Dose- and time-dependent polystyrene microplastic exposure alters brain metabolic markers and behavior in male Wistar rats

Abstract

Background: As plastic production increased, researchers have continued to focus on the health effects of microplastics (MPs). Energy depletion and bioenergetics alterations caused by MPs could negatively affect cognition and lead to neurodegenerative diseases. The current study aims to assess metabolic parameters in the cerebral cortex and cerebellum across various doses and time points spanning sub-acute to sub-chronic periods. Materials and Methods: Rat brain metabolism was evaluated after oral exposure to polystyrene microplastics (PS-MPs) at three doses (0.5, 5, and 50 mg/L) for 28, 56, and 84 days. Results: Blood glucose was significantly decreased in the treated groups at all time points. Enhanced lactate dehydrogenase (LDH) activity in the cerebral cortex with shorter durations was reversed with longer exposure. Pyruvate depletion was observed in the PS-MPs-treated cerebral cortex, whereas enhanced pyruvate levels were found in the cerebellum. Decreased cerebral free amino nitrogen (FAN) was observed at the lowest dose after 28 days, whereas FAN increased in other doses and durations. The cerebral GOT activity was enhanced at the middle and high doses after 28 days, but decreased after longer exposures. However, cerebral GPT activity was stimulated after 8 and 12 weeks of treatment. The FAN content was elevated among different doses and durations in the cerebellum. Cerebellar transaminase functions were reduced after PS-MPs treatment. Discussion: The study indicates that PS-MPs induce hypoglycemia. In the cerebral cortex, reduced glycolysis was associated with increased glycolysis in the cerebellum. Additionally, behavioral studies indicate that rats treated with PS-MPs exhibited greater curiosity and exploratory behavior at 56 and 84 days after exposure to middle and high doses. The study suggests that the effects of PS-MPs on brain metabolic markers and resulting behavioral changes depend on treatment duration and dose, acting in a dose-dependent manner and leading to differential alterations in cerebral and cerebellar metabolism.