Plastics have become an integral part of our daily lives. In the environment, plastics break down into small pieces (<5 mm) that are referred to as microplastics. Microplastics are ubiquitous and widespread in the environment, and all living organisms are exposed to their effects. The present study provides new insights into the potential effects of polyethylene terephthalate (PET) microplastics on organisms via extracellular vesicle (EV)-mediated communication. The study demonstrated that serum-derived EVs are able to transport plastic particles. In addition, PET microplastics alter the content of miRNA in EVs. The identified differentially regulated miRNAs may target genes associated with lifestyle diseases, such as cardiovascular or metabolic diseases, and carcinogenesis. This work expands our understanding of PET microplastics' effects on organisms via EV-mediated communication and identifies directions for further research and strategies.

Inflammation in the female reproductive system causes serious health problems including infertility. The aim of this study was to determine the in vitro effects of peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) ligands on the transcriptomic profile of the lipopolysaccharide (LPS)-stimulated pig corpus luteum (CL) in the mid-luteal phase of the estrous cycle using RNA-seq technology. The CL slices were incubated in the presence of LPS or in combination with LPS and the PPARβ/δ agonist—GW0724 (1 μmol/L or 10 μmol/L) or the antagonist—GSK3787 (25 μmol/L). We identified 117 differentially expressed genes after treatment with LPS; 102 and 97 differentially expressed genes after treatment, respectively, with the PPARβ/δ agonist at a concentration of 1 μmol/L or 10 μmol/L, as well as 88 after the treatment with the PPARβ/δ antagonist. In addition, biochemical analyses of oxidative status were performed (total antioxidant capacity and activity of peroxidase, catalase, superoxide dismutase, and glutathione S-transferase). This study revealed that PPARβ/δ agonists regulate genes involved in the inflammatory response in a dose-dependent manner. The results indicate that the lower dose of GW0724 showed an anti-inflammatory character, while the higher dose seems to be pro-inflammatory. We propose that GW0724 should be considered for further research to alleviate chronic inflammation (at the lower dose) or to support the natural immune response against pathogens (at the higher dose) in the inflamed corpus luteum.

Microplastics and their effects on the body have recently been of great concern. Today it is clear that they are not indifferent to human health, but the full spectrum of their impact has not yet been fully described. Pancreatic diseases are becoming increasingly common worldwide, and their etiology is not well understood. Worryingly, these diseases have been increasingly diagnosed in children over the last 20 years, which was previously considered unusual. The aim of the study was therefore to determine the changes in the pancreas caused by PET microplastics in young organisms. For this purpose, the global metabolomic profile of the pancreas of piglets treated with a low (0.1 g/day) or high dose (1 g/day) of PET microplastics for 4 weeks was determined by UPLC-MS analysis. In addition, insulin levels and various biochemical parameters in the blood were analyzed. The study showed that PET microplastics affected the physiological processes in the pancreas at both low and high doses. We found that PET microplastics increased the tissue levels of important metabolites such as glucose, γ-aminobutyric acid, lysophosphatidylcholine or lysophosphatidylethanolamine. In addition, PET microplastics increased blood insulin concentrations and dose-dependently regulated lipase, cholesterol and calcium levels. These results suggest that PET microplastics increase the risk of insulin resistance and pancreatitis.

Type 1 diabetes is a chronic autoimmune disease, the incidence of which has been steadily increasing in recent years, particularly among adolescents. The disease results from a combination of genetic and environmental factors that lead to the destruction of insulin-producing beta cells in the pancreas. Recently, the potential role of microplastics in the pathogenesis of various diseases has gained attention. Therefore, the aim of this study was to investigate the impact of PET microplastics on the pancreas using immature pigs as a model organism. The global transcriptomic profile of the pancreas was analyzed in piglets treated with either a low (0.1 g/day) or high dose (1 g/day) of PET microplastics for 4 weeks using RNA-Seq. The analysis revealed a dose-dependent effect of PET microplastics on gene expression. A low dose affected the expression of one gene, while a high dose impacted the expression of 86 genes. The differentially expressed genes, including immune cell markers, cytokines and chemokines, may activate the immune system in the pancreas in a way that is characteristic of the pathogenesis of type 1 diabetes. It suggests that oral exposure to PET microplastics may be a new risk factor for the development of this disease.

Microplastics are a relatively new discovered environmental hazard that can contribute to the disruption of many physiological processes in the organism. There is evidence that they affect the physiology of the pancreas, but research in this area remains limited. Therefore, the aim of the study was to determine the effects of PET microplastics on the global proteomic profile of the pancreas using LC–MS/MS analysis, with the pig as a model organism. The pigs were treated either with a low (0.1 g/day) or a high dose (1 g/day) of PET microplastics for four weeks. The analysis revealed that PET microplastics affected protein abundance in a dose-dependent manner – the low dose altered the abundance of 7 proteins, while the high dose – 17. The differentially regulated proteins were involved in fatty acid biosynthesis (FASN, KAS), lipid peroxidation (CBR1) and digestive enzyme production (trypsinogen). Complementary colorimetric assays confirmed a significant increase in free fatty acids under the influence of a high dose of PET microplastics. Taken together, these results indicate that PET microplastics may affect oxidative status, induce lipotoxic stress and impair pancreatic exocrine function, suggesting a novel pathway through which microplastics may cause metabolic disturbances.