Nanotoxicology最新文献

The intensive use of rare earth elements (REEs) raises concerns about their effects on soil organisms, particularly under mixture exposure scenarios. This study evaluated the toxicity of lanthanum oxide (La₂O₃) and yttrium oxide (Y₂O₃) nanoparticles (NPs) and bulk forms on Folsomia candida. Single (0-2500 mg/kg) and dual mixture exposures were tested for effects on survival, reproduction, avoidance behavior, and biochemical markers. No effects on survival and avoidance behavior were observed. NPs were more toxic than bulk forms. La₂O₃ NPs reduced reproduction (≥ 1250 mg/kg) and acetylcholinesterase (AChE) activity (2500 mg/kg), whereas Y₂O₃ NPs exhibited greatest toxicity, reducing reproduction (≥ 313 mg/kg) and increasing catalase (CAT) (156 and 625 mg/kg) and glutathione reductase (GR) (625 and 2500 mg/kg) activities. Mixture exposures revealed complex interactions (synergism, antagonism, or no interaction), with toxicity depending on concentration, endpoint, and material form. Besides, higher number of biochemical endpoints were affected by mixture exposures, but dissimilar responses were observed with different concentrations: 2500 mg/kg Y₂O₃ NPs + 2500 mg/kg La₂O₃ NPs decreased reproduction and increased GR, glutathione S-transferases (GST) and AChE activities; 2500 mg/kg Y₂O₃ NPs + 625 mg/kg La₂O₃ NPs increased CAT, GR, GST and AChE activities; 625 mg/kg Y₂O₃ NPs + 625 mg/kg La₂O₃ NPs increased GR activity; 156 mg/kg Y₂O₃ NPs + 2500 mg/kg La₂O₃ NPs decreased AChE activity, increased GR activity and lipid peroxidation levels. This study highlights that REE exposures, particularly mixtures, can pose risks to soil organisms and emphasizes the need to include mixture interactions in risk assessments.

Increasing usage of nanoparticles or nanomaterials may lead to their release into the environment. The toxicity of these structures, classified as contaminants of emerging concern, is not yet sufficiently understood. However, as in the case of other environmental stressors, the effects of exposure to them should be analyzed on a multigenerational scale to predict the consequences for exposed populations. Therefore, this project aimed to assess the impact of graphene oxide (GO) nanomaterial on digestive enzyme activities in the house cricket Acheta domesticus as a model species, depending on GO concentration (0.2 or 0.02 µg·g^-1dry weight of food), previous selection for longevity and the number of generations (1-5) that have occurred since the beginning of exposure. The last and sixth generations were insects for which GO was withdrawn from the diet (recovery generation). Enzymatic activity was tested using API Zym kit modified for spectrophotometric reads. The tests revealed that GO intervenes with some digestive enzymes. Moreover, the effects of GO depend on the population's previous selection for longevity. The impact of mechanisms mitigating the consequences of aging supports the possible tolerance to GO intoxication. It demonstrated itself in diverse patterns of multigenerational response to GO in wild and long-lived insects. Also, multigenerational exposure revealed the 'third generation' effect. Finally, the impact of GO elimination depended on the concentration of nanomaterial used for the tests. Also, the potential impact of concentration-dependent agglomeration of GO in the context of hormesis has been discussed.

The rapid growth of nanotechnology applications and increased incorporation of engineered nanomaterials (ENMs) into consumer products across most industry sectors necessitate a comprehensive understanding of their potential long-term risks to human health. Over the past two decades, significant progress has been made in establishing the fundamentals of nanotoxicology, which has improved our understanding of ENM toxicity particularly regarding their physicochemical properties (e.g. size, shape, surface charge). Furthermore, substantial efforts have been devoted to elucidating the molecular mechanisms underlying nano-bio interactions, which are not only important for understanding health risks but are also critical for advancing therapeutic applications. However, the assessment of ENM adverse responses at low and subtoxic exposure levels, chronically or within specific contexts (e.g. co-exposure to other toxicants) has not received much attention. This is particularly important as real-world exposure to ENMs (e.g. occupational, medicinal, consumer products) typically occurs at low exposure levels, over long periods of time, in the presence of other exposures or preexisting disease. Accumulating research is demonstrating that even in the absence of overt toxicity, exposure to ENMs may contribute to adverse health outcomes, including exacerbation of co-toxicities and co-diseases. This underscores the critical need for evaluating ENM-induced adverse responses beyond conventional toxicological endpoints which are often carried out at unrealistically high doses. In this review article, we discuss the current state of the literature and highlight key emerging findings demonstrating adverse consequences of ENM exposure at low and subtoxic levels. We also discuss current challenges and future directions to address existing knowledge gaps.

