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Some basic research has shown that nanomaterials can aggravate allergic asthma. However, its potential mechanism is insufficient. Based on the research that alumina nanopowder (nAl 2 O 3 ) has been reported to cause lung tissue damage, the purpose of this study was to explore the relationship between nAl 2 O 3 and allergic asthma as well as its molecular mechanism. In this study, Balb/c mice were sensitized with ovalbumin (OVA) to construct the allergic asthma model while intratracheally administered 0.5, 5 or 50 mg kg -1 ·day -1 nAl 2 O 3 for 3 weeks. It was observed that exposure to nAl 2 O 3 exacerbated airway hyperresponsiveness (AHR), airway remodeling, and inflammation cell infiltration, leading to lung function damage in mice. Results revealed that nAl 2 O 3 could increase ROS levels and decrease GSH levels in lung tissue, promote the increases of the T-IgE, TGF-β, IL-1β and IL-6 levels, stimulate the overexpression of transcription factors GATA-3 and RORγt, decrease the levels of IFN-γ and IL-10 and increase the levels of IL-4 and IL-17A, resulting in the imbalance of Th1/Th2 and Treg/Th17 immune responses. In addition, antioxidant Vitamin E (Vit E) could alleviate asthma-like symptoms through blocking oxidative stress. The study displayed that exposure of nAl 2 O 3 deteriorated allergic asthma through promoting the imbalances of Th1/Th2 and Treg/Th17., (Copyright © 2019. Published by Elsevier Ltd.)

Because of its unique magnetic properties, the iron oxide (Fe₃O₄) nanoparticle has been widely exploited and its application in various fields has promised immense benefits. However, doubts exist over the use of Fe₃O₄-nanoparticles in human beings. Thus, the aim of the current study was to find out the potential safety range of medical use. Twenty-five Kunming mice were exposed to Fe₃O₄-nanoparticles via intraperitoneal injection daily for 1 week at doses of 0, 5, 10, 20, and 40 mg/kg. Hepatic and renal tissues were sliced for physiological observation. Injuries were observed in the high-dose groups (20 and 40 mg/kg) compared with the control group (0 mg/kg). Biomarkers of reactive oxygen species, glutathione, malondialdehyde, DNA-protein crosslinks, and 8-hydroxy-2'-deoxyguanosine in the hepatic and renal tissues were detected. Injury to tissues and oxidative damage to cells at the molecular level was found. The safest dose recommended from the results of this study is 5 mg/kg, as we believe this to be an upper limit balancing the benefits and risks for sub-long-term exposure.

Although the biological effects of some nanomaterials have already been assessed, information on toxicity and possible mechanisms of various particle types are insufficient. Moreover, the role of particle properties in the toxic reaction remains to be fully understood. In this paper, we aimed to explore the interrelationship between particle size, shape, chemical composition and toxicological effects of four typical nanomaterials with comparable properties: carbon black (CB), single wall carbon nanotube, silicon dioxide (SiO(2)) and zinc dioxide (ZnO) nanoparticles. We investigated the cytotoxicity, genotoxicity and oxidative effects of particles on primary mouse embryo fibroblast cells. As observed in the methyl thiazolyl tetrazolium (MTT) and water-soluble tetrazolium (WST) assays, ZnO induced much greater cytotoxicity than non-metal nanoparticles. This was significantly in accordance with intracellular oxidative stress levels measured by glutathione depletion, malondialdehyde production, superoxide dismutase inhibition as well as reactive oxygen species generation. The results indicated that oxidative stress may be a key route in inducing the cytotoxicity of nanoparticles. Compared with ZnO nanoparticles, carbon nanotubes were moderately cytotoxic but induced more DNA damage determined by the comet assay. CB and SiO(2) seemed to be less effective. The comparative analysis demonstrated that particle composition probably played a primary role in the cytotoxic effects of different nanoparticles. However, the potential genotoxicity might be mostly attributed to particle shape., (Copyright (c) 2008 John Wiley & Sons, Ltd.)

