UNASSIGNED: Studies have shown that microplastics (MPs) and nanoplastics (NPs) could accumulate in the human body and pose a potential threat to human health. The purpose of this study is to evaluate the biodistribution and toxicity of MPs/NPs with different particle sizes comprehensively and thoroughly.
UNASSIGNED: The purpose of this study was to investigate the biodistribution and in vivo toxicity of polystyrene (PS) MPs/NPs with different sizes (50 nm, 100 nm, and 500 nm). The BALB/c mice were given 100 μL of PS50, PS100 and PS500 at the dosage of 1 mg/kg BW or 10 mg/kg BW, respectively, by gavage once a day. After 28 consecutive days of treatment, the biodistribution of differently sized PS MPs/NPs was determined through cryosection fluorescence microscopy and fluorescent microplate reader analysis, and the subsequent effects of differently sized PS MPs/NPs on histopathology, hematology and blood biochemistry were also evaluated.
UNASSIGNED: The results showed that the three different sizes of PS MPs/NPs were distributed in the organs of mice, mainly in the liver, spleen, and intestine. At the same time, the smaller the particle size, the more they accumulate in the body and more easily penetrate the tissue. During the whole observation period, no abnormal behavior and weight change were observed. The results of H&E staining showed that no severe histopathological abnormalities were observed in the main organs in the low-dose exposure group, while. Exposure of three sizes of PS MPs/NPs could cause some changes in hematological parameters or biochemical parameters related to heart, liver, and kidney function; meanwhile, there were size- and dose-dependencies.
UNASSIGNED: The biological distribution and toxicity of plastic particles in mice were more obvious with the decrease of particle size and the increase of concentration of plastic particles. Compared with MPs, NPs were easier to enter the tissues and produce changes in liver, kidney, and heart functions. Therefore, more attention should be paid to the toxicity of NPs.

Lactation women, a highly concerned demographic in society, face health risks that deserve attention. Zinc oxide nanoparticles (ZnO NPs) are widely utilized in food and daily products due to their excellent physicochemical properties, leading to the potential exposure of lactating women to ZnO NPs. Hence, assessing the potential risks associated with ZnO NP exposure during lactation is critical. While studies have confirmed that exposure to ZnO NPs during lactation can induce toxic responses in multiple organs through blood circulation, the effects of lactational exposure on mammary tissue remain unclear. This research investigated the impairment of mammary tissue induced by ZnO NPs and its potential mechanisms. Through administering multiple injections of ZnO NPs into the tail vein of lactating ICR mice, our study revealed that ZnO NPs can deposit in the mammary tissues, downregulating key components of mammary epithelial barrier such as ZO-1, occludin, and claudin-3. In vivo, we also found that ZnO NPs can simultaneously induce apoptosis, necroptosis, and pyroptosis, called PANoptosis. Additionally, using EpH4-Ev cells to simulate an in vitro mammary epithelial barrier model, we observed that ZnO NPs effectively disrupted the integrity of mammary epithelial barrier and induced PANoptosis. Furthermore, we confirmed that PANoptosis was responsible for the mammary epithelial barrier disruption induced by ZnO NPs. Moreover, we identified that ZBP1 was the primary mechanism of ZnO NPs inducing PANoptosis. These discoveries are designed to enhance our comprehension of the mechanisms underlying mammary epithelial barrier disruption caused by ZnO NPs, and we aim to highlight the potential hazards associated with daily usage and therapeutic exposure to ZnO NPs during lactation.

The widespread use of nanomaterials in agriculture may introduce multiple engineered nanoparticles (ENPs) into the environment, posing a combined risk to crops. However, the precise molecular mechanisms explaining how plant tissues respond to mixtures of individual ENPs remain unclear, despite indications that their combined toxicity differs from the summed toxicity of the individual ENPs. Here, we used a variety of methods including physicochemical, biochemical, and transcriptional analyses to examine the combined effects of graphene nanoplatelets (GNPs) and titanium dioxide nanoparticles (TiO2 NPs) on hydroponically exposed lettuce (Lactuca sativa) seedlings. Results indicated that the presence of GNPs facilitated the accumulation of Ti as TiO2 NPs in the seedling roots. Combined exposure to GNPs and TiO2 NPs caused less severe oxidative damage in the roots compared to individual exposures. Yet, GNPs and TiO2 NPs alone and in combination did not cause oxidative damage in the shoots. RNA sequencing data showed that the mixture of GNPs and TiO2 NPs led to a higher number of differentially expressed genes (DEGs) in the seedlings compared to exposure to the individual ENPs. Moreover, the majority of the DEGs encoding superoxide dismutase displayed heightened expression levels in the seedlings exposed to the combination of GNPs and TiO2 NPs. The level of gene ontology (GO) enrichment in the seedlings exposed to the mixture of GNPs and TiO2 NPs was found to be greater than the level of GO enrichment observed after exposure to isolated GNPs or TiO2 NPs. Furthermore, the signaling pathways, specifically the \"MAPK signaling pathway-plant\" and \"phenylpropanoid biosynthesis,\" exhibited a close association with oxidative stress. This study has provided valuable insights into the molecular mechanisms underlying plant resistance against multiple ENPs.

