Related Experiment Video
Updated: Jan 20, 2026
Analyzing Mitochondrial Transport and Morphology in Human Induced Pluripotent Stem Cell-Derived Neurons in Hereditary Spastic Paraplegia
Published on: February 9, 2020
Effect of trehalose on manganese-induced mitochondrial dysfunction and neuronal cell damage in mice
Kuan Liu1, Meng-Jiao Jing1, Chang Liu1
1Department of Environmental Health, School of Public Health, China Medical University, Shenyang, China.
Abstract:
Chronic overexposure to manganese (Mn) has been verified to induce mitochondrial dysfunction, which is related to oxidative damage. The autophagic-lysosomal degradation pathway plays a vital role in the removal of impaired mitochondria through a specific quality control mechanism termed mitophagy. However, trehalose functions as an inducer of autophagy by an mTOR-independent mechanism, and little data report its effect on Mn-induced mitochondrial dysfunction. To explore the possibility that trehalose could be effective in interfering with the Mn-induced mitochondrial dysfunction, we used trehalose (2% and 4% (g/vol (mL))) in a mouse model of manganism. Our data showed that mice developed weary motor and behavioural deficits after exposure to Mn for 6 weeks. Overexposure to Mn resulted in mitochondrial dysfunction and neuronal cell damage in the basal nuclei of mice, which could be ameliorated by trehalose pre-treatment. Moreover, our results indicated that trehalose pre-treatment significantly reduced the oxidative damage and enhanced the activation of mitophagy. The findings clearly demonstrated that trehalose could relieve Mn-induced mitochondrial and neuronal cell damage through its antioxidative and mitophagy-inducing effects.
Insights
Trehalose treatment ameliorates manganese-induced mitochondrial dysfunction and neuronal damage in mice. This study shows trehalose enhances mitophagy and reduces oxidative stress, offering a potential therapeutic strategy for manganism.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Chronic manganese (Mn) overexposure causes mitochondrial dysfunction and oxidative damage.
- Mitophagy, a key cellular process, removes damaged mitochondria.
- Trehalose induces autophagy via an mTOR-independent pathway, but its role in Mn-induced damage is unclear.
Purpose of the Study:
- To investigate trehalose's efficacy in mitigating Mn-induced mitochondrial dysfunction and neuronal damage.
- To explore trehalose's effects on oxidative stress and mitophagy in a mouse model of manganism.
Main Methods:
- Mice were exposed to manganese for 6 weeks.
- Trehalose (2% and 4%) was administered as a pre-treatment.
- Mitochondrial function, neuronal damage, oxidative stress, and mitophagy were assessed.
Main Results:
- Manganese exposure induced motor and behavioral deficits, mitochondrial dysfunction, and neuronal damage.
- Trehalose pre-treatment ameliorated these deficits and damage.
- Trehalose significantly reduced oxidative damage and enhanced mitophagy activation.
Conclusions:
- Trehalose effectively relieves manganese-induced mitochondrial and neuronal cell damage.
- Its therapeutic effects are attributed to antioxidative properties and mitophagy induction.
- Trehalose presents a potential intervention for manganism.
Related Concept Videos
07:32Analyzing Mitochondrial Transport and Morphology in Human Induced Pluripotent Stem Cell-Derived Neurons in Hereditary Spastic Paraplegia
04:25A Mice Model of Chlorhexidine Gluconate-Induced Peritoneal Damage
06:05An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model
09:02Manganese Oxide Nanoparticle Synthesis by Thermal Decomposition of Manganese(II) Acetylacetonate
08:48Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models
10:00Assaying DNA Damage in Hippocampal Neurons Using the Comet Assay