As a new type of environmental pollutant, microplastics have been increasingly receiving attention for their impact on human health. Current research indicates that microplastics can enter the human body through various routes and exert neurotoxic effects. This article reviews the types, sources, and exposure pathways of microplastics, with a focus on the neurotoxic effects and potential mechanisms of microplastic exposure at different life stages in humans (fetal, infant, adult, and elderly). This review provides a comprehensive understanding of the neurotoxicity of microplastic exposure and its implications for human health risk assessment and effective prevention strategies. [ABSTRACT FROM AUTHOR]

Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death. Therefore, understanding the toxic effects and molecular mechanisms of environmental pollution underlying these processes is crucial for developing effective strategies to mitigate the adverse effects of environmental pollutants on human health. In the present study, we summarized and reviewed the toxic effects and molecular mechanisms of mitochondrial damage, ERS, and oxidative stress caused by exposure to environmental pollutants as well as interactions inducing the cell apoptosis and the roles in exposure to environmental pollutants. [ABSTRACT FROM AUTHOR]

Extensive environmental pollution by microplastics has increased the risk of human exposure to plastics. However, the biosafety of polypropylene microplastics (PP-MPs), especially of PP particles < 10 μm, in mammals has not been studied. Thus, here, we explored the mechanism of action and effect of exposure to small and large PP-MPs, via oral ingestion, on the mouse intestinal tract. Male C57BL/6 mice were administered PP suspensions (8 and 70 μm; 0.1, 1.0, and 10 mg/mL) for 28 days. PP-MP treatment resulted in inflammatory pathological damage, ultrastructural changes in intestinal epithelial cells, imbalance of the redox system, and inflammatory reactions in the colon. Additionally, we observed damage to the tight junctions of the colon and decreased intestinal mucus secretion and ion transporter expression. Further, the apoptotic rate of colonic cells significantly increased after PP-MP treatment. The expression of pro-inflammatory and pro-apoptosis proteins significantly increased in colon tissue, while the expression of anti-inflammatory and anti-apoptosis proteins significantly decreased. In summary, this study demonstrates that PP-MPs induce colonic apoptosis and intestinal barrier damage through oxidative stress and activation of the TLR4/NF-κB inflammatory signal pathway in mice, which provides new insights into the toxicity of MPs in mammals. [ABSTRACT FROM AUTHOR]

Neutral mucin is purplish red, and acidic mucin is blue; the tissues and cells containing both neutral and acidic mucins show different degrees of purple. The values are the means ± SDs (normalized amounts of AB-PAS and immunohistochemistry, I n i = 3; intestinal-barrier-related protein level, I n i = 5). In Section 2.2, Animals and Experimental Design, in the first paragraph, lines 3-5, we make the following correction: "All animal experiments were approved by the Experimental Animal Welfare Ethics Committee of the Tianjin Institute of Environmental and Operational Medicine, IACUC approval code AMMS-04-2021-014.". [Extracted from the article]

Some basic research has shown that nanomaterials can aggravate allergic asthma. However, its potential mechanism is insufficient. Based on the research that alumina nanopowder (nAl 2 O 3) has been reported to cause lung tissue damage, the purpose of this study was to explore the relationship between nAl 2 O 3 and allergic asthma as well as its molecular mechanism. In this study, Balb/c mice were sensitized with ovalbumin (OVA) to construct the allergic asthma model while intratracheally administered 0.5, 5 or 50 mg kg−1·day−1 nAl 2 O 3 for 3 weeks. It was observed that exposure to nAl 2 O 3 exacerbated airway hyperresponsiveness (AHR), airway remodeling, and inflammation cell infiltration, leading to lung function damage in mice. Results revealed that nAl 2 O 3 could increase ROS levels and decrease GSH levels in lung tissue, promote the increases of the T-IgE, TGF-β, IL-1β and IL-6 levels, stimulate the overexpression of transcription factors GATA-3 and RORγt, decrease the levels of IFN-γ and IL-10 and increase the levels of IL-4 and IL-17A, resulting in the imbalance of Th1/Th2 and Treg/Th17 immune responses. In addition, antioxidant Vitamin E (Vit E) could alleviate asthma-like symptoms through blocking oxidative stress. The study displayed that exposure of nAl 2 O 3 deteriorated allergic asthma through promoting the imbalances of Th1/Th2 and Treg/Th17. Image 1 • Evaluated the effect of nAl 2 O 3 on allergic asthma mice. • Revealed that exposure to nAl 2 O 3 via intratracheal instillation could exacerbate AHR in mice. • It was the imbalance between Th2 and Th17 type immune responses induced by oxidative stress that aggravated asthma symptoms. Intratracheal instillation of nAl 2 O 3 aggravated the imbalance of th2-type th17-type immune, induced airway hyperresponsiveness and subsequently deteriorated allergic asthma in mice. [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]