Because of the intricate interactions between bacteria internalization in periodontal cells and chronic inflammatory activation, periodontal disorders remain difficult. Furthermore, the primary cause of adult tooth loss is periodontitis, one of the most common dental disorders worldwide. The key to preventing periodontitis has been to reduce the development of bacteria and the generation of substances that eventually erode the tissue surrounding and supporting the teeth. Furthermore, there are several disadvantages to treating periodontitis with antibiotics administered systemically. A naturally occurring polymer with antibacterial and anti-inflammatory properties is chitosan (CS). CS is highly interested in treating periodontal disease as a medicine carrier due to its actions against anaerobic microorganisms and possible anti-inflammatory properties. Due to the multifactorial pathophysiology of periodontitis, combining antimicrobial medications in a single drug delivery method is preferable to administering them separately since it increases the therapeutic range when numerous organisms are present. As a result, CS-based drug delivery technologies, such as gels, micro, and nanoparticles (NPs), were created to transport drugs to the periodontal pocket over an extended period. This research provides an overview of the existing therapeutic benefits of CSNP on periodontitis. This information might be used to create therapeutic substitutes based on CSNP for treating periodontal infections.

The data available in the literature on the toxicity of fullerenes are numerous but contradictory. The ambiguity of research results hinders the transition from scientific research to real-world drug development. The ability of fullerenes to accumulate in some organs and tissues is interpreted in most cases as their disadvantage, while a number of studies have shown that there is no relationship between the accumulation of fullerenes and toxic effects. Moreover, fullerenes often exert potent protective effects. The pharmacokinetics and toxicity of fullerenes depend on the route of administration and are closely related to their functionalization, since pristine fullerenes are generally harmless. These factors, as well as the risk-benefit ratio, need to be considered when developing fullerene-based drugs. In this review, open-source data on in vivo toxicity, biodistribution, metabolism, and some protective properties of both native fullerene and a number of its derivatives are collected and analyzed. The problems and prospects for using fullerenes through various methods of delivery to the body, such as through the gastrointestinal tract, intravenous administration, intraperitoneal administration, dermal application or respiratory exposure are described.

The early development of nanotechnology has spurred major interest on the toxicity of nanoparticles (NPs) due to their ability to penetrate the biological barriers such as the BBB. This review aims at addressing how silver (AgNPs), titanium dioxide (TiO₂NPs), zinc oxide (ZnONPs), iron oxide (Fe₃O₄NPs), carbon NPs, Copper (Cu-NPs), silicon oxide (SiO₂ NPs) nanoparticles and quantum dots cause neurotoxicity. Some of the major signaling that occur are the signaling related to oxidative stress, neuroinflammation, mitochondrial dysfunction and cell equilibrium, hence results in neuronal damage and neurodegeneration. It is critical to describe that there are multiple ways by how NPs may be toxic based on their size and surface, dosage, and the recipient's age and health condition. A review on in vitro and in vivo analysis provides information about the toxic potentials of NPs and preventive measures including modification of NP surface and antioxidant treatment. The results underline the necessity of comprehensive safety assessments to allow the further utilization of nanoparticles across the economy.

The understanding of nanomaterial toxicity is aided by biokinetic information pointing to potential target organs. Silver (Ag), copper oxide (CuO), and zinc oxide (ZnO) are often referred to as soluble materials in the literature. In addition, data suggest gold (Au) nanoparticles to be soluble in the mammalian body. We identified inhalation studies on these materials and extracted data on physicochemical properties, organ distribution, and excretion. Silver and gold were retained in the lung for an extended period (>2,000 and >672 hours, respectively); copper initially increased in lung and then returned to baseline at ∼500 hours. Zinc increased in the lungs after short-term exposure to zinc oxide, but not after prolonged exposure. In blood, silver initially increased after inhalation but then gradually declined over ∼200 hours. Gold was elevated in the blood after exposure to 4, 7, 11, and 13 nm particles (but not particles of 20, 34, and 105 nm) and remained elevated for at least 672 hours after exposure to the 4 and 11 nm particles. Silver increased in the liver and spleen and was still present 2,000 hours post exposure. Gold was elevated in several organs, including the spleen and kidney, for more than 600 hours post exposure, indicating persistence in some organs. Both silver and gold were increased in the brain and olfactory bulb. Overall, we found no large differences in the biodistribution of the four nanomaterials but note that silver and gold were still increased in several organs at the last investigated post-exposure time points.

