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Tungsten trioxide nanoparticles (WO3 NPs) have shown increasing promise in biological and biomedical fields in recent years. However, their possible hazards, especially the adverse effects related to their sizes on human health and environment, are still yet poorly understood. In this study, we compared the hepatotoxicity in mice induced by WO3 nanorods of two different lengths (125−200 nm and 0.8−2 μm) via intraperitoneal injection, and explored the protective role of melatonin, an antioxidant, against the hepatotoxicity. The results showed that 10 mg/kg/day of shorter WO3 nanorods could cause obvious hepatic function impairment, histopathological lesions, and significant enhancement in levels of oxidative stress and inflammation in mouse liver. However, similar effects were found only in the 20 mg/kg/day longer WO3 nanorods–treated mice, and these adverse effects were attenuated by pretreatment with melatonin. These findings indicate that WO3 nanorods can exert hepatotoxicity in mice in a dose- and length-dependent manner, and that shorter WO3 nanorods cause more severe hepatotoxicity than their longer counterparts. Melatonin could serve as an effective protective agent against the longer WO3 nanorods–induced hepatotoxicity by decreasing the oxidative stress level. This study is important for determining the environmental and human health risks of exposure to WO3 NPs and their size-dependent toxicity, and provides an appealing strategy to avoid the adverse effects. [ABSTRACT FROM AUTHOR]

Ultrafine particles (UFPs) referred to particular matters with aerosol diameter less than 100 nm. Because of the lightweight and small size, UFPs have become an occupational inhalation risk. The UFPs will be accumulated in the deep lung through inhalation, and then reach into all the organs via circulation system; some UFPs even stay in the brain. As previous study reported, UFPs exposure is usually associated with cardiovascular disease, such as atherosclerosis (AS). In our study, we tried to understand how acute UFP exposure caused the biological dysregulation in atherosclerosis. Acute exposure of UFPs were applied to mice for 6 consecutive days, mice were sacrificed after 3, 5, 7, and 10 days post-exposure. Aorta and serum were collected for histological and biomarkers analysis. Mice aortic adventitial fibroblasts (MAFs) were isolated from mice and used to further study to understand the mechanism of UFPs induced atherosclerosis. Compared to the untreated control, the inflammation responses and nitrate stress were observed after acute exposure of UFPs, with increased IL-6, MCP-1, p47phox, and 3-NT levels in the mice serum. Besides, upregulation of microRNAs: miR-301b-3p and Let-7c-1-3p, and their downstream target: Smad2, Smad3, and TGFβ1 were also observed in mouse aorta after acute exposure of UFPs. Similar results were identified in vitro as well. Acute exposure of UFPs induced the systematic nitrate stress and inflammation responses, along with the changes of vascular permeability. Dysregulated miRNAs and TGFβ/Smads signaling pathway indicated the higher risk of atherosclerosis/vasculature remodeling when exposed to UFPs. [ABSTRACT FROM AUTHOR]

Nanomaterials have been widely used in a number of applications; however, these nanomaterials may potentially be risky for human health, particularly for the respiratory system. In this study, we used a mouse asthma model to study whether graphene oxide (GO), a promising carbonaceous nanomaterial with unique physicochemical properties, aggravates allergic asthma via the oxidative stress pathway. Mice were sensitized with ovalbumin (OVA) to trigger immune reactions, while vitamin E (Ve) was administered as an antioxidant. Our results showed that GO aggravated OVA-induced allergic asthma in mice, as suggested by increased reactive oxygen species (ROS), elevated total immunoglobulin E (IgE), upregulated Th2 response, and the aggravation of allergic asthma symptoms, such as airway remolding, collagen deposition with mucus hypersecretion, and airway hyperresponsiveness (AHR). The administration of Ve dramatically attenuated all of the above effects. In conclusion, Ve showed anti-allergic properties in antagonizing the exacerbation of allergic asthma induced by GO, providing a new possibility for the treatment of allergic asthma. [ABSTRACT FROM AUTHOR]

Growing concern has been raised over the potential hazard of nanoparticles (NPs) on human health from ambient particulate air pollution. Silicon dioxide (SiO) NPs are one of the most widely used nanoparticles in many sectors of industry. Research on NPs has focused mainly on their toxicity in organs. Meanwhile, NPs are present in the air year-round, but are more serious in winter. Thus, the aim of this study was to evaluate the inflammatory response to SiO NPs using in vivo test systems. The composition of particulate matter is complicated; however, elemental silicon accounts for a significant proportion. Cold exposure can induce many kinds of systemic reactions. Thus, the second aim of this study was also to evaluate the combined effect of NPs and cold exposure on human health. There is little research on the combined effects of nanoparticles and cold on inflammation. Sprague-Dawley rats were randomly divided into four groups: those exposed to SiO NPs by intratracheal instillation, those exposed to at 4 °C 4 h/day for 4 weeks, a combined SiO NPs and cold exposure group, and a control group. Inflammatory cell infiltration in the lungs was mainly observed after exposure to SiO NPs or cold. Hematoxylin and eosin staining revealed that inflammation of the lungs was more serious in the combined group. In the white adipose tissue and brown adipose tissue of the combined groups, the mRNA expressions of pro-inflammatory cytokines were upregulated. In conclusion, SiO NPs combined with cold exposure induced a stronger systemic inflammatory response, accompanied by more serious health hazards. [ABSTRACT FROM AUTHOR]

