Dual-action selenium nanodrugs confer synergistic protection against Parkinson’s Disease via mitochondrial-targeted antioxidant therapy and selenoprotein p-mediated selenium mobilization

Mitochondrial dysfunction, primarily induced by oxidative stress, triggers excessive reactive oxygen species (ROS) production. This cascade results in ATP depletion, the opening of mitochondrial permeability transition pores, and a consequent cytokine surge. These pathological events ultimately lead to the loss of dopaminergic neurons and α-synuclein accumulation, both of which are key factors in the pathogenesis and progression of Parkinson’s disease (PD). However, achieving a synergistic strategy that combines potent exogenous ROS scavenging with activation of endogenous antioxidant defenses has remained challenging. Here, we introduce glutathione (GSH)–modified selenium nanoparticles (G-Se NPs) that specifically eliminate bursts of neuronal mitochondrial ROS (mtROS) while simultaneously upregulating selenoprotein P (SelP) to strengthen intrinsic antioxidant capacity. On the one hand, G-Se NPs directly remove excess ROS through multi-enzymatic activity; on the other hand, they accumulate in the liver to promoting SelP synthesis. Notably, SelP can cross the blood-brain barrier, making it the principal transporter for delivering selenium to the brain, thereby initiating endogenous antioxidant pathways and conferring robust overall antioxidant effects. Consequently, G-Se NPs protect mitochondria, reverse neuroinflammation, and inhibit neuronal apoptosis. Across cell, nematode, and mouse PD models, G-Se NPs produced restoring dopaminergic neuron counts by 87.5% and extending lifespan in nematodes by 22 days, with an ultralow dose (1.5 mg/kg) sufficient to reverse behavioral disorders, noting that G-Se NPs are safe and well tolerated at therapeutic doses. This exogenous–endogenous synergy—combining nanoparticle-mediated ROS clearance with SelP-driven antioxidant amplification—signals a paradigm shift in PD nanotherapy, advancing from symptomatic relief toward modification of disease progression and supporting their promise as a safe, translatable PD nanotherapy.

Authors

Institutions

Publication Details

Journal
Advanced Composites and Hybrid Materials
Published
2026-04-25
DOI
https://doi.org/10.1007/s42114-026-01809-4
Primary Topic
Selenium in Biological Systems
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Dual-action selenium nanodrugs confer synergistic protection against Parkinson’s Disease via mitochondrial-targeted antioxidant therapy and selenoprotein p-mediated selenium mobilization

C Zhang, Yongsheng Huang, Xincheng Long, Qiuxia Tu et al.
Advanced Composites and Hybrid Materials
Selenium in Biological Systems
article

Dual-action selenium nanodrugs confer synergistic protection against Parkinson’s Disease via mitochondrial-targeted antioxidant therapy and selenoprotein p-mediated selenium mobilization

C Zhang, Yongsheng Huang, Xincheng Long, Qiuxia Tu, Lingli Song, Qihang Ao, Li Lei, Lei Tang, Shengkai Li, Jiaojiao Wang, Haijun Yu, Wen Zheng, Qian Zheng
article en

Abstract

Mitochondrial dysfunction, primarily induced by oxidative stress, triggers excessive reactive oxygen species (ROS) production. This cascade results in ATP depletion, the opening of mitochondrial permeability transition pores, and a consequent cytokine surge. These pathological events ultimately lead to the loss of dopaminergic neurons and α-synuclein accumulation, both of which are key factors in the pathogenesis and progression of Parkinson’s disease (PD). However, achieving a synergistic strategy that combines potent exogenous ROS scavenging with activation of endogenous antioxidant defenses has remained challenging. Here, we introduce glutathione (GSH)–modified selenium nanoparticles (G-Se NPs) that specifically eliminate bursts of neuronal mitochondrial ROS (mtROS) while simultaneously upregulating selenoprotein P (SelP) to strengthen intrinsic antioxidant capacity. On the one hand, G-Se NPs directly remove excess ROS through multi-enzymatic activity; on the other hand, they accumulate in the liver to promoting SelP synthesis. Notably, SelP can cross the blood-brain barrier, making it the principal transporter for delivering selenium to the brain, thereby initiating endogenous antioxidant pathways and conferring robust overall antioxidant effects. Consequently, G-Se NPs protect mitochondria, reverse neuroinflammation, and inhibit neuronal apoptosis. Across cell, nematode, and mouse PD models, G-Se NPs produced restoring dopaminergic neuron counts by 87.5% and extending lifespan in nematodes by 22 days, with an ultralow dose (1.5 mg/kg) sufficient to reverse behavioral disorders, noting that G-Se NPs are safe and well tolerated at therapeutic doses. This exogenous–endogenous synergy—combining nanoparticle-mediated ROS clearance with SelP-driven antioxidant amplification—signals a paradigm shift in PD nanotherapy, advancing from symptomatic relief toward modification of disease progression and supporting their promise as a safe, translatable PD nanotherapy.

Advanced Composites and Hybrid Materials
Guiyang Medical University (CN), Chinese Academy of Sciences (CN), Affiliated Hospital of Guizhou Medical University (CN), Shanghai Institute of Materia Medica (CN)
National Natural Science Foundation of China
Openalex Percentile: Top 7%
Selenium in Biological Systems
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.