Vehicle engine exhausts contain complex mixtures of gaseous and particulate pollutants, which are known to affect lung functions adversely. Many in vitro studies have shown that exposure to engine exhaust can induce oxidative stress in lung cells, leading to cellular inflammation and cytotoxicity. However, it remains challenging to identify key harmful components and their specific adverse effects via traditional toxicological assessments. Machine learning (ML) methods offer new ways of analyzing such complex datasets and have gained attention in predicting toxicity outcomes and identifying key pollutants in mixtures responsible for adverse effects in a non-biased way. This study aims to understand the contribution of exhaust components to lung cell toxicity using ML techniques. Data were reanalyzed from previous studies (2015-2018), where a 3D human epithelial airway tissue model was exposed to gasoline and diesel engine exhausts under air-liquid interface (ALI) conditions with different fuels and exhaust after-treatment systems. This dataset included exhaust characteristics (particle number (PN), carbon monoxide (CO), total gaseous hydrocarbons (THC), and nitrogen oxides (NOx) levels) and corresponding biological responses (cytotoxicity, oxidative stress, and inflammatory responses). The relationships between pollutants and biological responses were explored using ML techniques, including hierarchical and nonhierarchical clustering and principal component analysis. The findings reveal both gaseous (CO, THC, and NOx) and particulate pollutants contribute to oxidative stress, inflammation, and cytotoxicity in lung cells, highlighting the significant role of each gaseous component. In addition, unmeasured factors beyond CO, THC, NOx, and PN likely contribute to biological effects, indicating the need for a more detailed characterization of exhaust parameters in ML analysis. By successfully integrating ML techniques, this study shows the potential of ML in identifying pollutant-specific contributions to cell toxicity. These insights can guide the analysis of complex exposure scenarios and inform regulatory measures and technical developments in emission control.

Titanium dioxide nanoparticles (TiO₂-NPs) are one of the most commercially manufactured and widely applied NPs. However, often TiO₂-NPs leak into the environment and make aquatic animals exposure inevitable. Consequently, a deeper comprehension of TiO₂-NPs toxicity is utmost important. The 96-hour lethal concentration of TiO₂-NP in rohu (Labeo rohita) was 77.49 mg/L. An in-vivo toxicity assessment of TiO₂-NP was conducted at sub lethal concentration of 1 mg/L (2%), 2.5 mg/L (5%), and 5 mg/L (10%) at 24 hours post exposure (hpe), 4 days post exposure (dpe), and 14 dpe in an aquatic lower vertebrate, rohu. Quantitative bioaccumulation analysis showed highest TiO₂-NPs bioaccumulation in intestine followed by liver, gill, kidney, spleen, and negligible in muscle. TiO₂-NP at 5 mg/L concentration induced the immunotoxic response by destabilization of serum lysozyme and antiprotease activity which was further potentiated by increased production of myeloperoxidase, respiratory burst activity leading to higher production of reactive oxygen species that contribute to oxidative stress, inflammation and cellular damage. Molecular study demonstrated that TiO₂-NP is recognized and processed by signaling PRR, TLR22 leading to initiation of the downstream immune-signaling cascade and pro-inflammatory cytokines production. The TiO₂-NP induced the oxidative stress gene (SOD, CAT, and GPx) expression significantly at 1, 2.5 and 5 mg/L. Nevertheless, apoptotic biomarker (caspase3, BAX and p53) were induced significantly on 14th dpe at 5 mg/L dose exposure. Our study infer that TiO₂-NP induced immunotoxic response at higher concentration of 5 mg/L, nevertheless it acts as immunostimulator at lower concentration of 1 mg/L in L. rohita.

The mouth cavity is the second most complex microbial community in the human body. It is composed of bacteria, viruses, fungi, and protozoa. An imbalance in the oral microbiota may lead to various conditions, including caries, soft tissue infections, periodontitis, root canal infections, peri-implantitis (PI), pulpitis, candidiasis, and denture stomatitis. Additionally, several locally administered antimicrobials have been suggested for dentistry in surgical and non-surgical applications. The main drawbacks are increased antimicrobial resistance, the risk of upsetting the natural microbiota, and hypersensitivity responses. Because of their unique physiochemical characteristics, nanoparticles (NPs) can circumvent antibiotic-resistance mechanisms and exert antimicrobial action via a variety of new bactericidal routes. Because of their anti-microbial properties, carbon-based NPs are becoming more and more effective antibacterial agents. Periodontitis, mouth infections, PI, dentin and root infections, and other dental diseases are among the conditions that may be treated using carbon NPs (CNPs) like graphene oxide and carbon dots. An outline of the scientific development of multifunctional CNPs concerning oral disorders will be given before talking about the significant influence of CNPs on dental health. Some of these illnesses include Periodontitis, oral infections, dental caries, dental pulp disorders, dentin and dental root infections, and PI. We also review the remaining research and application barriers for carbon-based NPs and possible future problems.