as histopathological changes and subcellular distribution following PVP-AgNPs exposure, were also investigated. After 90 days of treatment, AgNPs were found within hepatic and ileum cells. The major tissue concentration of Ag was found in ileum of treated animals. However, all tissues of PVP-AgNPs-exposed animals showed increased levels of Ag in comparison with those of rats in the control group. No harmful effects in liver and kidney, as well as in biochemical markers were noted at any treatment dose. In addition, no hematological or histopathological changes were found in treated animals. However, significant differences in Cu and Zn levels were found in thymus and brain of PVP-AgNPs-treated rats.     

Repeated oral dose toxicity study of nickel oxide nanoparticles in Wistar rats: a histological and biochemical perspective

Despite the increasing use of nickel oxide (NiO) nanoparticles (NPs), limited information is available on their toxicological effects. Health consequences of 28 days repeated oral exposure to NiO NPs have not been explored thoroughly. Hence, toxicity investigations were performed after 28‐day daily exposure in albino Wistar rats with NiO NPs following Organization for Economic Co‐operation and Development test guideline 407. Histopathology, biochemical indices including oxidative stress and biodistribution patterns were evaluated to decipher the toxicological impact of NiO NPs. NiO NP characterization by transmission electron microscopy showed an average size of 12.9 (±3.4) nm. Histological studies depicted a prominent impact on the vital organs of the rats. A dose‐dependent rise in both aminotransferase enzyme values was recorded in the homogenates of liver and kidney tissues. A significant decrease in superoxide dismutase activity and increase in catalase activity was noted. Further, a dose‐dependent decrease in reduced glutathione content was recorded in rats, which suggested generation of reactive oxygen species and oxidative stress. Increase in the malondialdehyde levels was observed with an increase in the dose substantiating the antioxidant enzyme activity profiles. Biodistribution studies indicated maximum accumulation of Ni content in liver followed by kidney. Excretion of Ni was predominantly through feces and a little through renal clearance. Our study indicated that NiO NPs adversely alter the biochemical profile of the rats and cause histological damage. Further investigations are warranted to address the mechanism by which physiological path these NiO NPs exhibit their toxic nature in in vivo.     

Health hazards of nanoparticles: understanding the toxicity mechanism of nanosized ZnO in cosmetic products

In recent years, nanoparticles are being used extensively in personal healthcare products such as cosmetics, sunscreens, soaps, and shampoos. Particularly, metal oxide nanoparticles are gaining competence as key industrial constituents, progressing toward a remarkable rise in their applications. Zinc oxide and titanium oxide nanoparticles are the most commonly employed metal oxide nanoparticles in sunscreens, ointments, foot care, and over the counter topical products. Dermal exposure to these metal oxides predominantly occurs through explicit use of cosmetic products and airway exposure to nanoparticle dusts is primarily mediated via occupational exposure. There is a compelling need to understand the toxicity effects of nanoparticles which can easily enter the cells and induce oxidative stress. Consequently, these products have become a direct source of pollution in the environment and thereby greatly impact our ecosystem. A complete understanding of the toxicity mechanism of nano-ZnO is intended to resolve whether and to what extent such nanoparticles may pose a threat to the environment and to human beings. In this review article, we have discussed the characteristics of metal oxide nanoparticles and its applications in the cosmetic industry. We have also highlighted about their toxicity effects and their impact on human health.