In vitro effects of polystyrene microplastics exposure on adipose tissue dysfunction

Background Environmental pollution represents, to date, a global safety problem. In this regard, attention has recently been paid to the potential human exposure to microplastics (MPs, 1 μm - 5 mm in size) and their health effects. MPs result from the manufacturing and degradation of plastic objects and, recently, were detected in human blood, demonstrating that these particles can circulate in the human body and can reach various organs in the human body. Recently, reports emphasized the potential impact of MPs on the early exposure of infants and the early development of tissue and organs. In addition, epidemiological studies demonstrated an association between MPs exposure and the incidence of obesity and metabolic syndrome, due to the potential persistence of these compounds on adipose tissue level. For this purpose, in this work we intended to evaluate, the in vitro effects of polystyrene MPs exposure of murine preadipocytes (3T3-L1) on adipogenesis and inflammation processes. Methods Polystyrene microplastics (5 µm) 5-100 µg/ml were added to 3T3-L1 preadipocytes during the 10 days of the differentiation process. The effect on lipid accumulation was evaluated by Oil Red O (ORO) staining, whereas the main markers involved in adipogenesis, ER stress and proinflammatory mechanisms were evaluated by Western blot and qPCR. ROS levels were assessed fluorometrically. Experiments were carried out on three experimental units each in triplicate and data were considered statistically significant with p value < 0.05 (one-way ANOVA with Tukey’s HSD). Results ORO staining showed that chronic MPs exposure dose-dependently induced lipid accumulation and hypertrophic adipocytes. This effect was supported by a marked increase in C/EBP-β and PPARγ levels and their transcriptional activity (FABP4, FASN and SREBP-1 gene expression). Furthermore, MPs altered endoplasmic reticulum (ER) homeostasis inducing ROS increase, ER stress markers (XBP 1s and pEIF2a) and downstream genes (Grp78 and CHOP) in a dose-dependent way. Lastly chronic MPs exposure induced proinflammatory response activating IL-6 and MCP-1 gene expression. Conclusions This study clearly indicates the mechanism involved in microplastics exposure on adipocytes dysfunction, demonstrating, therefore, how chronic exposure to these particles can represent a relevant factor for the development of obesity and related disorders.