Sidestream cigarette smoke, the major component of environmental tobacco smoke, is a complex and reactive aerosol. The particulate matter (PM) in sidestream smoke is one of the carriers of chemical constituents. However, particle size-dependent toxicological effects of PM are poorly understood. In this study, we evaluated the relationship between the PM size and in vitro cytotoxicity and mutagenicity of sidestream cigarette smoke. A NanoMoudi-II 125A was used to collect PM samples ranging from 10 nm to 10 μm. The in vitro toxicity of PM was evaluated using a neutral red cytotoxicity assay and Salmonella mutagenicity assay. The results showed that the cytotoxicity and mutagenicity of PM larger than 1 μm was significantly lower than PM sized 10 nm-1 μm. Furthermore, there was a noticeable trend that the smaller the size of the PM of sidestream cigarette smoke, the greater the toxicity. This study suggests that the toxicity of PM in sidestream cigarette smoke is size-dependent. [ABSTRACT FROM AUTHOR]

Environmental pollutants co-exist and exhibit interaction effects that are different from those associated with a single pollutant. As one of the more commonly manufactured nanomaterials, titanium dioxide nanoparticles (TiO-NPs) are most likely to bind to other contaminants in water. In this paper, we aimed to study the combined toxicological effects of TiO-NPs and bisphenol A (BPA) on organism. First, in vitro adsorption experiments were conducted to determine the adsorptive interaction between TiO-NPs and BPA. Second, zebrafish embryo toxicity tests were performed to monitor for changes in the toxicological effects associated with the two chemicals. The study results demonstrated that adsorptive interactions exist between the two chemicals and increased toxicity effects which included an advanced toxicological effect time, decreased survival, increased morphological abnormalities, and delayed embryo hatching. Also, we suggest that the mode of combined action has a synergistic effect. Based on this, we postulate that concomitant exposure to TiO-NPs and BPA increased BPA bioavailability and uptake into cells and organisms. Further studies are required to understand the mechanisms of interactions of this mixture. [ABSTRACT FROM AUTHOR]

Chronic noise exposure has been implicated in increased risk of diabetes. However, there is limited experimental evidence of the mechanisms linking chronic noise stress and glucose metabolism. We addressed this in the present study by examining glucose metabolism, immune response, and changes in gut microbiota/host inflammatory homeostasis in rats exposed to noise for 30 consecutive days. Chronic noise exposure increased blood glucose and corticosterone levels for at least 14 days after cessation of noise. Stressed rats also exhibited elevated levels of glycogen and triglyceride in the liver and impaired hepatic insulin production via insulin-induced insulin receptor/insulin receptor substrate 1/glycogen synthase kinase 3β signalling, which persisted for 3-14 days after cessation of noise exposure. Chronic noise altered the percentage of Proteobacteria and Actinobacteria in the gut, increasing Roseburia but decreasing Faecalibacterium levels in the cecum relative to controls. Immunoglobulin A, interleukin 1β, and tumor necrosis factor α levels were also elevated in the intestine of these animals, corresponding to noise-induced abnormalities in glucose regulation and insulin sensitivity. These results suggest that lifelong environmental noise exposure could have cumulative effects on diabetes onset and development resulting from alterations in gut microbiota composition and intestinal inflammation. [ABSTRACT FROM AUTHOR]

This study mainly investigated the neurotoxicity induced by zinc oxide nanoparticle (ZnO NP) in different-aged mice and the interaction between age and ZnO NP exposure. Sixty adult and old male C57BL/6J mice were assigned to four groups based on a two-factor (age and ZnO NP exposure) design. Results showed that ZnO NPs (5.6 mg/kg, intraperitoneal) induced increased production of pro-inflammatory cytokines in the serum and the brain of mice. A synergistic reaction between aging and ZnO NP exposure occurred regarding serum interleukin 1 (IL-1) and interleukin 6 (IL-6). In the brain, increased oxidative stress level, impaired learning and memory abilities, and hippocampal pathological changes were identified, especially in old mice, following ZnO NP exposure. Then, a potential mechanism of cognitive impairment was examined. The contents of hippocampal cAMP response element binding protein (CREB), phosphorylated CREB, synapsin I, and cAMP were decreased in an age-dependent manner, and the most substantial decrease occurred in old mice treated with ZnO NPs. These findings demonstrated for the first time that aging and ZnO NP exposure synergistically influenced systemic inflammation, and indicated old individuals were more susceptible to ZnO NP-induced neurotoxicity. One of the mechanisms might due to the supression of cAMP/CREB signaling. [ABSTRACT FROM AUTHOR]