Introduction

Microplastics (MPs) are emerging environmental pollutants that have attracted increasing scientific concern due to their widespread presence in ecosystems and potential risks to human and animal health. While their effects have been extensively studied in aquatic organisms, data regarding their impact on mammalian systems remain limited. In particular, the mechanisms underlying MP-induced toxicity at the cellular and molecular levels are still poorly understood.

Material and Methods

Adult female Wistar rats were exposed to polystyrene microplastics (PS-MPs) through oral gavage over four consecutive estrous cycles. Two types of particles were used: pristine polystyrene microplastics (PPS-MPs) and fluorescent polystyrene microplastics (FPS-MPs), both with a diameter of 5 µm. FPS-MPs were employed specifically to assess tissue distribution and translocation, while PPS-MPs were used for toxicological evaluation. At the end of the exposure period, liver tissues were collected for biochemical, histological, and molecular analyses.

Results

FPS-MPs were detected in hepatic tissue (133 ± 35 particles), confirming their translocation. Exposure to PPS-MPs increased superoxide dismutase (SOD) (2.58-fold) and catalase (CAT) activity (1.36-fold), while reducing protein sulfhydryl levels (PSH) (0.35-fold), indicating oxidative stress. Histological analysis and quantitative assessment revealed significant alterations, including a significant decrease in glycogen content (2.4- fold). Immunofluorescence analysis showed a pronounced increase in α-tubulin and a decrease in DAAM-1 signals, a formin protein essential for actin filament assembly and cytoskeletal organization, suggesting impaired cytoskeletal dynamics. These observations were further supported by molecular analyses, which showed α-tubulin overexpression (3.35-fold) and reduced DAAM-1 expression (0.5-fold).

Conclusion

Our findings indicate that exposure to environmentally relevant concentrations of MPs induces early hepatocellular alterations, suggesting that oxidative stress and cytoskeletal remodeling may be central mechanisms underlying MP-induced hepatotoxicity.