The production, use, and waste of plastics increased worldwide, which resulted in environmental pollution and a growing public health problem. In particular, microplastics have the potential to accumulate in humans and mammals through the food chain. However, the toxicity of microplastics is not well understood. In this study, we investigated the toxicity of 10–50 μm polyethylene microplastics following single- and 28-day repeated oral administration (three different doses of microplastics of 500, 1000, and 2000 mg/kg/day) in ICR mice. For the investigation, we administered the microplastics orally for single- and 28-day repeated. Then, the histological and clinical pathology evaluations of the rodents were performed to evaluation of the toxicity test, and Raman spectroscopy was used to directly confirm the presence of polyethylene microplastics. In the single oral dose toxicity experiments, there were no changes in body weight and necropsy of the microplastics-treated group compared with that of controls. However, a histopathological evaluation revealed that inflammation from foreign bodies was evident in the lung tissue from the 28-day repeated oral dose toxicity group. Moreover, polyethylene microplastics were detected in the lung, stomach, duodenum, ileum, and serum by Raman spectroscopy. Our results corroborated the findings of lung inflammation after repeated oral administration of polyethylene microplastics. This study provides evidence of microplastic-induced toxicity following repeated exposure to mice.

Spinal cord injury (SCI) is a life-threatening condition that leads to permanent disability with partial or complete loss of motor, sensory, and autonomic functions. SCI is usually caused by initial mechanical insult, followed by a cascade of several neuroinflammation and structural changes. For ameliorating the neuroinflammatory cascades, MSC has been regarded as a therapeutic agent. The animal SCI research has demonstrated that MSC can be a valuable therapeutic agent with several growth factors and cytokines that may induce anti-inflammatory and regenerative effects. However, the therapeutic efficacy of MSCs in animal SCI models is inconsistent, and the optimal method of MSCs remains debatable. Moreover, there are several limitations to developing these therapeutic agents for humans. Therefore, identifying novel agents for regenerative medicine is necessary. Extracellular vesicles are a novel source for regenerative medicine; they possess nucleic acids, functional proteins, and bioactive lipids and perform various functions, including damaged tissue repair, immune response regulation, and reduction of inflammation. MSC-derived exosomes have advantages over MSCs, including small dimensions, low immunogenicity, and no need for additional procedures for culture expansion or delivery. Certain studies have demonstrated that MSC-derived extracellular vesicles (EVs), including exosomes, exhibit outstanding chondroprotective and anti-inflammatory effects. Therefore, we reviewed the principles and patho-mechanisms and summarized the research outcomes of MSCs and MSC-derived EVs for SCI, reported to date.

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.

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.