Polystyrene microplastics (PS-MPs) disturb skeleto-muscular energy metabolism and tissue architecture following...

Polystyrene microplastic (PS-MP), known as a white pollutant, exhibited adverse effects on aquatic and terrestrial animals. The present study aims to evaluate the dose-dependent effect of polystyrene microplastics on skeletal muscle energy metabolism in Wistar rats. PS-MP was administered orally in Wistar rats at doses of 0.5 mg/L, 5 mg/L, and 50 mg/L in drinking water for 28 days daily. After the treatment, metabolic profile and tissue histological analyses were performed. Average food consumption by the treated rats was decreased by PS-MPs. Glycogen and pyruvate contents were depleted in a dose-responsive fashion. Lactate dehydrogenase and transaminase activities were decreased by PS-MP exposure. Free amino nitrogen was mobilized from blood to skeletal muscle in response to stress. Protein content depleted in the muscular tissue whereas enhanced carbonylated protein formation. Pronase and cathepsin activities were increased by PS-MP. Inhibited TCA cycle enzyme activities were observed in the target tissue. Moreover, muscle hypertrophy, nuclear migration, and fibrillation were seen in histological sections. Decreased food consumption by PS-MP exposure could promote glucose scarcity in blood. Depletion of muscular glycogen may result from increased glycogenolysis to replenish loss of blood glucose. Reduction in pyruvate content may result from decreased glycolysis which could perturb the lactate dehydrogenase function. Lack of transaminase in the target tissue was indicative of tissue damage. Muscular protein breakdown might be due to oxidative denaturation of native proteins as well as increased proteolysis. Due to less pyruvate production, the TCA cycle enzyme functions were suppressed. Histopathological studies established significant degenerative changes in muscular morphology following PS-MP exposure. The present study suggests that PS-MP perturbed skeleto-muscular energy metabolism and promoted muscle fiber degeneration following sub-acute exposure.