The molecular mechanisms of PM 2.5 exposure in the male reproductive system, have scarcely been studied. Here, we demonstrate the possible relationship and molecular mechanisms between endoplasmic reticulum stress (ERS), oxidative stress, and reproductive toxicity caused by PM 2.5. A "PM 2.5 real-time online concentrated animal whole-body exposure system" was employed to expose male Wistar rats to PM 2.5 for 12 weeks, which could induce sperm quality decline, apoptosis, inflammation, oxidative stress, ERS, and histopathological damage in the testis. In vitro study on cultured primary testicular spermatogonia and Leydig cells confirmed that treatment with PM 2.5 (0–320 μg/mL) for 24 h decreased cell survival rate, increased reactive oxygen species, lactate dehydrogenase and 8-hydroxydeoxyguanosine levels, induced DNA damage, ERS and apoptosis, and inhibit the secretion and synthesis of testosterone in Leydig cells. These results clarified that ERS pathways triggered by oxidative stress could significantly induce CHOP and caspase-12 activation, which are significantly associated with cell apoptosis. However, oxidative stress and ERS inhibitors significantly inhibited the occurrence of these injuries. In conclusion, PM 2.5 triggers the ERS pathway and induces DNA damage in rat testicular cells through oxidative stress, ultimately leading to cellular apoptosis. Furthermore, high-concentration intermittent inhalation was more harmful than low-concentration continuous inhalation when the total mass of PM 2.5 exposure was the same. [Display omitted] • PM 2.5 can cause reproductive toxicity in male Wistar rats. • PM 2.5 can cause DNA damage and ERS in male rat germ cells through oxidative stress. • PM 2.5 can activate ERS-mediated CHOP and Caspase-12 apoptosis pathways. • PM 2.5 can activate the DNA damage-mediated mitochondrial apoptosis pathway. • High-dose PM 2.5 intermittent exposure is more toxic than low-dose continuous exposure. [ABSTRACT FROM AUTHOR]

The toxic effects of coal combustion related fine particulate matter (PM 2.5 ), collected from Datong, Shanxi province, China, on nematode Caenorhabditis elegans were investigated. Exposure to PM 2.5 resulted in deficits in development, reproduction, locomotion behavior, and lifespan, and induction of intestinal autofluorescence or reactive oxygen species (ROS) production. Prolonged exposure to PM 2.5 led to more severe toxicity on nematodes than acute exposure. In addition, exposure to PM 2.5 induced altered expression patterns of genes required for the control of oxidative stress. Reduction in mean defecation cycle length and developmental deficits in AVL and DVB neurons, which are involved in the control of defecation behavior, were also triggered by PM 2.5 exposure. Thus, oxidative stress and abnormal defecation behavior may contribute greatly to the toxicity of coal combustion related PM 2.5 in nematodes. The results also imply that the long-term adverse effects of coal combustion related PM 2.5 on environmental organisms should be carefully considered. [ABSTRACT FROM AUTHOR]

• Nano-CuO can be transported to rat liver and cause hepatotoxicity. • Nano-CuO caused histopathological damage and apoptosis in rat liver. • Nano-CuO induced oxidative stress and inflammatory response in rat liver. • Nano-CuO caused cytotoxicity and apoptosis in BRL-3A cells. • Nano-CuO activated ERS-mediated CHOP, JNK, and Caspase-12 apoptosis pathways. Copper oxide nanoparticles (Nano-CuO) toxicity has been researched widely in recent years. However, the relationship between oxidative stress and ER-stress and the possible mechanisms induced by Nano-CuO have been rarely studied. Here, the mechanism of hepatotoxicity and apoptosis through oxidative stress and ER-stress induced by Nano-CuO was investigated in vivo and in vitro. In in vivo experiments, male Wistar rats were intranasally instilled 10 μg Nano-CuO/g body weight daily for 60 days, which caused liver function impairment, oxidative stress, inflammatory response, histopathological and ultrastructural damage, ER-stress and apoptosis in liver tissue. in vitro experiments on rat hepatocytes BRL-3A cells showed that exposure to Nano-CuO for 24 h resulted in excess production of reactive oxygen species leading to decrease in mitochondria membrane potential causing cell death by inducing apoptosis. However, administration of n-acetyl cysteine decreased the apoptosis in Nano-cuo treated group. The in vivo and in vitro experiments confirmed that oxidative stress triggered ER-stress pathway, leading to the opening of apoptosis pathways of CHOP, JNK, and Caspase-12. In summary, treatment of Nano Cuo triggered oxidative stress by ROS, which in turn resulted in activation of ER stress pathways causing cell death in liver tissue and BRL-3A cells. [ABSTRACT FROM AUTHOR]