Heart failure represents a primary cause of hospitalization and mortality in both developed and developing countries, often necessitating heart transplantation as the only viable recovery path. Despite advances in transplantation medicine, organ rejection remains a significant post-operative challenge, traditionally monitored through invasive endomyocardial biopsies (EMB). This study introduces a rapid prototyping approach to organ rejection monitoring via a sensor-integrated flexible patch, employing electrical impedance spectroscopy (EIS) for the non-invasive, continuous assessment of resistive and capacitive changes indicative of tissue rejection processes. Utilizing titanium-dioxide-coated electrodes for contactless impedance sensing, this method aims to mitigate the limitations associated with EMB, including procedural risks and the psychological burden on patients. The biosensor\'s design features, including electrode passivation and three-dimensional microelectrode protrusions, facilitate effective monitoring of cardiac rejection by aligning with the heart\'s curvature and responding to muscle contractions. Evaluation of sensor performance utilized SPICE simulations, scanning electron microscopy, and cyclic voltammetry, alongside experimental validation using chicken heart tissue to simulate healthy and rejected states. The study highlights the potential of EIS in reducing the need for invasive biopsy procedures and offering a promising avenue for early detection and monitoring of organ rejection, with implications for patient care and healthcare resource utilization.

In recent years, the intensive production of nanoparticles with a wide application has led to their transfer to the environment, including the water ecosystem. The accumulation of nanoparticles in fish, causing various pathological changes in the host, raises certain concerns. In the current study, we investigated the penetration and bioaccumulation of Fe3O4 nanoparticles, in the liver of common carp (Cyprinus carpio Linnaeus, 1758). Common carp juveniles were exposed to Fe3O4 nanoparticles at concentrations of 10 and 100 mg. After 7 days, their livers were examined by light and transmission electron microscopes. Compared to normal fish\'s liver, after using a small concentration (10 mg) of nanoparticles, changes were observed in erythrocytes, hepatocytes, intracellular canaliculi, and bile ducts of the liver. At a high concentration (100 mg), the intensity of changes increased significantly. The liver\'s capsule was damaged, and a considerable number of hepatocytes were completely destroyed. Additionally, the walls of blood vessels and biliary ductule walls was notably disturbed. It was found that the intensity of pathologies occurring in the liver, increases proportionally with higher concentrations of nanoparticles. Confirmation via electron microscopic methods revealed that Fe3O4 nanoparticles, when administered with food to common carp, enter the fish\'s liver through erythrocytes localized in the lumen of blood vessels. From there, they traverse through the endothelium of vessels, proceed to hepatocytes, including cytoplasmic organelles, intracellular canaliculi, biliary ductules, and eventually reach the bile ducts. Fe3O4 nanoparticles in all structural elements of fish liver was up to 20 nm. Therefore, high concentrations of nanoparticles in the environment harms the bodies of aquatic organisms, including fish. The changes identified in the liver of common carp in the present study are valuable information in assessing possible risks to other components of the aquatic ecosystem and organisms.

The ubiquity of nanoparticles, sourced from both natural environments and human activities, presents critical challenges for public health. While offering significant potential for innovative biomedical applications-especially in enhancing drug transport across the blood-brain barrier-these particles also introduce possible hazards due to inadvertent exposure. This concise review explores the paradoxical nature of nanoparticles, emphasizing their promising applications in healthcare juxtaposed with their potential neurotoxic consequences. Through a detailed examination, we delineate the pathways through which nanoparticles can reach the brain and the subsequent health implications. There is growing evidence of a disturbing association between nanoparticle exposure and the onset of neurodegenerative conditions, highlighting the imperative for comprehensive research and strategic interventions. Gaining a deep understanding of these mechanisms and enacting protective policies are crucial steps toward reducing the health threats of nanoparticles, thereby maximizing their therapeutic advantages.

