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Vitamin D3 Neuroprotection Against Rotenone and MPTP in SH-SY5Y Cells
Ekramy M Elmorsy1, Ayat B Al-Ghafari2,3, Huda A Al Doghaither2
1Center for Health Research, Northern Border University, Arar, Saudi Arabia.
Basic & Clinical Pharmacology & Toxicology
|May 4, 2026
Summary
Active vitamin D3 protects against rotenone (RO) and MPTP neurotoxicity in human neuroblastoma cells. Vitamin D3 preserves mitochondrial function, reduces oxidative stress, and maintains neurochemical balance, suggesting therapeutic potential for neurological disorders.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Environmental neurotoxicants like rotenone (RO) and MPTP induce cytotoxicity in neural cells.
- Neurodegenerative diseases are often linked to mitochondrial dysfunction and oxidative stress.
Purpose of the Study:
- To investigate the neuroprotective effects of active vitamin D3 against RO- and MPTP-induced cytotoxicity.
- To elucidate the mechanisms underlying vitamin D3's neuroprotective actions in SH-SY5Y cells.
Main Methods:
- Exposure of undifferentiated human neuroblastoma (SH-SY5Y) cells to RO and MPTP.
- Assessment of cell viability, noradrenaline turnover, and acetylcholinesterase activity.
- Analysis of cellular bioenergetics (ATP levels, mitochondrial function, lactate), oxidative stress markers (ROS, lipid peroxidation, CAT activity), and gene expression (CAMK2A, CAMK2B).
Main Results:
- RO and MPTP exposure reduced cell viability and disrupted neurochemical balance.
- Vitamin D3 cotreatment significantly mitigated neurotoxin-induced cytotoxicity and neurochemical alterations.
- Vitamin D3 preserved mitochondrial function, reduced oxidative stress, and counteracted neurodevelopmental gene upregulation.
Conclusions:
- Vitamin D3 confers significant neuroprotection against RO- and MPTP toxicity in SH-SY5Y cells.
- Neuroprotection is mediated by modulating mitochondrial function, oxidative stress, and neurochemical balance.
- Vitamin D3 shows potential for preventing or treating neurological disorders associated with mitochondrial dysfunction and oxidative damage.
