Nanotoxicology最新文献

Selenite(Se) is a trace mineral that is essential for cardiac health. This study aims to investigate the beneficial effects of Se on cardiomyocyte damage induced by silver nanoparticles (AgNPs) and to explore the underlying protective mechanisms. H9C2 cells were incubated with AgNPs with or without Se . Cell viability, reactive oxygen species (ROS), mitochondrial membrane potential, NAD⁺/NADH ratios, ATP levels, the mTOR signaling pathway, and autophagic proteins were measured. The results showed that AgNPs exposure significantly decreased cell viability, inhibited cell proliferation, and changed cell morphology. AgNPs dramatically elevated ROS production and descended mitochondrial membrane potential. Furthermore, the NAD⁺/NADH ratio and ATP level of the AgNPs exposure group were significantly lower than those of the control group. AgNPs activated AMPK, depressed mTOR, and increased LC3 II/I and P62(P < 0.05). Interestingly, treatment with Se effectively salvaged AgNPs-induced cardiomyocyte damage, reduced ROS accumulation, stabilized mitochondrial membrane potential, restored the NAD⁺/NADH ratio and ATP level, and prevented the activation of mTOR and autophagy dysfunction induced by AgNPs. Se mitigates AgNPs-induced cardiomyocyte damage by utilizing antioxidative properties and suppressing mitochondrial dysfunction mediated autophagy through regulating AMPK/mTOR signaling pathway.

With advances in the application of graphene oxide (GO), the major hindering factor is its toxicity. It is crucial to understand the immediate effects on the parent generation as well as the long-term multigenerational effects on subsequent generations. In this paper we investigated the multigenerational effect of GO from the parent to subsequent generations (F0, F1, F2, F3 to F4) in Drosophila melanogaster model organism. Flies were exposed to GO through the ingestion method at concentrations ranging from 50 µg/mL, 100 µg/mL, and 250 µg/mL. The effects of GO were studied at different levels via climbing assay, longevity assay, oxidative stress and phenotypic screening in subsequent generations. Significant declines were observed in the climbing ability, an increase in oxidative stress (F2), and a decrease in lifespan of the parent (F0) to progeny (F1, F2) flies exposed to GO. Critically, the reversal of these toxic effects in the later generations (F3-F4), suggests the development of adaptive mechanisms through which flies overcome the detrimental impacts of prolonged GO exposure. These findings underscore the importance of examining the multigenerational effects of nanomaterials (NMs), as the initial toxicity may not persist over time due to the emergence of adaptive responses in subsequent generations. Understanding and mitigating the toxicity of GO over generations is essential for its safe application in various fields.

Bone, a complex nanocomposite, has yet to be successfully replicated in a commercially available bone regenerative product that fully recapitulates this dual-phase nanoscale architecture. This study investigated the biocompatibility and safety of a nanoalloplastic composed of spherical nanohydroxyapatite (nHA; 30-45 nm)/tricalcium phosphate (TCP) and osteogenic, angiogenic and immunomodulatory self-assembling peptide nanofibers (15-20 nm), designed to mimic the natural nanocomposite structure of bone. Adhering to ISO 10993 protocols, the nanocomposite was subjected to rigorous biocompatibility evaluation by IFDA laboratories. This assessment encompassed cytotoxicity, genotoxicity, hemocompatibility, sensitization, and irritation, as well as acute and chronic systemic toxicity studies. Results demonstrated the material's non-cytotoxic nature, with no significant reduction in cell viability. Hemocompatibility testing revealed acceptable hemolytic activity, while genotoxicity assays showed no evidence of DNA damage. Neither irritation nor sensitization was observed. Systemic toxicity studies in mice revealed no adverse clinical signs, weight changes, or organ pathologies. Bone regeneration study showed complete and osteoinductive potential over one month in rabbits. The peptide nanofibers contribute to the material's biocompatibility through their ECM-mimicking sequences, nanofibrous architecture, biodegradability, and toxic- and solvent-free nature. TCP and spherical nHA with an optimum particle size, morphology, crystallinity, dissolution rate, and significant pH stability, collectively ensure its biocompatibility and vascularized bone formation. These findings validate the biocompatibility and safety of this osteoinductive nanocomposite. The integration of spherical nHA and self-assembling peptide nanofibers appears to generate a biomimetic microenvironment that improves cellular interactions, thereby accelerating bone regeneration and confirming its biocompatibility, positioning it as a revolutionary solution for bone regeneration.

The objective of this state-of-the-art review is to summarize contemporary data on the potential toxic effects of aluminum nanoparticles (AlNPs) and discuss the underlying molecular mechanisms. In vivo studies using laboratory rodents demonstrate that lungs, liver, brain, and the immune system are the primary targets for AlNPs toxicity. Specifically, inhalation exposure to AlNPs induces lung damage by promoting inflammatory infiltration, airway remodeling, septal thickening, and bronchial hyperresponsiveness. AlNPs-induced liver damage is characterized by hepatocyte degeneration and necrosis, liver sinusoid congestion, inflammation, and fibrosis. AlNPs induces neurotoxicity resulting in neurodegeneration, neuroinflammation, altered neurotransmitter metabolism, and subsequent adverse neurobehavioral outcome. In turn, immunotoxicity of AlNPs is characterized by promotion of systemic inflammation along with impaired phagocytosis. In addition to the toxicity exerted by Al₂O₃NPs itself, the observed toxic effects of AlNPs may be attributed to Al³⁺ release from the particles with the subsequent induction of oxidative stress, inflammation, mitochondrial dysfunction, genotoxicity, cell cycle dysregulation, and cell death due to apoptosis, necrosis, and ferroptosis. It is also evident that both the size and the form of AlNPs significantly affect its cytotoxicity. However, further studies are required to explore the mechanisms of toxic effects of AlNPs, as well as its potential adverse effects on human health.

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.