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<p>Copper oxide nanoparticles (CuO-NPs) are known to trigger systemic toxicity through the disruption of copper homeostasis and the generation of profound oxidative stress. Given their widespread&#xa0;industrial applications, concerns&#xa0;persist&#xa0;regarding environmental and human exposure. This cascade of molecular injury drives multi-organ damage, immune suppression, and genomic instability. To address this&#xa0;concern, the present study systematically evaluates the potential of engineered curcumin nanoparticles (Cur-NPs) against CuO-NPs-induced toxicity in a rodent model as a proof of principle.&#xa0;Sixty adult male Sprague–Dawley rats were randomized into five experimental groups: control, vehicle (corn oil), CuO-NPs (50 mg/kg), Cur-NPs (50 mg/kg), and CuO-NPs + Cur-NPs co-treatment, administered orally for 30 days. Toxicological endpoints included oxidative stress biomarkers, immune functional assays (total leukocyte count, phagocytic index), regulation of apoptotic pathways (Bax/Bcl-2 ratio, caspase-3 activity), DNA integrity via the alkaline comet assay, and detailed histopathological examination of the liver, kidneys, and spleen. Exposure to CuO-NPs alone triggered severe oxidative damage, marked immunosuppression, a pro-apoptotic imbalance, and significant hepatic DNA fragmentation. Histopathology confirmed systemic injury, including hepatic necrosis, renal tubular degeneration, and splenic lymphoid depletion. Co-treatment with Cur-NPs significantly mitigated these effects, restoring antioxidant defences, immune competence, and apoptotic balance, while reducing DNA damage and tissue pathology. Cur-NPs alone maintained profiles comparable to controls, confirming their safety. Collectively, these findings&#xa0;reveal&#xa0;that Cur-NPs confer potent protection primarily by re-establishing redox&#xa0;homeostasis&#xa0;and modulating critical immune and apoptotic pathways, with copper chelation representing a proposed but unconfirmed contributory mechanism. This study provides a strong rationale for a plant-based, nanomaterial-enabled intervention to systemically protect against engineered nanomaterial toxicity in&#xa0;occupational settings, offering a foundation for developing exposure mitigation strategies.</p>

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Curcumin nanoparticles attenuate copper nanoparticle-induced systemic toxicity in rats: a proof-of-concept study for a systemic protective strategy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月28日

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  • Asmaa S. Morsi,
  • Hager M. Ramadan,
  • Ahmed M. Youssef,
  • Nadia A. Taha

摘要

Copper oxide nanoparticles (CuO-NPs) are known to trigger systemic toxicity through the disruption of copper homeostasis and the generation of profound oxidative stress. Given their widespread industrial applications, concerns persist regarding environmental and human exposure. This cascade of molecular injury drives multi-organ damage, immune suppression, and genomic instability. To address this concern, the present study systematically evaluates the potential of engineered curcumin nanoparticles (Cur-NPs) against CuO-NPs-induced toxicity in a rodent model as a proof of principle. Sixty adult male Sprague–Dawley rats were randomized into five experimental groups: control, vehicle (corn oil), CuO-NPs (50 mg/kg), Cur-NPs (50 mg/kg), and CuO-NPs + Cur-NPs co-treatment, administered orally for 30 days. Toxicological endpoints included oxidative stress biomarkers, immune functional assays (total leukocyte count, phagocytic index), regulation of apoptotic pathways (Bax/Bcl-2 ratio, caspase-3 activity), DNA integrity via the alkaline comet assay, and detailed histopathological examination of the liver, kidneys, and spleen. Exposure to CuO-NPs alone triggered severe oxidative damage, marked immunosuppression, a pro-apoptotic imbalance, and significant hepatic DNA fragmentation. Histopathology confirmed systemic injury, including hepatic necrosis, renal tubular degeneration, and splenic lymphoid depletion. Co-treatment with Cur-NPs significantly mitigated these effects, restoring antioxidant defences, immune competence, and apoptotic balance, while reducing DNA damage and tissue pathology. Cur-NPs alone maintained profiles comparable to controls, confirming their safety. Collectively, these findings reveal that Cur-NPs confer potent protection primarily by re-establishing redox homeostasis and modulating critical immune and apoptotic pathways, with copper chelation representing a proposed but unconfirmed contributory mechanism. This study provides a strong rationale for a plant-based, nanomaterial-enabled intervention to systemically protect against engineered nanomaterial toxicity in occupational settings, offering a foundation for developing exposure mitigation strategies.