Silver nanoparticles (AgNPs) are increasingly incorporated in diverse products to confer antimicrobial properties. They are released into the environment during manufacture, after disposal, and from the products during use. Because AgNPs bioaccumulate in brain, it is important to understand how they interact with neural cell physiology. We found that the focal adhesion (FA)-associated protein cadherin aggregated in a dose-dependent response to AgNP exposure in differentiating cultured B35 neuroblastoma cells. These aggregates tended to colocalize with F-actin inclusions that form in response to AgNP and also contain β-catenin. However, using hyperspectral microscopy, we demonstrate that these multi-protein aggregates did not colocalize with the AgNPs themselves. Furthermore, expression and organization of the FA protein vinculin did not change in cells exposed to AgNP. Our findings suggest that AgNPs activate an intermediate mechanism which leads to formation of aggregates via specific protein-protein interactions. Finally, we detail the changes in hyperspectral profiles of AgNPs during different stages of cell culture and immunocytochemistry processing. AgNPs in citrate-stabilized solution present mostly blue with some rainbow spectra and these are maintained upon mounting in Prolong Gold. Exposure to tissue culture medium results in a uniform green spectral shift that is not further altered by fixation and protein block steps of immunocytochemistry.

Solid lipid nanoparticles (SLN) are widely recognized for their biocompatibility, scalability, and long-term stability, making them versatile formulations for drug and gene delivery. Cellular interactions, governed by complex endocytic and signaling pathways, are pivotal for successfully applying SLN as a therapeutic agent. This study aims to enhance our understanding of the intricate interplay between SLN and cells by investigating the influence of specific endocytic and cell signaling pathways, with a focus on the impact of the TGF-βpathway on SLN-mediated cell transfection in both cancerous and non-cancerous prostate cells. Here, we systematically explored the intricate mechanisms governing the interactions between solid lipid nanoparticles and cells. By pharmacologically manipulating endocytic and signaling pathways, we analyzed alterations in SLNplex internalization, intracellular traffic, and cell transfection dynamics. Our findings highlight the significant role of macropinocytosis in the internalization and transfection processes of SLNplex in both cancer and non-cancer prostate cells. Moreover, we demonstrated that the TGF-βpathway is an important factor influencing endosomal release, potentially impacting gene expression and modulating cell transfection efficiency. This study provides novel insights into the dynamic mechanisms governing the interaction between cells and SLN, emphasizing the pivotal role of TGF-βsignaling in SLN-mediated transfection, affecting internalization, intracellular transport, and release of the genetic cargo. These findings provide valuable insight for the optimization of SLN-based therapeutic strategies in prostate-related applications.

In recent years, the rapid development of nanotechnology has caused the products obtained with this technology to be used more daily. Information on the effects of these products, which provide great advantages in every respect, on human health and the environment is insufficient. It has been suggested that these nanoparticles may have toxic effects on living things, mostly in animal experiments and cell cultures. In this paper, the organism Caenorhabditis elegans (C. elegans), which contains a genome and biochemical ways highly similar to humans, is used to understand and reveal the metabolism of Zinc oxide nanoparticles (ZnO NPs) toxicological effects. The toxicological effects of ZnO NPs on C. elegans organisms were investigated and the results were evaluated in terms of environment and human health. C. elegans was exposed to commercial ZnO NPs and green synthesized ZnO NPs from Olea europaea (olive tree, OLE). LC50 values were determined by probit analysis (green synthesized ZnO NP LC5024h = 84.97 mg/L, LC5072h = 33.27 mg/L, commercial ZnO NPs LC5024h = 5.75 mg/L, LC5072h = 1.91 mg/L). When the survival times of C. elegans were evaluated by the Kaplan-Meier method, it was seen that commercial ZnO NPs were more toxic than green synthesized ZnO NPs. In MTT tests, it was clearly seen that commercial ZnO NPs and green synthesized ZnO NPs entered the cell and caused different cytotoxicity. While there was a difference between control and 0.5, 2.5, 5, 10, 25, and 50 mg/L doses in commercial ZnO NP applications, there were significant differences between control and 25, 50 mg/L concentrations in green synthesized ZnO NP applications.

Topical infection affects nearly one-third of the world\'s population; it may result from poor sanitation, hygienic conditions and crowded living and working conditions that accelerate the spread of topical infectious diseases. The problems associated with the anti-infective agents are drug resistance and long-term therapy. Secondary metabolites are obtained from plants, microorganisms and animals, but they are metabolized inside the human body. The integration of nanotechnology into secondary metabolites is gaining attention due to their interaction at the subatomic and skin-tissue levels. Hydrogel, liposomes, lipidic nanoparticles, polymeric nanoparticles and metallic nanoparticles are the most suitable carriers for secondary metabolite delivery. Therefore, the present review article extensively discusses the topical applications of nanomedicines for the effective delivery of secondary metabolites.