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Microplastic pollution: A potent threat for metabolic disruption in mammals
Summary
This review examines the evidence linking microplastic exposure to metabolic disruption, covering mechanisms by which microplastics and their associated chemical additives may interfere with hormonal regulation, glucose metabolism, and lipid homeostasis. The authors identify microplastics as a potent emerging threat to metabolic health.
Polystyrene (PS) is one of the major primary microplastics that are factory-made and widely used as consumer goods, insulation materials, and equipment used in information technology. Animals are exposed to PS via freshwater, marine water, drinking water, food, and atmosphere, as well as via agroecosystems due to their low density, strong durability, and small size characteristics. Several health problems are caused by polystyrene, such as neurotoxicity, digestive disorders, reproductive dysfunction, immunotoxicity, genotoxicity, and oxidative damage in marine creatures. Sub-acute oral exposure to different doses of polystyrene microplastic (PS-MP) in male Wistar rats stimulated glycogenolysis in skeletal muscle as evidenced by depletion of tissue glycogen. Pyruvic acid in the kidney and skeletal muscle was reduced in a dose-dependent fashion after PS-MP exposure. Free amino nitrogen was significantly increased in muscle, whereas it decreased in the kidney. The LDH function was compromised in skeletal muscle whereas enhanced in the kidney following PS-MP exposure. Glucose 6-phosphatase and succinate dehydrogenase activities were stimulated in the kidneys of the PS-MP-exposed rats, whereas transaminase activities were deceased in both kidney and skeletal muscle after polystyrene exposure. It is submitted that sub-acute polystyrene exposure significantly altered glucose metabolism in renal and skeletal muscle by decreasing glycolysis, as well as by stimulating the TCA cycle and gluconeogenic activities in the renal tissue of rats. Metabolic adjustment was made differentially in skeletal muscle and kidney of exposed animals in accordance with dose-dependent alteration of biochemical and enzymatic parameters.