Modulation of copper-induced neurotoxicity by monoisoamyl 2,3-dimercaptosuccinic acid loaded nanoparticles through inhibition of mitophagy and reduction of oxidative stress in SH-SY5Y cells
Copper (Cu2 +) dysregulation, often stemming from ATP7B gene mutations, exacerbates neurological disorders like Huntington’s, Alzheimer’s, and Parkinson's diseases. Monoisoamyl 2,3-dimercaptosuccinic acid (MiADMSA) shows promise in mitigating Cu2+ induced neurotoxicity by chelating intracellula...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-06-01
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| Series: | Toxicology Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2214750024002579 |
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| Summary: | Copper (Cu2 +) dysregulation, often stemming from ATP7B gene mutations, exacerbates neurological disorders like Huntington’s, Alzheimer’s, and Parkinson's diseases. Monoisoamyl 2,3-dimercaptosuccinic acid (MiADMSA) shows promise in mitigating Cu2+ induced neurotoxicity by chelating intracellular Cu2+ ions, reducing oxidative stress, and restoring antioxidant enzyme function. However, challenges such as poor bioavailability hinder its therapeutic efficacy. Nano-delivery systems offer a solution by improving MiADMSA's solubility, stability, and targeted delivery, potentially minimizing off-target effects. In this study, MiADMSA was loaded into a polymer conjugated with lipoic acid (LA) and human serum albumin (HSA) using a coacervation crosslinking method. The prepared nanoparticles were optimized using a Box-Behnken design. Evaluation in SH-SY5Y cells revealed promising neuroprotective effects against Cu2+ induced neurotoxicity, highlighting the potential of MiADMSA-loaded nanocarriers as a therapeutic strategy for neurodegenerative diseases associated with metal dysregulation. |
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| ISSN: | 2214-7500 |