Spinal cord injury (SCI) interferes with the normal function of the autonomic nervous system by blocking circuits between the sensory and motor nerves. Although many studies focus on functional recovery after neurological injury, effective neuroregeneration is still being explored. Recently, extracellular vesicles such as exosomes have emerged as cell-free therapeutic agents owing to their ability of cell-to-cell communication. In particular, exosomes released from mesenchymal stem cells (MSCs) have the potential for tissue regeneration and exhibit therapeutic effectiveness in neurological disorders. In this study, we isolated exosomes from human epidural adipose tissue-derived MSCs (hEpi AD–MSCs) using the tangential flow filtration method. The isolated exosomes were analyzed for size, concentration, shape, and major surface markers using nanoparticle tracking analysis, transmission electron microscopy, and flow cytometry. To evaluate their effect on SCI recovery, hEpi AD–MSC exosomes were injected intravenously in SCI-induced rats. hEpi AD–MSC exosomes improved the locomotor function of SCI-induced rats. The results of histopathological and cytokine assays showed that hEpi AD–MSC exosomes regulated inflammatory response. Genetic profiling of the rat spinal cord tissues revealed changes in the expression of inflammation-related genes after exosome administration. Collectively, hEpi AD–MSC exosomes are effective in restoring spinal functions by reducing the inflammatory response.

Currently, polypropylene (PP) is used in various products, thus leading to high daily exposure in humans. Thus, it is necessary to evaluate the toxicological effects, biodistribution, and accumulation of PP microplastics in the human body. In this study, administration of two particle sizes of PP microplastics (approximately 5 and 10–50 µm) did not lead to any significant changes in several toxicological evaluation parameters, including body weight and pathological examination, compared with the control group in ICR mice. Therefore, the approximate lethal dose and no-observed-adverse-effect level of PP microplastics in ICR mice were established as ≥2000 mg/kg. Furthermore, we manufactured cyanine 5.5 carboxylic acid (Cy5.5-COOH)-labeled fragmented PP microplastics to monitor real-time in vivo biodistribution. After oral administration of the Cy5.5-COOH-labeled microplastics to the mice, most of the PP microplastics were detected in the gastrointestinal tract and observed to be out of the body after 24 h in IVIS Spectrum CT. Therefore, this study provides a new insight into the short-term toxicity, distribution, and accumulation of PP microplastics in mammals.

Microplastics (MPs), plastic particles with a diameter of < 5 mm, are intentionally produced or formed by the breakdown of a variety of larger plastics. Polyethylene terephthalate (PET) is a common source of MPs and PET-MPs are prevalent in the environment. Owing to their persistence, PET-MPs can enter ecosystems, air, and food sources, posing significant health risks. This study aimed to investigate the toxicological effects and in vivo accumulation of PET-MPs smaller than 10 µm. To track their biodistribution, fluorescently labeled PET-MPs were prepared. Particle size and morphology were confirmed using physical and chemical characterization. Following the oral administration of PET-MPs in ICR (CD-1®) outbred mice, accumulation occurred predominantly in lungs, as confirmed by IVIS spectrum CT analysis and in vivo and ex vivo imaging. Toxicity assays revealed the development of granulomatous inflammation in the lungs at medium and high doses, indicating a concentration-dependent response. The recorded no-observed-adverse-effect levels were 1.75 mg/kg for males and 7 mg/kg for females. This study highlights the potential of PET-MPs to induce persistent inflammation in respiratory tissues and reveals the need for further research to support the regulatory standards and long-term health effects of MP exposure.

The increased use of plastics has led to severe environmental pollution, particularly by microplastics—plastic particles 5 mm or less in diameter. These particles are formed by environmental factors such as weathering and ultraviolet irradiation, thereby making environmental pollution worse. This environmental pollution intensifies human exposure to microplastics via food chains. Despite potential negative effects, few toxicity assessments on microplastics are available. In this study, two sizes of polytetrafluoroethylene (PTFE) microplastics, approximately 5 μm and 10–50 μm, were manufactured and used for single and four-week repeated toxicity and pharmacokinetic studies. Toxicological effects were comprehensively evaluated with clinical signs, body weight, food and water consumption, necropsy findings, and histopathological and clinical-pathological examinations. Blood collected at 15, 30 60, and 120 min after a single administration of microplastics were analyzed by Raman spectroscopy. In the toxicity evaluation of single and four-week repeated oral administration of PTFE microplastics, no toxic changes were observed. Therefore, the lethal dose 50 (LD₅₀) and no-observed-adverse-effect-level (NOAEL) of PTFE microplastics in ICR mice were established as 2000 mg/kg or more. PTFE microplastics were not detected in blood, so pharmacokinetic parameters could not be calculated. This study provides new insight into the long-term toxicity and pharmacokinetics of PTFE microplastics.

As the production, usage, and disposal of plastics increase, the microplastics generated—plastic particles smaller than 5 mm—increases, exacerbating environmental pollution. In turn, various organisms become increasingly exposed to contaminated environments, potentially affecting humans through the food chain. Crucial findings from in vivo experiments indicate histopathological changes caused by microplastics impact the morphology and physiological function of organisms. This study describes the histopathological changes induced by microplastics across the circulatory, nervous, digestive, respiratory, and reproductive systems and explains associated functional alterations. Except in the nervous system, the main morphological changes involve degenerative changes throughout the body, such as apoptosis, inflammation, and fibrosis. Most changes were induced by inflammatory responses to microplastics, leading to fibrosis and subsequent functional impairments. Various studies confirm that microplastics stimulate cells, leading to increased reactive oxygen species production, inflammation, and cell death. Consequently, these morphological changes impair related systemic functions. This review highlights fundamental morphological changes in organs and cells due to microplastics and discusses the limitations involving systems showing no changes.

Microplastics are pollutants that occur in various environments and habitats. Inflammatory bowel disease (IBD) is a chronic inflammatory disease accompanied with diarrhea, and the number of patients has increased worldwide. In this study, manufactured fragmented polyethylene-microplastics in the size range of 10-30 ㎛, were oxidized by exposure to ultraviolet light, and then administered to a dextran sodium sulfate-induced colitis mouse model to observe the effects of polyethylene-microplastics on IBD. In the microplastics-treated groups, an increase in disease activity index score, histopathological score, and a decrease in the areas of goblet cells were observed. In addition, the tight junction proteins, ZO-1 and Occludin, were significantly decreased, whereas MPO was significantly increased. Interestingly, E-cadherin, which is an adheren junction, was also decreased, presumably because of the physical effects of microplastics. The results suggest that polyethylene-microplastics worsen IBD and microplastics can affect not only tight junctions, but also adheren junctions.