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Evaluation of the hepatorenal subacute toxicity of polystyrene nanoplastics on immunohistochemical, histopathological, endoplasmic reticulum stress, and biochemical changes: The protective role of ellagic acid
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Researchers demonstrated that 28-day oral exposure to polystyrene nanoplastics in rats caused liver and kidney toxicity—marked by elevated oxidative stress, inflammation, endoplasmic reticulum stress, and histopathological damage—and that co-administration of the antioxidant ellagic acid significantly attenuated these harmful effects.
Plastic products are widely used for a variety of purposes. Therefore, exposure to polystyrene nanoplastics (PS-NPs) products may affect the biological systems of humans and other organisms. Ellagic acid (EA) is a naturally occurring flavonoid compound that exhibits antioxidant activities. This study investigated the potential harmful effects of PS-NPs on the liver and kidney, and to determine the molecular and cellular mechanisms related with exposure to PS-NPs 24 male rats were divided randomly and equally into 4 groups; control (distilled water), PS-NPs (15 mg/kg/day) exposed group, EA (35 mg/kg/day) exposed group and PS-NPs plus EA exposed group via orally using gavage for 28 days. The application of PS-NPs for 28 days led to a decrease in Nrf2 levels and the antioxidant content (SOD, CAT, GPx, and GST) liver and kidney tissues, while the MDA level, which is an indicator of cellular lipid peroxidation, increased. Additionally, changes were observed in serum indicators such as ALT, AST, LDH, urea and creatinine. Similarly, 8-OHdG, NF-κB, IL-1β levels, TNF-α and caspase-3 expression increased. Histopathological changes were observed in liver and kidney tissues, along with an increase in ER stress (HSP70, HSP90, GRP78, PERK, and CHOP). The combination of EA treatment and PS-NPs led to a reduction in PS-NPs-induced hepatic and renal toxicity and an enhancement in the parameters that were investigated.
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Researchers orally exposed Wistar rats to polystyrene nanoplastics at multiple doses for five weeks and observed dose-dependent increases in oxidative stress. The study found significant alterations in liver and kidney function markers, disrupted energy metabolism, and changes in antioxidant enzyme activity, suggesting that nanoplastic exposure may affect multiple organ systems in mammals.
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Researchers exposed Wistar rats to polystyrene nanoplastics and found significant kidney damage mediated through endoplasmic reticulum stress, marked by elevated oxidative stress markers, histopathological abnormalities, and upregulation of ER stress proteins GRP78, CHOP, and caspase-12 — damage that was substantially reduced by co-administration of the antioxidant edaravone.
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Exposure to polystyrene nanoplastics caused significant liver damage in rats, including oxidative stress, inflammation, and cell death, along with elevated liver enzymes that are markers of liver injury in clinical settings. Treatment with sinensetin — a natural plant flavonoid — substantially reversed these effects, restoring antioxidant enzyme activity and reducing inflammatory markers. The findings establish a potential protective role for natural compounds against nanoplastic-induced organ toxicity and illuminate the mechanisms by which nanoplastics harm the liver.
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